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Sample records for anti-helicobacter pylori activity

  1. Screening test for anti-Helicobacter pylori activity of traditional Chinese herbal medicines

    Institute of Scientific and Technical Information of China (English)

    2010-01-01

    AIM:To evaluate the anti-Helicobacter pylori (H.pylori) activity of 50 traditional Chinese herbal medicines in order to provide the primary evidence for their use in clinical practice.METHODS:A susceptibility test of water extract from 50 selected traditional Chinese herbal medicines for in vitro H.pylori Sydney strain 1 was performed with broth dilution method.Anti-H.pylori activity of the selected Chinese herbal medicines was evaluated according to their minimum inhibitory concentration (MIC).RESULTS:The ...

  2. In vitro evaluation of Bacopa monniera on anti-Helicobacter pylori activity and accumulation of prostaglandins.

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    Goel, R K; Sairam, K; Babu, M Dora; Tavares, I A; Raman, A

    2003-01-01

    Bacopa monniera is an Indian tratidional medicine widely used to improve intellectual functions. Earlier, we had reported the prophylactic and curative effects of standardized extract of Bacopa monniera (BME) in various gastric ulcer models. The effect was due to augmentation of the defensive mucosal factors like increase in mucin secretion, life span of mucosal cells and gastric antioxidant effect rather than on the offensive acid-pepsin secretion. The present study includes evaluation of standardized BME (bacoside A content--35.5 +/- 0.9) on other contributing factors towards ulcerogenesis. BME in the dose of 1000 microg/ml showed anti-Helicobacter pylori activity in vitrol and in the dose of 10 microg/ml increased in vitro of prostanoids (PGE and PGI2) in human colonic mucosal incubates. It may be concluded that these factors may contribute to antiulcerogenic activity of BME.

  3. Preparation, characterization, and anti-Helicobacter pylori activity of Bi3+-Hericium erinaceus polysaccharide complex.

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    Zhu, Yang; Chen, Yao; Li, Qian; Zhao, Ting; Zhang, Ming; Feng, Weiwei; Takase, Mohammed; Wu, Xueshan; Zhou, Zhaoxiang; Yang, Liuqing; Wu, Xiangyang

    2014-09-22

    Two new Bi3+-Hericium erinaceus polysaccharide (BiHEP) complexes were prepared using Bi3+ and two purified polysaccharides from H. erinaceus (HEPs), respectively. The complexes were characterized by elemental analysis, FT-IR, CD, SEM, AFM, XRD, and TG. The anti-Helicobacter pylori (Hp) activities in vitro by agar dilution assay of the complexes were evaluated. The molecular weights of HEPs were 197 and 20 kDa, respectively. All the analyses confirmed the formation of new BiHEP complexes with lower content of Bi3+ compared with colloidal bismuth subcitrate (CBS), the most utilized bismuth preparation clinically. Furthermore, HEPs themselves have definite inhibition effects on Hp, and BiHEP complexes have lower content of Bi exhibited strong inhibition effects on Hp (MIC=20 μg/mL), similar to that of CBS with higher content of Bi. The study provides a basis for further development of multiple treatments of Hp infection or new medicines.

  4. In vitro and In vivo Anti-Helicobacter pylori Activities of Centella asiatica Leaf Extract

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    Zheng, Hong-Mei; Choi, Myung-Joo; Kim, Jae Min; Lee, Kye Wan; Park, Yu Hwa; Lee, Don Haeng

    2016-01-01

    Helicobacter pylori infection is associated with an increased risk of developing upper gastrointestinal tract diseases. However, treatment failure is a major cause of concern mainly due to possible recurrence of infection, the side effects, and resistance to antibiotics. The aim of this study was to investigate the activities of Centella asiatica leaf extract (CAE) against H. pylori both in vitro and in vivo. The minimum inhibitory concentrations (MICs) against 55 clinically isolated strains of H. pylori were tested using an agar dilution method. The MICs of CAE ranged from 0.125 mg/mL to 8 mg/mL, effectiveness in inhibiting H. pylori growth was 2 mg/mL. The anti-H. pylori effects of CAE in vivo were also examined in H. pylori-infected C57BL/6 mice. CAE was orally administrated once daily for 3 weeks at doses of 50 mg/kg and 250 mg/kg. CAE at the 50 mg/kg dose significantly reduced H. pylori colonization in mice gastric mucosa. Our study provides novel insights into the therapeutic effects of CAE against H. pylori infection, and it suggests that CAE may be useful as an alternative therapy. PMID:27752495

  5. Anti-Helicobacter pylori activity and immunostimulatory effect of extracts from Byrsonima crassa Nied. (Malpighiaceae

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    Vilegas Wagner

    2009-01-01

    Full Text Available Abstract Background Several in vitro studies have looked at the effect of medicinal plant extracts against Helicobacter pylori (H. pylori. Regardless of the popular use of Byrsonima crassa (B. crassa as antiemetic, diuretic, febrifuge, to treat diarrhea, gastritis and ulcers, there is no data on its effects against H. pylori. In this study, we evaluated the anti-H. pylori of B. crassa leaves extracts and its effects on reactive oxygen/nitrogen intermediates induction by murine peritoneal macrophages. Methods The minimal inhibitory concentration (MIC was determined by broth microdilution method and the production of hydrogen peroxide (H2O2 and nitric oxide (NO by the horseradish peroxidase-dependent oxidation of phenol red and Griess reaction, respectively. Results The methanolic (MeOH and chloroformic (CHCl3 extracts inhibit, in vitro, the growth of H. pylori with MIC value of 1024 μg/ml. The MeOH extract induced the production H2O2 and NO, but CHCl3 extract only NO. Conclusion Based in our results, B. crassa can be considered a source of compounds with anti-H. pylori activity, but its use should be done with caution in treatment of the gastritis and peptic ulcers, since the reactive oxygen/nitrogen intermediates are involved in the pathogenesis of gastric mucosal injury induced by ulcerogenic agents and H. pylori infections.

  6. Anti-Helicobacter pylori activity of plant extracts traditionally used for the treatment of gastrointestinal disorders

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    Laura Lúcia Cogo

    2010-06-01

    Full Text Available The antibacterial activity of plant extracts obtained from Bixa orellana L., Chamomilla recutita L., Ilex paraguariensis A. St.-Hil., Malva sylvestris L., Plantago major L. and Rheum rhaponticum L. has been evaluated against two reference strains and eleven clinical isolates of Helicobacter pylori. All the plant species chosen are used in popular Brazilian cuisine and folk medicine in the treatment of gastrointestinal disorders. Initial screening was made by the disk diffusion test and then minimum inhibitory concentration was determined by the agar dilution method. The results presented in this work demonstrated that among the plant preparations analyzed, B. orellana L., C. recutita L., I. paraguariensis A. St.-Hil. and M. sylvestris L. were capable of inhibiting the in vitro growth of H. pylori.

  7. Anti-Helicobacter pylori activity of plant extracts traditionally used for the treatment of gastrointestinal disorders.

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    Cogo, Laura Lúcia; Monteiro, Cristina Leise Bastos; Miguel, Marilis Dallarmi; Miguel, Obdulio Gomes; Cunico, Miriam Machado; Ribeiro, Marcelo Lima; de Camargo, Eloá Ramalho; Kussen, Gislene Maria Botão; Nogueira, Keite da Silva; Costa, Libera Maria Dalla

    2010-04-01

    The antibacterial activity of plant extracts obtained from Bixa orellana L., Chamomilla recutita L., Ilex paraguariensis A. St.-Hil., Malva sylvestris L., Plantago major L. and Rheum rhaponticum L. has been evaluated against two reference strains and eleven clinical isolates of Helicobacter pylori. All the plant species chosen are used in popular Brazilian cuisine and folk medicine in the treatment of gastrointestinal disorders. Initial screening was made by the disk diffusion test and then minimum inhibitory concentration was determined by the agar dilution method. The results presented in this work demonstrated that among the plant preparations analyzed, B. orellana L., C. recutita L., I. paraguariensis A. St.-Hil. and M. sylvestris L. were capable of inhibiting the in vitro growth of H. pylori.

  8. Mechanochemical synthesis and in vitro anti-Helicobacter pylori and uresase inhibitory activities of novel zinc(II)-famotidine complex.

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    Amin, Muhammad; Iqbal, Mohammad S; Hughes, Roy W; Khan, Safyan A; Reynolds, Paul A; Enne, Virve I; Sajjad-ur-Rahman; Mirza, Akmal S

    2010-06-01

    The mechanochemical synthesis and characterization of a zinc complex with famotidine is described. The complex was characterized by microanalysis and a number of spectroscopic techniques. The complex was of M:L dihydrate type. Derivatization of famotidine with zinc appears to enhance the activity of the drug by inhibiting the growth of Helicobacter pylori (two reference and 34 clinical isolates). The complex inhibited the growth of H. pylori in an MIC range of 1-8 microg mL(-1). The anti-H. pylori activity of the zinc-famotidine complex against antibiotic-resistant strains was nearly comparable to that of antibiotic-susceptible strains. The complex was found to be far less toxic than the parent drug, as demonstrated by its higher LD(50) value. In the human urease enzyme inhibition assay the complex exhibited significant inhibition. The new complex appears to be more useful in eradicating both the antibiotic-susceptible and antibiotic-resistant strains of H. pylori.

  9. Preliminary Phytochemical Screening and In Vitro Anti-Helicobacter pylori Activity of Extracts of the Stem Bark of Bridelia micrantha (Hochst., Baill., Euphorbiaceae

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    Pascal O. Bessong

    2011-07-01

    Full Text Available Helicobacter pylori is a major risk factor for gastritis, ulcers and gastric cancer. This study was aimed to determine the antimicrobial activity of the stem bark of Bridelia. micrantha on H. pylori isolated in South Africa. Extracts and clarithromycin were tested against 31 clinical strains, including a standard strain (NCTC 11638 of H. pylori, by measuring the diameters of the corresponding inhibition zones, followed by determination of the Minimum Inhibitory Concentration (MIC (using metronidazole, and amoxicillin as control antibiotics and the rate of kill. Preliminary phytochemical screening was also done. Inhibition zone diameters which ranged from 0–23 mm were observed for all five of the extracts and 0–35 mm for clarithromycin. Marked susceptibility of strains (100% was noted for the acetone extract (P < 0.05, followed by ethyl acetate extract (93.5%. The MIC50 values ranged from 0.0048 to 0.156 mg/mL for the ethyl acetate extract and 0.0048 to 0.313 mg/mL for the acetone extract. The MIC90 values ranged from 0.0048 to 2.5 mg/mL for the ethyl acetate extract and 0.078 to >0.625 mg/mL for the acetone extract, respectively. Insignificant statistical difference in potency was observed when comparing the crude ethyl acetate extract to metronidazole and amoxicillin (P > 0.05. Complete killing of strain PE430C by the ethyl acetate extract was observed at 0.1 mg/mL (2 × MIC and 0.2 mg/mL (4 × MIC at 66 and 72 h. For strain PE369C, 100% killing was observed at 0.1 mg/mL (2 × MIC in 66 and 72 h. The ethyl acetate extract could thus be a potential source of lead molecules for the design of new anti-Helicobacter pylori therapies as this study further confirmed the presence of phytochemicals including alkaloids, flavonoids, steroids, tannins and saponins.

  10. Anti-Helicobacter pylori therapy significantly reduces Helicobacter pylori-induced gastric mucosal damage in Mongolian gerbils

    Institute of Scientific and Technical Information of China (English)

    Chun-Chao Chang; Sheng-Hsuan Chen; Gi-Shih Lien; Yuarn-Jang Lee; Horng-Yuan Lou; Ching-Ruey Hsieh; Chia-Lang Fang; Shiann Pan

    2005-01-01

    AIM: To investigate the effectiveness of 4 d' anti-Helicobacter pyloritherapy on the H pylori-infected Mongolian gerbils based on physiological and pathological changes.METHODS: We used 6-wk-old male gerbils orally inoculated with H pylori (ATCC43504, 2x108 CFU/mL).Seven weeks after H pylori inoculation, the animals of study group received 4 d' anti-H pylori triple therapy (H pylorieradicated group). Seven days later, all animals of the H pylori-eradicated and control groups (H pylori-infected& H pylori-uninfected groups) were sacrificed. We examined gastric mucosal lesions macroscopically, studied gastritis microscopically and determined the stomach weight ratio, myeloperoxidase (MPO) activity and prostaglandin (PG) E2 level.RESULTS: The results showed that both macroscopic and histological gastric damages were significantly less in H pylori-eradicated group than H pylori-infected group.Stomach weight ratio, MPO activity and PGE2 levels were significantly higher in H pylori-infected group than those in the other two groups.CONCLUSION: Four days' anti-H pylori therapy was effective in the improvement of H pylori-induced gastric lesions in Mongolian gerbils.

  11. Anti-Helicobacter pylori activity and oxidative burst inhibition by the naphthoquinone 5-methoxy-3,4-dehydroxanthomegnin from Paepalanthus latipes

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    Rodrigo Rezende Kitagawa

    2012-02-01

    Full Text Available Helicobacter pylori is a bacterium recognized as the major cause of chronic gastritis and peptic ulcers. Infection by H. pylori induces inflammatory responses and pathological changes in the gastric microenvironment. The host Keywords: immune cells (especially neutrophils release inflammatory mediators and large 5-methoxy-3,4-dehydroxanthomegnin amounts of reactive oxygen species (ROS, which are associated with an increased Helicobacter pyloririsk of developing gastric cancer. In this study, we evaluated the anti-H. pylori and oxidative burst antioxidantactivitiesofa1,4-naphthoquinone-5-methoxy-3,4-dehydroxanthomegnin. Paepalanthus latipes The antimicrobial activity was assessed using a spectrophotometric microdilution technique, and antioxidant activity was assessed by noting the effect of 5-methoxy3,4-dehydroxanthomegnin on the neutrophil oxidative burst using luminol-and lucigenin-amplified chemiluminescence. The results showed that 5-methoxy-3,4dehydroxanthomegnin is a potent anti-H. pylori compound (MIC 64 µg/mL and MBC 128 µg/mL and a strong antioxidant. 5-Methoxy-3,4-dehydroxanthomegnin decreased luminol- and lucigenin-amplified chemiluminescence, with ED50 values of 1.58±0.09 µg/mL and 5.4±0.15 µg/mL, respectively, reflecting an inhibitory effect on the oxidative burst. These results indicate that 5-methoxy-3,4-dehydroxanthomegnin is a promising compound for the prevention and treatment of diseases caused by H. pylori infection, such as gastritis, peptic ulceration, and gastric cancer, because reactive oxygen intermediates are involved in the pathogenesis of gastric mucosal injury induced by H. pylori infections.

  12. Anti-Helicobacter pylori activity in vitro of chamomile flowers, coneflower herbs, peppermint leaves and thyme herbs – a preliminary report

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    Malm Anna

    2015-03-01

    Full Text Available Recently, several studies have been undertaken so as to develop more effective therapeutic approaches towards eradicating Helicobacter pylori. Among these is phytotherapy. The aim of this study was to investigate the activity in vitro of the plant extracts obtained from common herbs cultivated in the Lubelszczyzna region against the reference strain H. pylori ATCC 43504. Among these are thyme herbs, chamomile flowers, peppermint leaves and coneflower herbs. Herein, it was found that the MIC values of the assayed extracts were as follows: the extracts from coneflower herbs showed anti-H. pylori activity with MIC = 31.3-125 μg/ml; the extracts from chamomile flowers demonstrated MIC = 31.3-62.5 μg/ ml; the extracts from peppermint leaves had MIC = 15.6-250 μg/ml; and the extracts from thyme herbs revealed MIC = 15.6-62.5 μg/ml, depending on the solvent used. The most active were the extracts obtained with ethyl acetate or ethanol alcohol absolute 99.8%. These showing MIC within the range of 15.6-62.5 μg/ml, while the lowest activity was observed in case of the extract obtained with 70% aqueous ethanol. This last showing MIC within the range of 62.5-250 μg/ml. The MIC values of essential oil components were 15.6 μg/ml for bisabolol and menthol or 31.3 μg/ml for thymol. The obtained data indicate that the assayed herbs possessed promising anti-H. pylori bioactivity.

  13. In vitro and in vivo anti-Helicobacter pylori activities of FEMY-R7 composed of fucoidan and evening primrose extract.

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    Cai, Jingmei; Kim, Tae-Su; Jang, Ja Young; Kim, Jihyun; Shin, Kyungha; Lee, Sung-Pyo; Choi, Ehn-Kyoung; Kim, Sa-Hyun; Park, Min; Kim, Jong Bae; Kim, Yun-Bae

    2014-03-01

    Effects of FEMY-R7, composed of fucoidan and evening primrose extract, on the bacterial growth and intragastric infection of Helicobacter pylori as well as gastric secretion were investigated in comparison with a proton-pump inhibitor pantoprazole. For in vitro anti-bacterial activity test, H. pylori (1×10(8) CFU/mL) was incubated with a serially-diluted FEMY-R7 for 3 days. As a result, FEMY-R7 fully inhibited the bacterial growth at 100 µg/mL, which was determined to be a minimal inhibitory concentration. In addition, 6-hour incubation with H. pylori, FEMY-R7 inhibited urease activity in a concentration-dependent manner, showing a median inhibitory concentration of 1,500 µg/mL. In vivo elimination study, male C57BL/6 mice were infected with the bacteria by intragastric inoculation (5×10(9) CFU/mouse) 3 times at 2-day intervals, and simultaneously, orally treated twice a day with 10, 30 or 100 mg/kg FEMY-R7 for 7 days. In Campylobcter-like organism-detection test and bacterial identification, FEMY-R7 exerted a high bacteria-eliminating capacity at 30-100 mg/kg, comparably to 30 mg/kg pantoprazole. In contrast to a strong antacid activity of pantoprazole in a pylorus-ligation study, FEMY-R7 did not significantly affect gastric pH, free HCl, and total acidity, although it significantly decreased fluid volume at a low dose (10 mg/kg). The results indicate that FEMY-R7 eliminate H. pylori from gastric mucosa by directly killing the bacteria and preventing their adhesion and invasion, rather than by inhibiting gastric secretion or mucosal damage.

  14. A new look at anti-Helicobacter pylori therapy

    Institute of Scientific and Technical Information of China (English)

    Seng-Kee Chuah; Feng-Woei Tsay; Ping-I Hsu; Deng-Chyang Wu

    2011-01-01

    With the rising prevalence of antimicrobial resistance, the treatment success of standard triple therapy has recently declined to unacceptable levels (i.e., 80% or less) in most countries. Therefore, several treatment regimens have emerged to cure Helicobacter pylori (H .pylori)infection. Novel first-line anti-H. pylorii therapies in 2011 include sequential therapy, concomitant quadruple therapy, hybrid (dual-concomitant) therapy and bismuth-containing quadruple therapy. After the failure of standard triple therapy, a bismuth-containing quadruple therapy comprising a proton pump inhibitor (PPI), bismuth, tetracycline and metronidazole can be employed as rescue treatment. Recently, triple therapy combining a PPI, levofloxacin and amoxicillin has been proposed as an alternative to the standard rescue therapy. This salvage regimen can achieve a higher eradication rate than bismuth-containing quadruple therapy in some regions and has less adverse effects. The best second-line therapy for patients who fail to eradicate H. pylori with first-line therapies containing clarithromycin, amoxicillin and metronidazole is unclear. However, a levofloxacin-based triple therapy is an accepted rescue treatment. Most guidelines suggest that patients requiring third-line therapy should be referred to a medical center and treated according to the antibiotic susceptibility test. Nonetheless, an empirical therapy (such as levofloxacin-based or furazolidone-based therapies) can be employed to terminate H. pylorii infection if antimicrobial sensitivity data are unavailable.

  15. Does the antibody production ability affect the serum anti-Helicobacter pylori Ig G titer?

    Institute of Scientific and Technical Information of China (English)

    Hyun Ah Chung; Sun-Young Lee; Hee Won Moon; Jeong Hwan Kim; In-Kyung Sung; Hyung Seok Park; Chan Sup Shim; Hye Seung Han

    2016-01-01

    AIM: To investigate the relationship between serum titers of anti-Helicobacter pylori(H.pylori) immunoglobulin G(IgG) and hepatitis B virus surface antibody(HBsA b).METHODS: Korean adults were included whose samples had positive Giemsa staining on endoscopic biopsy and were studied in the hepatitis B virus surface antigen(HBsA g)/HBsA b serologic assay,pepsinogen(PG) assay,and H.pylori serologic test on the same day.Subjects were excluded if they were positive for HBs Ag,had a recent history of medication,or had other medical condition(s).We analyzed the effects of the following factors on serum titers of HBsA b and the anti-H.pylori IgG : Age,density of H.pylori infiltration in biopsy samples,serum concentrations of PG Ⅰ and PG Ⅱ,PG Ⅰ/Ⅱ ratio,and white blood cell count.RESULTS: Of 111 included subjects,74(66.7%) exhibited a positive HBsA b finding.The serum anti-H.pylori IgG titer did not correlate with the serum HBsA b titer(P = 0.185); however,it correlated with the degree of H.pylori infiltration on gastric biopsy(P < 0.001) and serum PG Ⅱ concentration(P = 0.042).According to the density of H.pylori infiltration on gastric biopsy,subjects could be subdivided into those with a marked(median: 3.95,range 0.82-4.00)(P = 0.458),moderate(median: 3.37,range 1.86-4.00),and mild H.pylori infiltrations(median: 2.39,range 0.36-4.00)(P < 0.001).Subjects with a marked H.pylori infiltration on gastric biopsy had the highest serological titer,whereas in subjects with moderate and mild H.pylori infiltrations titers were correspondingly lower(P < 0.001).After the successful eradication,significant decreases of the degree of H.pylori infiltration(P < 0.001),serum anti-H.pylori IgG titer(P < 0.001),and serum concentrations of PG I(P = 0.028) and PG Ⅱ(P = 0.028) were observed.CONCLUSION: The anti-H.pylori IgG assay can be used to estimate the burden of bacteria in immunocompetent hosts with H.pylori infection,regardless of the HBsA b titer after HBV vaccination.

  16. Anti-Helicobacter pylori activities of FEMY-R7 composed of fucoidan and evening primrose extract in mice and humans.

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    Kim, Tae-Su; Choi, Ehn-Kyoung; Kim, Jihyun; Shin, Kyungha; Lee, Sung-Pyo; Choi, Youngjin; Jeon, Joseph H; Kim, Yun-Bae

    2014-09-01

    Helicobacter pylori-eliminating effects of FEMY-R7, composed of fucoidan and evening primrose extract, were investigated in mice and humans. Male C57BL/6 mice were infected with the bacteria by intragastric inoculation (1×10(9) CFU/mouse) 3 times at 2-day intervals, and simultaneously, orally treated twice a day with 10 or 100 mg/kg FEMY-R7 for 2 weeks. In Campylobcter-like organism-detection test, FEMY-R7 markedly reduced the urease-positive reactivity. In a clinical sudy, human subjects, confirmed to be infected with Helicobacter pylori, were orally administered twice a day with a capsule containing 150 mg FEMY-R7 for 8 weeks. FEMY-R7 significantly decreased both the Delta over baseline-value in urea breath test and the serum pepsinogens I and II levels. The results indicate that FEMY-R7 not only eliminates H. pylori from gastric mucosa of animals and humans, but also improves gastric function.

  17. Chemical composition and anti-Helicobacter pylori effect of Satureja bachtiarica Bunge essential oil.

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    Falsafi, Tahereh; Moradi, Parisa; Mahboubi, Mohaddese; Rahimi, Ebrahim; Momtaz, Hassan; Hamedi, Behzhad

    2015-01-15

    Resistance of H. pylori strains to common antibiotics has been developed in different parts of the world and continues to increase. It is important to investigate the novel and efficient anti-H. pylori drugs, among which the plants would be suitable sources. Satureja bachtiarica Bunge is traditionally used as antimicrobial agent. In this study, we evaluated the antibacterial activity of S. bachtiarica Bunge essential oil against 10 clinical isolates of Helicobacter pylori by disc diffusion and agar dilution methods. The chemical composition of essential oil was analyzed by GC and GC-MS. Carvacrol (45.5%) and thymol (27.9%) were the primary constituents of oil, followed by p-cymene (4.4%), and γ-terpinene (4.0%). S. bachtiarica essential oil showed strong antibacterial activity against clinical isolates of H. pylori (17.6 ± 1.1 mm and 0.035 ± 0.13 μl/ml). Carvacrol, as the first main component, had a significant role in this effect, whereas in the presence of thymol, the antibacterial effect of carvacrol was reduced. Therefore, S. bachtiarica essential oil can be applied as an alternative agent for treatment of H. pylori infections. More studies would be required to better clarify its mechanism of action on H. pylori.

  18. Anti-helicobacter pylori effect of total alkaloids of sophora alopecuroides in vivo

    Institute of Scientific and Technical Information of China (English)

    Tian Aiping; Xu Ting; Liu Kaiyun; Zou Quanming; Yan Xiang

    2014-01-01

    Background Helicobacterpylori (H.pylori) infection could lead to most gastroduodenal diseases and is even identified as a carcinogen of gastric cancer.Total alkaloids of sophora alopecuroides (TASA) is widely used in herbal remedies to treat various infectious diseases,including stomach-associated diseases.This study is aimed at evaluating the antimicrobial activity of TASA on H.pylori-infected BALB/c mice mouse gastritis.Methods Totally 120 BALB/c mice were orally inoculated with H.pylori Bacterial liquid to construct BALB/c mice H.pylori infection gastritis animal model,after the model was successfully created.We randomly assigned 100 infected mice into 10 treatment groups,the first group (normal saline); the second group (bismuth pectin); the third group (omeprazole); the fourth group (TASA 2 mg/d); the fifth group (TASA 4 mg/d); the sixth group (TASA 5 mg/d); the seventh group (TASA + bismuth pectin); the eighth group (TASA + omeprazole); the ninth group (bismuth pectin + clarithromycin + metronidazole);the tenth group (omeprazole + clarithromycin + metronidazole),5 other non-infected mice as negative control.Mice were orally inoculated twice a day and 7 days continuously.Then the mice were killed 4 weeks after treatment,we used realtime PCR to detect 16sDNA of H.pylori to test both the colonization and the clearance mice of bacteria of each treatment.We applied hematoxylin and eosin (HE) staining and immunostaining of mice gastric mucosa to observe the general inflammation and related factors interleukin 8 (IL-8),cyclooxygenase 2 (COX-2),and nuclear factor-kappa B (NF-KB) expression change after treatments.Results Firstly,we ensured that after 6-week intragastric administration,the bacteria colonization reached an exceed peak which is far higher than positive threshold (P <0.001); secondly,after treatments,it is revealed that TASA combined with omeprazole or bismuth pectin showed promising antimicrobial activity against H.pylori as well as conventional

  19. Anti- Helicobacter pylori therapy followed by celecoxib on progression of gastric precancerous lesions

    Institute of Scientific and Technical Information of China (English)

    Li-Jing Zhang; Shi-Yan Wang; Xiao-Hui Huo; Zhen-Long Zhu; Jian-Kun Chu; Jin-Cheng Ma; Dong-Sheng Cui; Ping Gu; Zeng-Ren Zhao; Ming-Wei Wang; Jun Yu

    2009-01-01

    AIM:To evaluate whether celecoxib,a selective cyclooxygenase 2 (COX-2) inhibitor,could reduce the severity of gastric precancerous lesions following Helicobacter pylori (H pylori) eradication.METHODS:H pylori-eradicated patients with gastric precancerous lesions randomly received either celecoxib (n=30) or placebo (n=30) for up to 3 mo.COX-2 expression and activity was determined by immunostaining and prostaglandin E2 (PGE2) assay,cell proliferation by Ki-67 immunostaining,apoptosis by TUNEL staining and angiogenesis by microvascular density (MVD) assay using CD31 staining.RESULTS:COX-2 protein expression was significantly increased in gastric precancerous lesions (atrophy,intestinal metaplasia and dysplasia,respectively) compared with chronic gastritis,and was concomitant with an increase in cell proliferation and angiogenesis.A significant improvement in precancerous lesions was observed in patients who received celecoxib compared with those who received placebo (P<0.001).Of these three changes,84.6% of sites with dysplasia regressed in patients treated with celecoxib (P=0.002) compared with 60% in the placebo group,suggesting that celecoxib was effective on the regression of dysplasia.COX-2 protein expression (P<0.001) and COX-2 activity (P<0.001) in the gastric tissues were consistently lower in celecoxib-treated patients compared with the placebo-treated subjects.Moreover,it was also shown that celecoxib suppressed cell proliferation (P<0.01),induced cell apoptosis (P<0.01) and inhibited angiogenesis with decreased MVD (P<0.001).However,all of these effects were not seen in placebo-treated subjects.Furthermore,COX-2 inhibition resulted in the up-regulation of PPARg expression,a protective molecule with anti-neoplastic effects.CONCLUSION:H pylori eradication therapy followed by celecoxib treatment improves gastric precancerous lesions by inhibiting COX-2 activity,inducing apoptosis,and suppressing cell proliferation and angiogenesis.

  20. Tmplications of anti-parietal cell antibodies and anti-Helicobacter pylori antibodies in histological gastritis and patient outcome

    Institute of Scientific and Technical Information of China (English)

    Ching-Chu Lo; Nan-Jing Peng; Ping-I Hsu; Gin-Ho Lo; Kwok-Hung Lai; Hui-Hwa Tseng; Chiun-Ku Lin; Hoi-Hung Chan; Wei-Lun Tsai; Wen-Chi Chen

    2005-01-01

    AIM: To develop a serum or histological marker for early discovery of gastric atrophy or intestinal metaplasia.METHODS: This study enrolled 44 patients with gastric adenocarcinoma, 52 patients with duodenal ulcer, 14 patients with gastric ulcer and 42 consecutive healthy adults as controls. Each patient received an endoscopy and five biopsy samples were obtained. The degrees of histological parameters of gastritis were categorized following the Updated Sydney System. Anti-parietal cell antibodies (APCA)and anti- Helicobacter pylori( H pylori) antibodies (AHPA)were analyzed by immunoassays. Hpylori infection was diagnosed by rapid urease test and histological examination.RESULTS: Patients with gastric cancer and gastric ulcer are significantly older than healthy subjects, while also displaying higher frequency of APCA than healthy controls.Patients with positive APCA showed higher scores in gastric atrophy and intestinal metaplasia of corpus than patients with negative APCA. Patients with positive AHPA had higher scores in gastric atrophy, intestinal metaplasia, and gastric inflammation of antrum than those patients with negative AHPA. Elderly patients had greater prevalence rates of APCA. Following multivariant logistic regression analysis,the only significant risk factor for antral atrophy is positive AHPA, while that for corpus atrophy is positive APCA.CONCLUSION: The existence of positive APCA correlates with glandular atrophy in corpus and the presence of positive AHPA correlates with glandular atrophy in antrum.The existence of serum APCA and AHPA betokensglandular atrophy and requires further examination for gastric cancer.

  1. Comparison of Salivary Anti Helicobacter pylori IgG with Serum IgG and Bacteriological Tests in Detecting Helicobacter pylori Infections

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    H Ghasemian safaei

    2005-01-01

    Full Text Available Background: This study was conducted to compare the efficacy of enzyme-linked immunosorbent assay (ELISA for detecting anti-Helicobacter pylori (H. pylori specific IgG antibodies in specimens of oral fluid and serum with bacteriological tests. Methods: Antral biopsy specimens, as well as serum and oral fluid samples were collected from 97 patients who underwent upper gastrointestinal endoscopy. The presence or absence of current H. pylori infection was determined by culture, histology and urease detection. Anti-H. pylori specific IgG was detected in serum and oral fluid, using an established lab-made, and a commercial ELISA kit. The obtained data were compared with results of bacteriological tests. Results: In all, 62 (64% of 97 patients were positive for H. pylori by one or more of the gold standard tests (culture, histology and urease detection. Lab-made enzyme-linked immunoassay of oral fluid had a sensitivity and specificity of 92% and 83% respectively. A sensitivity and specificity of 87% and 83%, respectively, was obtained with the commercial kit. Lab-made enzyme-linked immunoassay of serum samples had a sensitivity and specificity of 90% and 88%, respectively. A sensitivity of 86% and specificity of 86% was obtained with the commercial kit. Conclusion: Detection of anti-H. pylori specific IgG in oral fluid by ELISA is comparable in sensitivity and specificity with serum based methods. Oral fluid based ELISA could provide a reliable, non-invasive method for the diagnosis of H. pylori infection. Saliva testing may have a role in epidemiological studies. Keywords: Helicobacter pylori, ELISA, Oral fluid

  2. Design and evaluation of controlled release mucoadhesive microspheres of amoxicillin for anti Helicobacter pylori therapy

    OpenAIRE

    N Venkateswaramurthy; Sambathkumar, R.; Perumal, P.

    2011-01-01

    The aim of this study was to develop controlled release mucoadhesive microspheres of amoxicillin trihydrate for the treatment of peptic ulcer disease caused by Helicobacter pylori (H. pylori). Microspheres were prepared by solvent evaporation technique using carbopol 974P, hydroxypropyl methyl cellulose K4M (HPMC K4M) and Eudragit RS 100. The prepared microspheres were subjected to evaluation for particle size, incorporation efficiency, in vitro mucoadhesion and in vitro drug release characte...

  3. Vitamin-C as anti-Helicobacter pylori agent: More prophylactic than curative- Critical review

    Directory of Open Access Journals (Sweden)

    Jagannath Pal

    2011-01-01

    Full Text Available Potential of nonantibiotic therapies for treatment of Helicobacter pylori-related acid peptic disease remains underexplored. Several clinical studies have shown that higher prevalence of H. pylori infection is associated with low Vitamin C (Vit C level in serum and gastric juice. However, there is no consensus regarding the usefulness of Vit C supplementation in the management of H. pylori infection. Surveying the existing literature we conclude that high concentration of Vit C in gastric juice might inactivate H. pylori urease, the key enzyme for the pathogen′s survival and colonization into acidic stomach. Once infection established, urease is not very important for its survival. The role of Vit-C as anti-H. pylori agent in peptic ulcer diseases appears to be preventive rather than curative. Rather than supplementing high dose of Vit C along with conventional triple therapy, it is preferable to complete the conventional therapy and thereafter start Vit C supplementation for extended period which would prevent reinfection in susceptible individuals, provided the patients are not achlorhydric. Further studies are required to prove the role of Vit C in susceptible population.

  4. Design and evaluation of controlled release mucoadhesive microspheres of amoxicillin for anti Helicobacter pylori therapy

    Directory of Open Access Journals (Sweden)

    N Venkateswaramurthy

    2011-01-01

    Full Text Available The aim of this study was to develop controlled release mucoadhesive microspheres of amoxicillin trihydrate for the treatment of peptic ulcer disease caused by Helicobacter pylori (H. pylori. Microspheres were prepared by solvent evaporation technique using carbopol 974P, hydroxypropyl methyl cellulose K4M (HPMC K4M and Eudragit RS 100. The prepared microspheres were subjected to evaluation for particle size, incorporation efficiency, in vitro mucoadhesion and in vitro drug release characteristics. Absence of drug-polymer interaction was confirmed using differential scanning calorimetry analysis and fourier transform infrared spectrophotometry. The prepared microspheres showed a strong mucoadhesive property. The polymer concentration influenced the in vitro drug release significantly in 0.1N HCl. The particle sizes of systems ranged between 123±8.35 μm and 524±11.54 μm. Percent drug entrapment and release profiles of amoxicillin trihydrate in 0.1 N HCl were determined using high-performance liquid chromatography. The percentage drug entrapment and percentage yield of formulations were about 56.71±1.66% to 88.32±0.65% and 39.20±1.62% to 92.40±1.32%, respectively. The stability of the drugs was assessed in 0.1 N HCl. The results further substantiated that mucoadhesive microspheres improved the gastric stability of amoxicillin trihydrate (due to entrapment within the microsphere. From the above results, it was concluded that the mucoadhesive microspheres of amoxicillin trihydrate has feasibility for eradicating H. pylori from the stomach more effectively because of the prolonged gastrointestinal residence time and controlled release of drug from the formulation.

  5. Serum anti-Helicobacter pylori immunoglobulin G titer correlates with grade of histological gastritis, mucosal bacterial density, and levels of serum biomarkers.

    Science.gov (United States)

    Tu, Huakang; Sun, Liping; Dong, Xiao; Gong, Yuehua; Xu, Qian; Jing, Jingjing; Yuan, Yuan

    2014-03-01

    OBJECTIVE. Clinical implications of serum anti-Helicobacter pylori immunoglobulin G (IgG) titer were unclear. This study investigated the associations of serum anti-H. pylori IgG titer with grade of histological gastritis, mucosal bacterial density and levels of serum biomarkers, including pepsinogen (PG) I, PGII, PGI/II ratio and gastrin-17. MATERIAL AND METHODS. Study participants were from a screening program in northern China. Serum anti-H. pylori IgG measurements were available for 5922 patients with superficial gastritis. Serum anti-H. pylori IgG titer and serum biomarkers were measured using ELISA, and gastric biopsies were evaluated using standardized criteria. RESULTS. In patients with mild, moderate or severe superficial gastritis, the mean serum anti-H. pylori IgG titers were 17.3, 33.4 and 54.4 EIU (p for trend gastritis, mucosal bacterial density and concentrations of serum PGI, PGII and gastrin-17, and negatively with PGI/II ratio.

  6. Development of pH-responsive chitosan/heparin nanoparticles for stomach-specific anti-Helicobacter pylori therapy.

    Science.gov (United States)

    Lin, Yu-Hsin; Chang, Chiung-Hung; Wu, Yu-Shiun; Hsu, Yuan-Man; Chiou, Shu-Fen; Chen, Yi-Jen

    2009-07-01

    The microorganism now known as Helicobacter pylori is considered to be an important factor in the etiology of peptic ulcers. It can secrete urease enzyme and buffer gastric acids to survive in the stomach. H. pylori can colonize the gastric mucosa and preferentially adheres near the cell-cell junctions of the gastric mucous cells. In this study, pH-responsive nanoparticles were produced instantaneously upon the addition of heparin solution to a chitosan solution with magnetic stirring at room temperature. The nanoparticles appeared to have a particle size of 130-300 nm, with a positive surface charge, and were stable at pH 1.2-2.5, allowing them to protect an incorporated drug from destructive gastric acids. We also demonstrated that the prepared nanoparticles can adhere to and infiltrate cell-cell junctions and interact locally with H. pylori infection sites in intercellular spaces.

  7. ASSESSMENT OF RELATED ANAMNESTIC AND CLINICAL FACTORS ON EFFICACY AND SAFETY OF ANTI-HELICOBACTER PYLORI THERAPY

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    D. N. Andreev

    2016-01-01

    Full Text Available The article presents the results of a prospective clinical study in which 100 patients with H. pylori-associated peptic ulcer disease of stomach/duodenum were examined. The aim of the study was to assess the effect of concomitant anamnestic and clinical factors on the efficacy and safety of eradication therapy (ET. Type 2 diabetes mellitus is a factor that significantly reduces the efficiency of ET with OR 0.21 (95% CI 0,06-0,69, p = 0,0102. Using a macrolide antibiotics prior to ET during the previous 12 months is associated with a reduction in the effectiveness of H. pylori eradication with OR 0.27 (95% CI 0,08-0,90, p = 0,0342. Despite the lack of statistical significance observed negative effect on the efficiency of ET factors such as smoking and increased BMI. Smoking, female gender, age over 50 years and the presence of type 2 diabetes mellitus had no significant impact on the safety profile of ET. 

  8. Non-pharmacological treatment of Helicobacter pylori

    Institute of Scientific and Technical Information of China (English)

    Haim Shmuely; Noam Domniz; Jacob Yahav

    2016-01-01

    Many food and plant extracts have shown in vitro antiHelicobacter pylori(H.pylori)activity,but are less effective in vivo.The anti-H.pylori effects of these extracts are mainly permeabilitization of the membrane,anti-adhesion,inhibition of bacterial enzymes andbacterial grown.We,herein,review treatment effects of cranberry,garlic,curcumin,ginger and pistacia gum against H.pylori in both in vitro,animal studies and in vivo studies.

  9. Bioactive compounds of Crocus sativus L. and their semi-synthetic derivatives as promising anti-Helicobacter pylori, anti-malarial and anti-leishmanial agents.

    Science.gov (United States)

    De Monte, Celeste; Bizzarri, Bruna; Gidaro, Maria Concetta; Carradori, Simone; Mollica, Adriano; Luisi, Grazia; Granese, Arianna; Alcaro, Stefano; Costa, Giosuè; Basilico, Nicoletta; Parapini, Silvia; Scaltrito, Maria Maddalena; Masia, Carla; Sisto, Francesca

    2015-12-01

    Crocus sativus L. is known in herbal medicine for the various pharmacological effects of its components, but no data are found in literature about its biological properties toward Helicobacter pylori, Plasmodium spp. and Leishmania spp. In this work, the potential anti-bacterial and anti-parasitic effects of crocin and safranal, two important bioactive components in C. sativus, were explored, and also some semi-synthetic derivatives of safranal were tested in order to establish which modifications in the chemical structure could improve the biological activity. According to our promising results, we virtually screened our compounds by means of molecular modeling studies against the main H. pylori enzymes in order to unravel their putative mechanism of action.

  10. Seroprevalence of anti-Helicobacter pylori and anti-CagA antibodies in peptic ulcer and healthy subjects in the city of Rafsanjan

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    Abdollah Jafarzadeh

    2006-12-01

    Full Text Available BACKGROUND: Helicobacter pylori (H. pylori infection is thought to play an etiologic role in several gastroduodenal diseases including gastric ulcer, duodenal ulcer, gastric MALT lymphoma, and distal gastric cancer. Several studies have suggested that H. pylori which express cytotoxin-associated gene A (CagA may be more virulent than those that do not, but limited populations have been studied to date. The aims of the present study were to evaluate the seroprevalence of anti-H. pylori IgG, IgA and anti-CagA antibodies in peptic ulcer (PU patients and healthy individuals in the city of Rafsanjan. METHODS: A total of 60 PU patients (30 males and 30 females, aged 17 to 60 years and 138 age-matched healthy individuals (65 males, 73 females were enrolled in this study. Diagnosis of PU disease was established on the basis of findings by gastrointestinal endoscopy. The control group was recruited from among healthy blood donors referred to Blood Transfusion Center of Rafsanjan. A blood sample was collected from each participant and the sera were tested for the presence of anti- H. pylori IgG and IgA antibodies and antibody to bacterial virulence factor (CagA by use of enzyme-linked immunosorbent assay. The serum concentrations of anti-H. pylori IgA and anti-CagA antibody were expressed as mean ± SD in each group. RESULTS: In PU patients the overall seroprevalence of anti-H. pylori IgG (95.8%, IgA (96.6% and anti-CagA (91.6% were higher than those observed in the control group (73.2%, P<0.003; 79%, P<0.002; 47.82%, P<0.0000001; respectively. In the control group the prevalence of serum anti-CagA IgG antibodies was significantly higher in males compared to females (58.46% vs. 38.35%; P<0.01. Moreover, the mean titer of anti-H. pylori IgA antibodies was significantly higher in anti-CagA+ subjects compared to anti-CagA- subjects (47.5 Uarb/ml ± 35 vs. 27 Uarb/ml ± 18; P<0.01. Furthermore, an inverse association was found between levels and the

  11. Antibacterial Activity of Twenty Iranian Plant Extracts Against Clinical Isolates of Helicobacter pylori

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    Farahnaz Nariman

    2009-06-01

    Full Text Available Objective(sDue to increasing emergence of drug-resistance in Helicobacter pylori isolates, traditional plants arepotentially valuable sources of novel anti-H. pylori agents. In this research, anti-H. pylori activity of theorganic extracts of twenty native Iranian plants was determined against ten clinical isolates of H. pylori.Materials and MethodsDisc diffusion was used to determine the biological activity of 20 plant extracts as well as 8 antibioticscommonly used to treat H. pylori infections. Minimum inhibitory concentrations were also measured by tubeand agar dilution methods for the biologically active plant extracts.ResultsOf the twenty plant extracts analyzed, sixteen exhibited good anti-H. pylori activity, using disc diffusion.The ten most active extracts were Carum bulbocastanum, Carum carvi, Mentha longifolia, Saliva limbata,Saliva sclarea, Ziziphora clinopodioides, Thymus caramanicus, Glycyrrhiza glabra, Xanthium brasilicumand Trachyspermum copticum. Minimum inhibitory concentrations measured for the 10 biologically activeplant extracts were within the range of 31.25 to 500 μg/ml.ConclusionAmong the ten plant extracts effective against H. pylori clinical isolates, Carum carvi, Xanthium brasilicumand Trachyspermum copticum showed the highest activity.Keywords: Anti-Helicobacter pylori, Iranian plants, Organic extracts

  12. Effects of Anti-Helicobacter pylori Treatment as Part of Antiemetic Cancer Chemotherapy%抗幽门螺杆菌治疗在肿瘤化疗止吐中的作用研究

    Institute of Scientific and Technical Information of China (English)

    朴瑛; 刘兆喆; 丁震宇; 徐龙; 郭放; 孙庆庆; 谢晓冬

    2012-01-01

    Objective: This work aims to assess the effects of anti-Helicobacter pylori (anti-H. pylori) therapy combined with antiemetic drugs on chemotherapy-induced gastrointestinal toxicity. Methods: Out of the 176 patients who were enrolled in the research from January 2010 to January 2011, 86 were infected by H. pylori. Infected patients were randomly divided into Groups A and B. Patients in Group A (n= 43) received anti-H. pylori therapy combined with antiemetic drugs (20 mg omeprazole, 500 mg clarithromycin, and 500 mg tinidazole, twice a day, plus 5 mg tropisetron, for four weeks) Patients in Group B (n=43) only received antiemetic drugs (5 mg tropisetron for four weeks). No statistical significance was observed between Groups A and B for gender, age, and clinical manifestations. Clinical symptoms were observed and evaluated based on the gastrointestinal reaction indexing standards of the World Health Organization. The H. pylori eradication rate was assessed by 4C-urea breath test. Results: The vomiting severity was higher in the patients who were infected by H. pylori and subsequently underwent chemotherapy compared with the non-infected patients. Significant differences were observed between grades Ⅲ and Ⅳ vomiting (x2=21.92, P<0.001), as well as between grades I and Ⅱvomiting (x2=9.73, PO.01). The degree of nausea and vomiting was reduced in the patients who underwent anti-H. pylori therapy combined with antiemetic drugs, compared with those who only received antiemetic drugs. The total efficiency of the treatment was significantly higher in group A than in group B (x2=4.46, P<0.05). Conclusion: Anti-H. pylori treatment combined with antiemetic drugs may effectively reduce and relieve chemotherapy-induced gastrointestinal toxicity for patients infected with H. pylori.%目的:评估抗幽门螺杆菌(Helicobacter pylori,HP)治疗及联合常规止吐药物对肿瘤患者化疗所致胃肠道不良反应的疗效.方法:2010年1月至2011年1

  13. Clinical study on verrucous gastritis treated with HF electrocoagulation and anti-helicobacter pylori drug under endoscope%药物联合内镜下高频电凝治疗疣状胃炎的疗效观察

    Institute of Scientific and Technical Information of China (English)

    程桐花; 朱贞祥

    2011-01-01

    Aim To investigate the effect on verrucous gastritis treated with high frequency( HF )electrocoagulation and anti-helicobacter pylori( HP)drug under endoscope. Methods After gastroscopic diagnosis,86 cases of patients with verrucous gastritis were divided into group A and B by random. In group A,HF electrocoagulation was conducted on verrucous lesions of the each case under gastroscope, and the eradication therapy for HP was conducted after the surgery. But for Group B, only the eradication therapy for HP was conducted. In four weeks later,we not only compared the eradication rate of HP in the two groups, but also the effect on verrucous lesions, and the effect in 6 months after the treatment. Results In four weeks later,eradication therapy of HP showed no difference in the two groups,but the effect were significantly different not only four weeks but also six months later. Conclusion The effect of the therapy with HF electrocoagulation under endoscope is better than that only with anti-HP drug for verrucous gastritis.%目的 探讨内镜下高频电凝联合药物抗幽门螺杆菌(HP)治疗疣状胃炎(VG)的疗效.方法 经胃镜诊断疣状胃炎86例患者,随机将其分为A(52例)、B(34例)两组.A组在胃镜下对所有疣状病变进行高频电凝疗法,术后予HP药物根除治疗.B组只予HP药物根除治疗.比较两组患者疗程结束后4周时HP根除率和疣状病变治疗效果,24周时疣状病变的治疗效果.结果 两组在疗程结束后4周HP根治率无明显差异,4周和24周疣状病变治效果有显著差异.结论 内镜下高频电凝联合药物抗HP疗法较单药物抗HP疗法治疗疣状胃炎效果更佳.

  14. 丁香对幽门螺杆菌的体外抑菌作用%Anti-Helicobacter Pylori Action of Eugenol and Essential Oil from Eugenia Caryophyllata in vitro

    Institute of Scientific and Technical Information of China (English)

    韩艳; 王庆伟; 张琰; 刘新友; 覃华; 杜小燕

    2011-01-01

    目的 考察丁香挥发油及丁香酚体外抑制幽门螺杆菌的活性.方法 水蒸气蒸馏法提取丁香挥发油,采用高效液相色谱法测定挥发油丁香酚的含量.以氨苄西林为对照,体外法测定丁香挥发油、丁香提取挥发油后的水提取物及丁香酚对8种幽门螺杆菌菌株的最小抑菌浓度(MIC).结果 氨苄西林对8种幽门螺杆菌菌株的MIC范围为1.25~2.50 μg·mL-1,丁香挥发油的MIC范围为5.00~10.00 μg·mL-1,丁香酚的MIC范围为2.50~5.00 μg·mL-1,丁香提取挥发油后的水提取物无抑菌作用.结论 丁香抑制幽门螺杆菌的活性成分是其挥发油中的主要成分丁香酚.%Objective To study the antibacterial effects of eugenol and essential oil from Euggenia Cairyphyllata against helicobacter pylori in vitro. Methods The essential oil was obtained by steam distillation. The concentration of eugenol was determined by HPLC. MIC against helicobacter pylori of eugenol, essential oil from Eugenia Caryophyllata and aqueous extract of Eugenia Caryophyllata except essential oil were determined in vitro with ampieillin as a control drug. Results The range of MIC against 8 helicobacter pylori was 1.25-2.50 μg· mL-1 for ampicillin, 5.00-10. 00 μg· mL-1 for the essential oil, 2.50-5.00 μg· mL-1 for eugenol. The aqueous extract showed no effect against helicobacter pylori. Conclusion The main active component from Eugenia Caryophyllata against H. pylori is eugenol of essential oil.

  15. In vitro characterization of the anti-bacterial activity of SQ109 against Helicobacter pylori.

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    Morris O Makobongo

    Full Text Available The most evident challenge to treatment of Helicobacter pylori, a bacterium responsible for gastritis, peptic ulcers and gastric cancer, is the increasing rate of resistance to all currently used therapeutic antibiotics. Thus, the development of novel therapies is urgently required. N-geranyl-N'-(2-adamantyl ethane-1, 2-diamine (SQ109 is an ethylene diamine-based antitubercular drug that is currently in clinical trials for the treatment of tuberculosis (TB. Previous pharmacokinetic studies of SQ109 revealed that persistently high concentrations of SQ109 remain in the stomach 4 hours post oral administration in rats. This finding, combined with the need for new anti-Helicobacter therapies, prompted us to define the in vitro efficacy of SQ109 against H. pylori. Liquid broth micro-dilution was used for susceptibility studies to determine the antimicrobial activity of SQ109 against a total of 6 laboratory strains and 20 clinical isolates of H. pylori; the clinical isolates included a multi-drug resistant strain. All strains tested were susceptible to SQ109 with MIC and MBC ranges of 6-10 µM and 50-60 µM, respectively. SQ109 killing kinetics were concentration- and time-dependent. SQ109 killed H. pylori in 8-10 h at 140 µM (2MBCs or 4-6 h at 200 µM (~3MBCs. Importantly, though the kinetics of killing were altered, SQ109 retained potent bactericidal activity against H. pylori at low pH. Additionally, SQ109 demonstrated robust thermal stability and was effective at killing slow growing or static bacteria. In fact, pretreatment of cultures with a bacteriostatic concentration of chloramphenicol (Cm synergized the effects of typically bacteriostatic concentrations of SQ109 to the level of five-logs of bacterial killing. A molar-to-molar comparison of the efficacy of SQ109 as compared to metronidazole (MTZ, amoxicillin (AMX, rifampicin (RIF and clarithromycin (CLR, revealed that SQ109 was superior to MTZ, AMX and RIF but not to CLR. Finally, the

  16. Identification of novel scaffolds for potential anti-Helicobacter pylori agents based on the crystal structure of H. pylori 3-deoxy-d-manno-octulosonate 8-phosphate synthase (HpKDO8PS).

    Science.gov (United States)

    Cho, Sujin; Im, Hookang; Lee, Ki-Young; Chen, Jie; Kang, Hae Ju; Yoon, Hye-Jin; Min, Kyung Hoon; Lee, Kang Ro; Park, Hyun-Ju; Lee, Bong-Jin

    2016-01-27

    The crystal structure of 3-deoxy-d-manno-octulosonate-8-phosphate synthase (KDO8PS) from Helicobacter pylori (HpKDO8PS) was determined alone and within various complexes, revealing an extra helix (HE) that is absent in the structures of KDO8PS from other organisms. In contrast to the metal coordination of the KDO8PS enzyme from Aquifex aeolicus, HpKDO8PS is specifically coordinated with Cd(2+) or Zn(2+) ions, and isothermal titration calorimetry (ITC) and differential scanning fluorimetry (DSF) revealed that Cd(2+) thermally stabilizes the protein structure more efficiently than Zn(2+). In the substrate-bound structure, water molecules play a key role in fixing residues in the proper configuration to achieve a compact structure. Using the structures of HpKDO8PS and API [arabinose 5-phosphate (A5P) and phosphoenolpyruvate (PEP) bisubstrate inhibitor], we generated 21 compounds showing potential HpKDO8PS-binding properties via in silico virtual screening. The capacity of three, avicularin, hyperin, and MC181, to bind to HpKDO8PS was confirmed through saturation transfer difference (STD) experiments, and we identified their specific ligand binding modes by combining competition experiments and docking simulation analysis. Hyperin was confirmed to bind to the A5P binding site, primarily via hydrophilic interaction, whereas MC181 bound to both the PEP and A5P binding sites through hydrophilic and hydrophobic interactions. These results were consistent with the epitope mapping by STD. Our results are expected to provide clues for the development of HpKDO8PS inhibitors.

  17. Antibacterial activity of Tabebuia impetiginosa Martius ex DC (Taheebo) against Helicobacter pylori.

    Science.gov (United States)

    Park, Byeoung-Soo; Lee, Hyun-Kyung; Lee, Sung-Eun; Piao, Xiang-Lan; Takeoka, Gary R; Wong, Rosalind Y; Ahn, Young-Joon; Kim, Jeong-Han

    2006-04-21

    The growth-inhibiting activity of Tabebuia impetiginosa Martius ex DC dried inner bark-derived constituents against Helicobacter pylori ATCC 43504 was examined using paper disc diffusion and minimum inhibitory concentration (MIC) bioassays. The activity of the isolated compounds was compared to that of the commercially available anti-Helicobacter pylori agents, amoxicillin, metronidazole, and tetracycline. The biologically active components of Tabebuia impetiginosa dried inner bark (taheebo) were characterized by spectroscopic analysis as 2-(hydroxymethyl)anthraquinone, anthraquinone-2-carboxylic acid, and 2-hydroxy-3-(3-methyl-2-butenyl)-1,4-naphthoquinone (lapachol). With the paper disc diffusion assay 2-(hydroxymethyl)anthraquinone exhibited strong activity against Helicobacter pylori ATCC 43504 at 0.01 mg/disc. Anthraquinone-2-carboxylic acid, lapachol and metronidazole were less effective, exhibiting moderate anti-Helicobacter pylori activity at 0.1 mg/disc. Amoxicillin and tetracycline were the most potent compounds tested, displaying very strong activity at 0.005 mg/disc. 2-(Hydroxymethyl)anthraquinone exhibited moderate activity at this dose. Tetracycline still had strong activity at 0.001 mg/disc while amoxicillin had little activity at this dose. In the MIC bioassay, 2-(hydroxymethyl)anthraquinone (2 microg/mL), anthraquinone-2-carboxylic acid (8 microg/mL), and lapachol (4 microg/mL) were more active than metronidazole (32 microg/mL) but less effective than amoxicillin (0.063 microg/mL) and tetracycline (0.5 microg/mL). The anti-Helicobacter pylori activity of seven 1,4-naphthoquinone derivatives (structurally related to lapachol), 1,4-naphthoquinone, 5,8-dihydroxy-1,4-naphthoquinone (naphthazarin), 2-methyl-1,4-naphthoquinone (menadione), 2-hydroxy-1,4-naphthoquinone (lawsone), 5-hydroxy-2-methyl-1,4-naphthoquinone (plumbagin), 5-hydroxy-1,4-naphthoquinone (juglone), and 2,3-dichloro-1,4-naphthoquinone (dichlone) was also evaluated using the paper disc

  18. Effective predictive factors for regression of gastric MALT lymphoma after anti-Helicobacter pylori treatment%胃粘膜相关淋巴样组织淋巴瘤抗H.Pylori治疗的有效预测因子

    Institute of Scientific and Technical Information of China (English)

    胡莲; 李昌平

    2006-01-01

    胃粘膜相关淋巴样组织(MALT)型结外边缘区B细胞淋巴瘤发病机制主要与幽门螺杆菌(H.pylori)感染有关,目前认为根治H.pylori治疗已成为胃粘膜相关淋巴样组织淋巴瘤的一线治疗.然而,抗H.pylori治疗不能使胃MALT淋巴瘤100%完全缓解,即使完全缓解后仍有复发的可能.随着研究的深入,哪些患者更能从抗H.pylori治疗中受益,抗H.pylori治疗后随访是目前研究的热点.此文对胃MALT淋巴瘤与H.pylori的关系,抗H.pylori治疗的有效预测、随访作一综述.

  19. Helicobacter pylori neutrophil activating protein as target for new drugs against H.pylori inflammation

    Institute of Scientific and Technical Information of China (English)

    Theodora Choli-Papadopoulou; Filippos Kottakis; Georgios Papadopoulos; Stefanos Pendas

    2011-01-01

    Helicobacter pylori (H. pylori ) infection is among the most common human infections and the major risk factor for peptic ulcer disease and gastric cancer. Within this work we present the implication of C-terminal region of H. pylori neutrophil activating protein in the stimulation of neutrophil activation as well as the evidence that the C-terminal region of H. pylori activating protein is indispensable for neutrophil adhesion to endothelial cells, a step necessary to H. pylori inflammation. In addition we show that arabino galactan proteins derived from chios mastic gum, the natural resin of the plant Pistacia lentiscus var. Chia inhibit neutrophil activation in vitro .

  20. Inhibition of Helicobacter pylori and Its Associate Urease by Labdane Diterpenoids Isolated from Andrographis paniculata.

    Science.gov (United States)

    Shaikh, Rafik U; Dawane, Ashwini A; Pawar, Rajendra P; Gond, Dhananjay S; Meshram, Rohan J; Gacche, Rajesh N

    2016-03-01

    The present study was carried out to evaluate anti-Helicobacter pylori and its associated urease activity of labdane diterpenoids isolated from Andrographis paniculata. A molecular docking analysis was performed by using ArgusLab 4.0.1 software. The results obtained indicate that compound A possesses strong inhibition to H. pylori, 28 ± 2.98 (minimum inhibitory concentration, 9 µg/mL), and its urease, 85.54 ± 2.62% (IC50 , 20.2 µg/mL). Compounds B, C, and D also showed moderate inhibition to H. pylori and its urease. The obtained results were in agreement with the molecular docking analysis of compounds. The phytochemicals under investigation were found to be promising antibacterial agents. Moreover, the isolated compounds can be considered as a resource for searching novel anti-H. pylori agents possessing urease inhibition.

  1. A study of Helicobacter pylori infection in diabetes mellitus

    OpenAIRE

    Khwaja Saifullah Zafar; Vidyasagar Ram; Manoj Kumar

    2016-01-01

    Background: Helicobacter pylori is the most common bacterial infection in human beings. The aim was to study the association of Helicobacter pylori infection in patients of diabetes mellitus. Design of the study was observational analytic cross sectional study. Methods: A total of 69 subjects were studied. Of these 30 were non diabetics and 39 were diabetics, with disease duration more than 1 year. The serological diagnosis of H. pylori was made by Anti- Helicobacter pylori antibody test....

  2. Detection of serum anti- Helicobacter pyloriimmunoglobulin G in patients with different digestive malignant tumors

    Institute of Scientific and Technical Information of China (English)

    Ke-Xia Wang; Xue-Feng Wang; Jiang-Long Peng; Yu-Bao Cui; Jian Wang; Chao-Pin Li

    2003-01-01

    AIM: To investigate the seroprevalence of Helicobacter pylori infection in patients with different digestive malignant tumors.METHODS: Enzyme linked immunosorbent assay (ELISA) was used to detect serum anti-Helicobacter pylori IgG antibody in 374 patients with different digestive malignant tumors and 310 healthy subjects (normal control group).RESULTS: The seroprevalence of Helicobacter pylori infection was 61.50 %(230/374) and 46.77 % (145/310),respectively, in patients with digestive tumors and normal controls (P<0.05). The seroprevalence was 52.38 % (33/63),86.60 % (84/97), 83.14 % (84/101), 45.24 (19/42),51.13 % (18/35) and 44.44 % (16/36), respectively in patients with carcinomas of esophagus, stomach, duodenum,rectum, colon and liver (P<0.01). In patients with intestinal and diffuse type gastric cancers, the seroprevalence was 93.75 % (60/64) and 72.73 % (24/33), respectively (P<0.05).In patients with gastric antral and cardiac cancers, the seroprevalence was 96.43 % (54/56) and 73.17 % (30/41),respectively (P<0.05). In patients with ulcerous and proliferous type duodenal cancers, the seroprevalence of H pylori infection was 91.04 % (61/67) and 52.27 % (23/44),respectively (P<0.05). In patients with duodenal bulb and descending cancers, the seroprevalence was 94.20 % (65/69) and 45.20 % (19/42), respectively (P<0.05).CONCLUSION:Hpyloriinfection is associated with occurrence and development of gastric and duodenal carcinomas.Furthermore, it is also associated with histological type and locations of gastric and duodenal carcinomas.

  3. [Is anti-helicobacter therapy a rational approach in treatment of erosive and ulcerous lesions of the gastroduodenal mucosa in patients with inflamatory bowel diseases?].

    Science.gov (United States)

    Maev, I V; Gadzhieva, M G

    2005-01-01

    The study revealed changes in the oesophagogastroduodenal mucosa in 110 patients with IBD; in 60.9% of cases these changes were associated with Helicobacter pylori. 35 patients with IBD were examined to form two groups. The first group (20 patients) received rabeprazol (pariet) in a dose of 20 mg per day; the rest 15 patients were administered 120 mg of de-nol four times a day; amoxicicline and furazolidon were used as additional therapy in cases with Helicobacter pylori. The study showed that successful eradication did not always result in erosion epithelization but, on the contrary, only 40% cases of clinical and endoscopic remission were associated with Helicobacter pylori elimination. These data suggest that anti-helicobacter therapy is not a rational approach in treatment of this category of patients.

  4. Carotenoid composition and in vitro pharmacological activity of rose hips.

    Science.gov (United States)

    Horváth, Györgyi; Molnár, Péter; Radó-Turcsi, Erika; Deli, József; Kawase, Masami; Satoh, Kazue; Tanaka, Toru; Tani, Satoru; Sakagami, Hiroshi; Gyémánt, Nóra; Molnár, József

    2012-01-01

    The aim of the present study was to compare carotenoid extracts of Rose hips (Rosa canina L.) with regard to their phytochemical profiles and their in vitro anti-Helicobacter pylori (H. pylori), cytotoxic, multidrug resistance (MDR) reversal and radical scavenging activity. Carotenoid composition was investigated in the different fractionation of rose hips, using extraction methods. Six main carotenoids - epimers of neochrome, lutein, zeaxanthin, rubixanthin, lycopene, β,β-carotene - were identified from Rose hips by their chromatographic behavior and UV-visible spectra, which is in accordance with other studies on carotenoids in this plant material. The active principles in the carotenoid extract might differ, depending upon the extraction procedures.

  5. Bactericidal activity of Pistacia lentiscus mastic gum against Helicobacter pylori.

    Science.gov (United States)

    Marone, P; Bono, L; Leone, E; Bona, S; Carretto, E; Perversi, L

    2001-12-01

    In this study we evaluated the antibacterial activity of mastic gum, a resin obtained from the Pistacia lentiscus tree, against clinical isolates of Helicobacter pylori. The minimal bactericidal concentrations (MBCs) were obtained by a microdilution assay. Mastic gum killed 50% of the strains tested at a concentration of 125 microg/ml and 90% at a concentration of 500 microg/ml. The influence of sub-MBCs of mastic gum on the morphologies of H. pylori was evaluated by transmission electron microscopy. The lentiscus resin induced blebbing, morphological abnormalities and cellular fragmentation in H. pylori cells.

  6. In vitro antagonistic activity of Lactobacillus casei against Helicobacter pylori.

    Science.gov (United States)

    Enany, Shymaa; Abdalla, Salah

    2015-01-01

    Helicobacter pylori is one of the most common causes of chronic infections in humans. Curing H. pylori infection is difficult because of the habitat of the organism below the mucus adherent layer of gastric mucosa. Lactobacilli are known as acid-resistant bacteria and can remain in stomach for a long time than any other organism, we aimed in this study to examine the efficacy of Lactobacillus casei as a probiotic against H. pylori in humans. Particularly, L. casei was opted as it is considered to be one of the widely used probiotics in dairy products. One hundred and seven strains of H. pylori were isolated from dyspeptic patients and were tested for their antibiotic susceptibility to metronidazole (MTZ), clarithromycin (CLR), tetracycline (TET), and amoxicillin (AMX) by the disc diffusion method. The strains were examined for their susceptibility toward L. casei - present in fermented milk products - by well diffusion method. It was found that 74.7% strains were resistant to MTZ; 1.8% to MTZ, TET, and CLR; 3.7% to MTZ and CLR; 4.6% to MTZ and TET; and 0.9% were resistant to MTZ, TET, and AMX. The antibacterial activity of L. casei against H. pylori was determined on all the tested H. pylori isolates including antibiotic resistant strains with different patterns. Our study proposed the use of probiotics for the treatment of H. pylori infection as an effective approach.

  7. HELICOBACTER PYLORI GROWTH INHIBITION BY SUBSTANCE PRODUCED PSEUDOMONAS BY AEROGINOSA: IN VTRO STUDY

    Directory of Open Access Journals (Sweden)

    A FAZELI

    2003-03-01

    Full Text Available Resistance of H.pylori against metronidazole is increasingly appeared in reports of investigators of gastric infections. So that, seeking to find more effective anti-helicobacter drugs is a necessity. In this study, inhibitory effect of the P. aeroginosa-produced substance on H. pylori growth was determined using two methods, Cross-streak and Well-diffusion Only two out of 37 P. aeroginosa isalates were able to inhibit H. pylori growth which one of them was chosen for further investigation. Its antibacterial activity was tested on 31 isolates of H. pylori consisting 27 metrondazole-sensitive and 4 metronidazole-resistant isolates. The inhibitory substance was enable to kill both metrondazole-sensitive and resistant isolates of H. pylori. The substance could also inhibit the of several other bacteria including E.coli, Salmonella sp., Klebsiella sp., S. aureus and a gram positive bacilli. While the inhibitory effect of the substance had no change at 40c for 30 days, its effect substantially reduced by treating at 600c for 15 minutes. Treatment of substance at 600c (30 min. 80?c and 100?c (15 & 30min, and freezing (-20?c and melting (37?c inactivated its inhibitory effect completely. Treatment with trips in also could inactivate it. Thus P. aeroginosa-produced substance, probably is a protein and may be classified in bacteriocin group.

  8. Antimicrobial activity of Northwestern Mexican plants against Helicobacter pylori.

    Science.gov (United States)

    Robles-Zepeda, Ramón E; Velázquez-Contreras, Carlos A; Garibay-Escobar, Adriana; Gálvez-Ruiz, Juan C; Ruiz-Bustos, Eduardo

    2011-10-01

    Helicobacter pylori is the major etiologic agent of such gastric disorders as chronic active gastritis and gastric carcinoma. Over the past few years, the appearance of antibiotic-resistant bacteria has led to the development of better treatments, such as the use of natural products. This study evaluated the anti-H. pylori activity of 17 Mexican plants used mainly in the northwestern part of Mexico (Sonora) for the empirical treatment of gastrointestinal disorders. The anti-H. pylori activity of methanolic extracts of the plants was determined by using the broth microdilution method. The 50% minimum inhibitory concentrations ranged from less than 200 to 400 μg/mL for Castella tortuosa, Amphipterygium adstringens, Ibervillea sonorae, Pscalium decompositum, Krameria erecta, Selaginella lepidophylla, Pimpinella anisum, Marrubium vulgare, Ambrosia confertiflora, and Couterea latiflora and were greater than 800 μg/mL for Byophyllum pinnatum, Tecoma stans linnaeus, Kohleria deppena, Jatropha cuneata, Chenopodium ambrosoides, and Taxodium macronatum. Only Equisetum gigantum showed no activity against H. pylori. This study suggests the important role that these plants may have in the treatment of gastrointestinal disorders caused by H. pylori. The findings set the groundwork for further characterization and elucidation of the active compounds responsible for such activity.

  9. Catechin-based procyanidins from Peumus boldus Mol. aqueous extract inhibit Helicobacter pylori urease and adherence to adenocarcinoma gastric cells.

    Science.gov (United States)

    Pastene, Edgar; Parada, Víctor; Avello, Marcia; Ruiz, Antonieta; García, Apolinaria

    2014-11-01

    In this work, the anti-Helicobacter pylori effect of an aqueous extract from dried leaves of Peumus boldus Mol. (Monimiaceae) was evaluated. This extract displayed high inhibitory activity against H. pylori urease. Therefore, in order to clarify the type of substances responsible for such effect, a bioassay-guided fractionation strategy was carried out. The active compounds in the fractions were characterized through different chromatographic methods (RP-HPLC; HILIC-HPLC). The fraction named F5 (mDP = 7.8) from aqueous extract was the most active against H. pylori urease with an IC50  = 15.9 µg gallic acid equivalents (GAE)/mL. HPLC analysis evidenced that F5 was composed mainly by catechin-derived proanthocyanidins (LC-MS and phloroglucinolysis). The anti-adherent effect of boldo was assessed by co-culture of H. pylori and AGS cells. Both the aqueous extract and F5 showed an anti-adherent effect in a concentration-dependent manner. An 89.3% of inhibition was reached at 2.0 mg GAE/mL of boldo extract. In conjunction, our results suggest that boldo extract has a potent anti-urease activity and anti-adherent effect against H. pylori, properties directly linked with the presence of catechin-derived proanthocyanidins.

  10. Evaluation of clinico-pathological features and Helicobacter pylori infection in gastric inflammatory fibroid polyps.

    Science.gov (United States)

    Albuquerque, Andreia; Rios, Elisabete; Carneiro, Fátima; Macedo, Guilherme

    2014-12-01

    Inflammatory fibroid polyps are rare mesenchymal lesions. The frequency of Helicobacter pylori infection in the gastric mucosa overlying inflammatory fibroid polyps and its relation with the histologic features of the polyps are undetermined. The clinico-pathological features of inflammatory fibroid polyps, the frequency of Helicobacter pylori infection in the overlying gastric mucosa, and its putative impact on the phenotype of the polyps were evaluated. Gastric inflammatory fibroid polyps diagnosed in our Hospital from 1998 to 2012 were reviewed and the histological. The histological sections were stained with hematoxylin and eosin and modified Giemsa for the evaluation of Helicobacter pylori infection. Inconclusive cases were further analyzed by immunohistochemistry with anti-Helicobacter pylori antibody. Diagnosis was confirmed in 54 polyps, 85 % developed in females, mean age 63 ± 11 years. Most polyps were sessile (74 %), with a mean size of 15 ± 12 mm, 96 % were located in the antrum and 85 % were removed by snare polypectomy. Helicobacter pylori infection was identified in 48 % of the polyps. Most inflammatory fibroid polyps developed in the submucosa, and mucosal extension was observed in 96 % of the cases. Chronic gastritis was observed in all cases (63 % with activity, 31 % with intestinal metaplasia, and 61 % with foveolar hyperplasia). Erosion and ulceration of the overlying gastric mucosa was observed in 48 % and 11 % of the polyps, respectively. Onion skin features were present in 52 % of the polyps and were more frequently observed in cases without evidence of Helicobacter pylori infection. Background changes in gastric mucosa were not distinctive according to Helicobacter pylori infection. Chronic atrophic gastritis with intestinal metaplasia was associated with the presence of perivascular onion skin lesions. To our knowledge, this is the second largest series of gastric inflammatory fibroid polyps. Helicobacter pylori infection was

  11. Komplet remission af højmalignt lymfom i ventriklen efter eradikation af Helicobacter pylori

    DEFF Research Database (Denmark)

    Høeg, Rasmus Tetens; Skau, Anne-Marie; Nørgaard, Peter

    2011-01-01

    A 91 year-old man was found to have diffuse large cell B-cell lymphoma (DLBCL), localized to the stomach. Because of his age, his only treatment was anti-Helicobacter pylori therapy. He achieved a complete remission, and six months after the initial presentation, there were no signs of recurrence...

  12. Two stomach-originated lactobacillus strains improve Helicobacter pylori infected murine gastritis

    Institute of Scientific and Technical Information of China (English)

    2010-01-01

    AIM:To investigate the potential anti-Helicobacter pylori(H.pylori ) and anti-inflammation in vivo effects of two lactobacillus strains from human stomach.METHODS:Forty H.pylori infected Balb/c mice were randomly divided into 4 groups:proton pump inhibitor and antibiotics triple treated group,Lactobacillus fermenti(L.fermenti ) treated group,Lactobacillus acidophilus treated group and normal saline control group.Ten uninfected mice were also included as blank control group.The infection of H.pylori was dete...

  13. Helicobacter pylori induces activation of human peripheral γδ+ T lymphocytes.

    Directory of Open Access Journals (Sweden)

    Benedetta Romi

    Full Text Available Helicobacter pylori is a gram-negative bacterium that causes gastric and duodenal diseases in humans. Despite a robust antibody and cellular immune response, H. pylori infection persists chronically. To understand if and how H. pylori could modulate T cell activation, in the present study we investigated in vitro the interaction between H. pylori and human T lymphocytes freshly isolated from peripheral blood of H. pylori-negative donors. A direct interaction of live, but not killed bacteria with purified CD3+ T lymphocytes was observed by microscopy and confirmed by flow cytometry. Live H. pylori activated CD3+ T lymphocytes and predominantly γδ+ T cells bearing the TCR chain Vδ2. Upon interaction with H. pylori, these cells up-regulated the activation molecule CD69 and produced cytokines (such as TNFα, IFNγ and chemokines (such as MIP-1β, RANTES in a non-antigen-specific manner. This activation required viable H. pylori and was not exhibited by other gram-negative bacteria. The cytotoxin-associated antigen-A (CagA, was at least partially responsible of this activation. Our results suggest that H. pylori can directly interact with T cells and modulate the response of γδ+ T cells, thereby favouring an inflammatory environment which can contribute to the chronic persistence of the bacteria and eventually to the gastric pathology.

  14. Structure-Based Inhibitors Exhibit Differential Activities against Helicobacter pylori and Escherichia coli Undecaprenyl Pyrophosphate Synthases

    Directory of Open Access Journals (Sweden)

    Chih-Jung Kuo

    2008-01-01

    Full Text Available Helicobacter pylori colonizes the human gastric epithelium and causes diseases such as gastritis, peptic ulcers, and stomach cancer. Undecaprenyl pyrophosphate synthase (UPPS, which catalyzes consecutive condensation reactions of farnesyl pyrophosphate with eight isopentenyl pyrophosphate to form lipid carrier for bacterial peptidoglycan biosynthesis, represents a potential target for developing new antibiotics. In this study, we solved the crystal structure of H. pylori UPPS and performed virtual screening of inhibitors from a library of 58,635 compounds. Two hits were found to exhibit differential activities against Helicobacter pylori and Escherichia coli UPPS, giving the possibility of developing antibiotics specially targeting pathogenic H. pylori without killing the intestinal E. coli.

  15. H pylori stimulates proliferation of gastric cancer cells through activating mitogen-activated protein kinase cascade

    Institute of Scientific and Technical Information of China (English)

    Yong-Chang Chen; Ying Wang; Jing-Yan Li; Wen-Rong Xu; You-Li Zhang

    2006-01-01

    AIM: To explore the mechanism by which H pylori causes activation of gastric epithelial cells.METHODS: A VacA (+) and CagA (+) standard Hpyloriline NCTC 11637 and a human gastric adenocarcinoma derived gastric epithelial cell line BGC-823 were applied in the study. MTT assay and 3H-TdR incorporation test were used to detect the proliferation of BGC-823 cells and Western blotting was used to detect the activity and existence of related proteins.RESULTS: Incubation with Hpylori extract increased the proliferation of gastric epithelial cells, reflected by both live cell number and DNA synthesis rate. The activity of extracellular signal-regulated protein kinase (ERK) signal transduction cascade increased within 20 min after incubation with Hpylori extract and appeared to be a sustained event. MAPK/ERK kinase (MEK) inhibitor PD98059abolished the action of H pylori extract on both ERK activity and cell proliferation. Incubation with H pyloriextract increased c-Fos expression and SRE-dependentgene expression. H pylori extract caused phosphorylation of several proteins including a protein with molecular size of 97.4 kDa and tyrosine kinase inhibitor genistein inhibited the activation of ERK and the proliferation of cells caused by H pylori extract.CONCLUSION: Biologically active elements in H pylori extract cause proliferation of gastric epithelial cells through activating tyrosine kinase and ERK signal transduction cascade.

  16. Activation of Helicobacter pylori causes either autoimmune thyroid diseases or carcinogenesis in the digestive tract.

    Science.gov (United States)

    Astl, J; Šterzl, I

    2015-01-01

    Helicobacter pylori has been implicated in stimulation of immune system, development of autoimmune endocrinopathies as autoimmune thyroiditis (AT) and on other hand induction of immunosupresion activates gastric and extra-gastric diseases such as gastric ulcer or cancer. It causes persistent lifelong infection despite local and systemic immune response. Our results indicate that Helicobacter pylori might cause inhibition of the specific cellular immune response in Helicobacter pylori-infected patients with or without autoimmune diseases such as AT. We cannot also declare the carcinogenic effect in oropharynx. However the association of any infection agents and cancerogenesis exists. The adherence of Helicobacter pylori expression and enlargement of benign lymphatic tissue and the high incidence of the DNA of Helicobacter pylori in laryngopharyngeal and oropharyngeal cancer is reality. LTT appears to be a good tool for detection of immune memory cellular response in patients with Helicobacter pylori infection and AT. All these complications of Helicobacter pylori infection can be abrogated by successful eradication of Helicobacter pylori.

  17. In vitro activity of artemisone and artemisinin derivatives against extracellular and intracellular Helicobacter pylori.

    Science.gov (United States)

    Sisto, Francesca; Scaltrito, Maria Maddalena; Masia, Carla; Bonomi, Arianna; Coccè, Valentina; Marano, Giuseppe; Haynes, Richard K; Miani, Alessandro; Farronato, Giampietro; Taramelli, Donatella

    2016-07-01

    The in vitro activity of the new artemisinin derivative artemisone as well as other molecules of the same class against Helicobacter pylori and their effects when combined with standard antibiotics were evaluated. Since H. pylori can be internalised into gastric epithelial cells, the effects of artemisinin, dihydroartemisinin and artemisone against intracellular H. pylori were also investigated. Bacteriostatic [minimum inhibitory concentration (MIC)] and bactericidal [minimum bactericidal concentration (MBC)] activities were assessed against 24 clinical strains of H. pylori with different antibiotics susceptibilities. Artemisone showed MIC50 and MIC90 values of 0.25 mg/L and 0.5 mg/L, respectively, and an MBC50 value of 0.5 mg/L. Artemisone was synergistic with amoxicillin in 60% of strains, with clarithromycin in 40% and with metronidazole in 20%. There was no interaction between artemisone and omeprazole or bismuth citrate. Against intracellular H. pylori, only dihydroartemisinin at 2× MIC caused a 1 log10 CFU decrease after 18 h and 24 h of incubation. This is the first demonstration in vitro of the activity of artemisinin derivatives against intracellular H. pylori and indicates that artemisone has the potential to be efficacious for the treatment of H. pylori infection, especially in combination with antibiotics.

  18. Helicobacter pylori neutrophil-activating protein: from molecular pathogenesis to clinical applications.

    Science.gov (United States)

    Fu, Hua-Wen

    2014-05-14

    Helicobacter pylori (H. pylori) neutrophil-activating protein (HP-NAP) was originally identified as a virulence factor of H. pylori for its ability to activate neutrophils to generate respiratory burst by releasing reactive oxygen species. Later on, HP-NAP was also found to be involved in the protection of H. pylori from DNA damage, supporting the survival of H. pylori under oxidative stress. This protein is highly conserved and expressed by virtually all clinical isolates of H. pylori. The majority of patients infected with H. pylori produced antibodies specific for HP-NAP, suggesting its important role in immunity. In addition to acting as a pathogenic factor by activating the innate immunity through a wide range of human leukocytes, including neutrophils, monocytes, and mast cells, HP-NAP also mediates adaptive immunity through the induction of T helper cell type I responses. The pro-inflammatory and immunomodulatory properties of HP-NAP not only make it play an important role in disease pathogenesis but also make it a potential candidate for clinical use. Even though there is no convincing evidence to link HP-NAP to a disease outcome, recent findings supporting the pathogenic role of HP-NAP will be reviewed. In addition, the potential clinical applications of HP-NAP in vaccine development, clinical diagnosis, and drug development will be discussed.

  19. Antibacterial activity of Boesenbergia rotunda (L. Mansf. and Myristica fragrans Houtt. against Helicobacter pylori

    Directory of Open Access Journals (Sweden)

    Gail Mahady

    2006-03-01

    Full Text Available Helicobacter pylori, a gram-negative bacterium, is recognized as the primary etiological agent for the development of gastritis, dyspepsia, peptic ulcer as well as gastric and colon cancer. In developing countries the incidence of H. pylori infection ranges from 50-100%. Two Thai plants, namely Boesenbergia rotunda (L.Mansf. and Myristica fragrans Houtt., have been used to treat dyspepsia and peptic ulcer in Thai Traditional Medicine. Their crude extracts were previously reported to possess anti- H. pylori activity. This investigation proposed to test previously isolated bioactive compounds from B. rotunda and M. fragrans if they possessed anti- H. pylori activity. Primary cultures of H. pylori from local hospital patients in Thailand were used in the investigation. In vitro anti- H. pylori testing had been performed with pinostrobin and red oil from roots of B. rotunda, and dihydroguaiaretic acid from arils of M. fragrans. Clarithromycin (MIC 120 µg/mL was used as a positive control. All three compounds showed positive clear zone in agar diffusion test at p<0.05 in all 10 clinical cultures. Pinostrobin, red oil and dihydroguaiaretic acid autoclaved in blood agar medium had MIC of 125, 150, 100 µg/mL and MBC of 150, 175, 125 µg/mL, respectively. All three compounds have their activities against H. pylori in the same range of that of drug currently used in the treatment of peptic ulcer. Thus, all three compounds from B. rotunda and M. fragrans show good potential for further drug development. This investigation demonstrates that food and spice plants used in Thai Traditional Medicine for treatment of dyspepsia and peptic ulcer contain compounds which inhibit the growth of H. pylori in vitro. The result suggests that ingredients of some Thai food in regular diet may contribute to the low incidence of gastric cancer in the Thai population by affecting the growth of H. pylori.

  20. Synthesis and activity of Helicobacter pylori urease and catalase at low pH.

    OpenAIRE

    Bauerfeind, P; Garner, R; Dunn, B E; Mobley, H L

    1997-01-01

    BACKGROUND: Helicobacter pylori produces large amounts of urease presumably to be prepared for the rare event of a sudden acid exposure. The hypothesis that H pylori is acid sensitive and protein production is inhibited by low pH was examined. METHODS: H pylori or its soluble enzymes were incubated buffered or unbuffered at a pH ranging from 2-7 in the presence of 5 mM urea for 30 minutes. After exposure, urease and catalase activities of whole cells, supernatants, and soluble enzyme preparat...

  1. In vitro bactericidal activities of Japanese rice-fluid against Helicobacter pylori strains

    Directory of Open Access Journals (Sweden)

    Yoshiyuki Kawakami, Kozue Oana, Masayoshi Hayama, Hiroyoshi Ota, Masahiko Takeuchi, Kazuhiro Miyashita, Tsunetomo Matsuzawa, Kiyomi Kanaya

    2006-01-01

    Full Text Available Background: Helicobacter pylori has now been widely recognized as a causative agent of gastroduodenal diseases. The development of safer anti- H. pylori compounds is desirable due to the antibiotic-resistant strains emerged to date. Methods: We successfully developed the compounds of Rice-fluid derived from unpolished, polished, and usually cooked Japanese rice, and investigated their in vitro antibacterial activities by means of the Time-Kill-Curve methods against various species of bacteria including H. pylori strains. Results: All of the compounds revealed keen bactericidal activities against H. pylori, followed by Streptococcus pneumoniae and Campylobacter jejuni strains, but failed to affect the viability of other bacterial species investigated including staphylococci, enterococci, Pseudomonas aeruginosa, and other gram-negative rods belonging to the family Enterobacteraceae. The bactericidal activities were demonstrated to be time- and concentration-dependent. Conclusions: The compounds of Rice-fluid are considered to be potentially new and safe therapeutic regimens against H. pylori infections. The mechanism of their bactericidal activities against H. pylori strains remains to be elucidated.

  2. Mechanism of antibacterial activity of liposomal linolenic acid against Helicobacter pylori.

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    Sung Woo Jung

    Full Text Available Helicobacter pylori infects approximately half of the world population and is a major cause of gastritis, peptic ulcer, and gastric cancer. Moreover, this bacterium has quickly developed resistance to all major antibiotics. Recently, we developed a novel liposomal linolenic acid (LipoLLA formulation, which showed potent bactericidal activity against several clinical isolated antibiotic-resistant strains of H. pylori including both the spiral and coccoid form. In addition, LipoLLA had superior in vivo efficacy compared to the standard triple therapy. Our data showed that LipoLLA associated with H. pylori cell membrane. Therefore, in this study, we investigated the possible antibacterial mechanism of LipoLLA against H. pylori. The antibacterial activity of LipoLLA (C18:3 was compared to that of liposomal stearic acid (LipoSA, C18:0 and oleic acid (LipoOA, C18:1. LipoLLA showed the most potent bactericidal effect and completely killed H. pylori within 5 min. The permeability of the outer membrane of H. pylori increased when treated with LipoOA and LipoLLA. Moreover, by detecting released adenosine triphosphate (ATP from bacteria, we found that bacterial plasma membrane of H. pylori treated with LipoLLA exhibited significantly higher permeability than those treated with LipoOA, resulting in bacteria cell death. Furthermore, LipoLLA caused structural changes in the bacterial membrane within 5 min affecting membrane integrity and leading to leakage of cytoplasmic contents, observed by both transmission electron microscopy (TEM and scanning electron microscopy (SEM. Our findings showing rapid bactericidal effect of LipoLLA suggest it is a very promising new, effective anti-H. pylori agent.

  3. Inhibition of Helicobacter pylori and Its Associated Urease by Palmatine: Investigation on the Potential Mechanism

    Science.gov (United States)

    Tan, Li-Hua; Xu, Yi-Fei; Liu, Yu-Hong; Mo, Zhi-Zhun; Dou, Yao-Xing; Su, Rui; Su, Zi-Ren; Huang, Ping; Xie, Jian-Hui

    2017-01-01

    In this paper, we evaluated the anti-Helicobacter pylori activity and the possible inhibitory effect on its associated urease by Palmatine (Pal) from Coptis chinensis, and explored the potential underlying mechanism. Results indicated that Pal exerted inhibitory effect on four tested H. pylori strains (ATCC 43504, NCTC 26695, SS1 and ICDC 111001) by the agar dilution test with minimum inhibitory concentration (MIC) values ranging from 100 to 200 μg/mL under neutral environment (pH 7.4), and from 75 to 100 μg/mL under acidic conditions (pH 5.3), respectively. Pal was observed to significantly inhibit both H. pylori urease (HPU) and jack bean urease (JBU) in a dose-dependent manner, with IC50 values of 0.53 ± 0.01 mM and 0.03 ± 0.00 mM, respectively, as compared with acetohydroxamic acid, a well-known urease inhibitor (0.07 ± 0.01 mM for HPU and 0.02 ± 0.00 mM for JBU, respectively). Kinetic analyses showed that the type of urease inhibition by Pal was noncompetitive for both HPU and JBU. Higher effectiveness of thiol protectors against urease inhibition than the competitive Ni2+ binding inhibitors was observed, indicating the essential role of the active-site sulfhydryl group in the urease inhibition by Pal. DTT reactivation assay indicated that the inhibition on the two ureases was reversible, further supporting that sulfhydryl group should be obligatory for urease inhibition by Pal. Furthermore, molecular docking study indicated that Pal interacted with the important sulfhydryl groups and inhibited the active enzymatic conformation through N-H ∙ π interaction, but did not interact with the active site Ni2+. Taken together, Pal was an effective inhibitor of H. pylori and its urease targeting the sulfhydryl groups, representing a promising candidate as novel urease inhibitor. This investigation also gave additional scientific support to the use of C. chinensis to treat H. pylori-related gastrointestinal diseases in traditional Chinese medicine. Pal might be

  4. Helicobacter pylori urease activates blood platelets through a lipoxygenase-mediated pathway.

    Science.gov (United States)

    Wassermann, German E; Olivera-Severo, Deiber; Uberti, Augusto F; Carlini, Célia R

    2010-07-01

    The bacterium Helicobacter pylori causes peptic ulcers and gastric cancer in human beings by mechanisms yet not fully understood. H. pylori produces urease which neutralizes the acidic medium permitting its survival in the stomach. We have previously shown that ureases from jackbean, soybean or Bacillus pasteurii induce blood platelet aggregation independently of their enzyme activity by a pathway requiring platelet secretion, activation of calcium channels and lipoxygenase-derived eicosanoids. We investigated whether H. pylori urease displays platelet-activating properties and defined biochemical pathways involved in this phenomenon. For that the effects of purified recombinant H. pylori urease (HPU) added to rabbit platelets were assessed turbidimetrically. ATP secretion and production of lipoxygenase metabolites by activated platelets were measured. Fluorescein-labelled HPU bound to platelets but not to erythrocytes. HPU induced aggregation of rabbit platelets (ED(50) 0.28 microM) accompanied by ATP secretion. No correlation was found between platelet activation and ureolytic activity of HPU. Platelet aggregation was blocked by esculetin (12-lipoxygenase inhibitor) and enhanced approximately 3-fold by indomethacin (cyclooxygenase inhibitor). A metabolite of 12-lipoxygenase was produced by platelets exposed to HPU. Platelet responses to HPU did not involve platelet-activating factor, but required activation of verapamil-inhibitable calcium channels. Our data show that purified H. pylori urease activates blood platelets at submicromolar concentrations. This property seems to be common to ureases regardless of their source (plant or bacteria) or quaternary structure (single, di- or tri-chain proteins). These properties of HPU could play an important role in pathogenesis of gastrointestinal and associated cardiovascular diseases caused by H. pylori.

  5. Helicobacter pylori Activates HMGB1 Expression and Recruits RAGE into Lipid Rafts to Promote Inflammation in Gastric Epithelial Cells

    Science.gov (United States)

    Lin, Hwai-Jeng; Hsu, Fang-Yu; Chen, Wei-Wei; Lee, Che-Hsin; Lin, Ying-Ju; Chen, Yi-Ywan M.; Chen, Chih-Jung; Huang, Mei-Zi; Kao, Min-Chuan; Chen, Yu-An; Lai, Hsin-Chih; Lai, Chih-Ho

    2016-01-01

    Helicobacter pylori infection is associated with several gastrointestinal disorders in the human population worldwide. High-mobility group box 1 (HMGB1), a ubiquitous nuclear protein, mediates various inflammation functions. The interaction between HMGB1 and receptor for advanced glycation end-products (RAGE) triggers nuclear factor (NF)-κB expression, which in turn stimulates the release of proinflammatory cytokines, such as interleukin (IL)-8, and enhances the inflammatory response. However, how H. pylori activates HMGB1 expression and mobilizes RAGE into cholesterol-rich microdomains in gastric epithelial cells to promote inflammation has not been explored. In this study, we found that HMGB1 and RAGE expression increased significantly in H. pylori-infected cells compared with -uninfected cells. Blocking HMGB1 by neutralizing antibody abrogated H. pylori-elicited RAGE, suggesting that RAGE expression follows HMGB1 production, and silenced RAGE-attenuated H. pylori-mediated NF-κB activation and IL-8 production. Furthermore, significantly more RAGE was present in detergent-resistant membranes extracted from H. pylori-infected cells than in those from -uninfected cells, indicating that H. pylori exploited cholesterol to induce the HMGB1 signaling pathway. These results indicate that HMGB1 plays a crucial role in H. pylori-induced inflammation in gastric epithelial cells, which may be valuable in developing treatments for H. pylori-associated diseases. PMID:27667993

  6. The assessment of carotid intima media thickness and serum Paraoxonase-1 activity in Helicobacter pylori positive subjects

    Directory of Open Access Journals (Sweden)

    Akbas Halide S

    2010-08-01

    Full Text Available Abstract Background The role of inflammation in the pathogenesis and progression of atherosclerosis has been increasingly discussed. Although the seroepidemiological studies have suggested a relationship between Helicobacter pylori (H. pylori infection and atherosclerosis; the issue is still controversial. It is well known that abnormal lipid profil is related to atherosclerosis and the measurement of carotid-intima media thickness (CIMT is one of the surrogate marker of atherosclerosis. The serum concentration of high-density lipoprotein (HDL-C has been known to have an inverse correlation with the development of atherosclerosis. Paraoxonase-1 (PON1 is a major anti-atherosclerotic component of HDL-C. PON1 activity is related to lipid peroxidation and prospective cardiovascular risk. The aim of this study was to investigate CIMT and serum PON1 activities along with lipid parameters in H. pylori positive and negative subjects. Methods Thirty H. pylori positive subjects and thirty-one negative subjects were enrolled. H. pylori infection was diagnosed by the presence of positivity of stool H. pylori antigen test or Carbon 14 labeled urea breath test. Serum PON1 activity was measured spectrophotometrically. Traditional cardiovascular risk factors were investigated and laboratory analysis included measurement of serum triglycerides (TG, total cholesterol (TC, high-density lipoprotein (HDL-C and low-density lipoprotein cholesterol (LDL-C. We assessed CIMT by high-resolution ultrasound of both common carotid arteries. Results We found that the mean and maximum values of right and overall CIMT in H. pylori positive subjects were significantly thicker than those of H. pylori negative subjects. There was no significant differences in serum HDL-C, LDL-C, TC levels and TC/HDL-C ratios between two groups. Serum TG levels of H. pylori positive subjects were significantly higher than those of H. pylori negative subjects (p = 0.014. We found that PON1

  7. Inhibition of urease activity but not growth of Helicobacter pylori by acetohydroxamic acid.

    OpenAIRE

    Goldie, J; Veldhuyzen van Zanten, S J; Jalali, S; H. Richardson; Hunt, R H

    1991-01-01

    The in vitro effects of acetohydroxamic acid (AHA), a potent urease inhibitor, were studied to determine the effect on the urease activity and growth of 38 strains of Helicobacter pylori. AHA in concentrations of 50-1000 mg/l had a noticeably reversible inhibitory effect on the urease activity of the organism but no effect on growth.

  8. Recombinant Helicobacter pylori catalase

    Institute of Scientific and Technical Information of China (English)

    Yang Bai; Ya-Li Zhang; Jian-Feng Jin; Ji-De Wang; Zhao-Shan Zhang

    2003-01-01

    AIM: To construct a recombinant strain which highly expresses catalase of Helicobacter pylori(H.pylori) and assay the activity of H. pylori catalase.METHODS: The catalase DNA was amplified from H. pylori chromosomal DNA with PCR techniques and inserted into the prokaryotie expression vector pET-22b (+), and then was transformed into the BL21 (DE3) E. coli strain which expressed catalase recombinant protein. The activity of H.pylori catalase was assayed by the Beers & Sizers.RESULTS: DNA sequence analysis showed that the sequence of catalase DNA was the same as GenBank's research. The catalase recombinant protein amounted to 24.4 % of the total bacterial protein after induced with IPTG for 3 hours at 37 ℃ and the activity of H. pylori catalase was high in the BL21 (DE3) E. coli strain.CONCLUSION: A clone expressing high activity H. pylori catalase is obtained, laying a good foundation for further studies.

  9. Direct measurement of gastric H + / K +-ATPase activities in patients with or without Helicobacter pylori-associated chronic gastritis

    Institute of Scientific and Technical Information of China (English)

    Duangporn Thong-Ngam; Pisit Tangkijvanich; Pichet Sampatanukul; Paungpayom Prichakas; Varocha Mahachai; Piyaratana Tosukowong

    2005-01-01

    AIM: The role of Helicobacter pylori (H pylori) infection in gastric acid secretion of patients with chronic gastritisremains controversial. This study was designed to elucidate the effect of H pylori on H+/K+-ATPase activities in gastric biopsy specimens.METHODS: Eighty-two patients with chronic gastritis who had undergone upper endoscopy were included in this study. H pylori infection was confirmed by rapid urease test and histology. Gastric H+/K+-ATPase activities and serum gastrin concentrations were measured by an enzymatic method and radioimmunoassay, respectively. For those patients who received triple therapy for eradicating H pylori, changes in the activity of gastric H+/K+-ATPase and serum gastrin levels were also measured. RESULTS: The mean gastric H+/K+-ATPase activity in H pyloripositive group (42 patients) was slightly higher than thatin H pylori-negative group (29 patients) (169.65±52.9 and eradication of H pylori, the gastric H+/K+-ATPase activities slightly decreased compared to prior therapy (165.03±59.50 The mean basal gastrin concentration was slightly higher in H pylori-positive patients than in H pylori-negative patients (87.92±39.65 pg/mL vs75.04± 42.57 pg/mL, P= 0.228). The gastrin levels fell significantly after the eradication of Hpylori. (Before treatment 87.00±30.78 pg/mL, aftertreatment 64.73±18.96 pg/mL, P = 0.015).CONCLUSION: Gastric H+/K+-ATPase activities are not associated with H pylori status in patients with chronicgastritis.

  10. Fusion expression of Helicobacter pylori neutrophil-activating protein in E.coli

    Institute of Scientific and Technical Information of China (English)

    Qiao-Zhen Kang; Guang-Cai Duan; Qing-Tang Fan; Yuan-Lin Xi

    2005-01-01

    AIM: To produce a recombinant protein rMBP-NAP, which was fusionally expressed by Helicobacter pylori(H pylori)neutrophil-activating protein (NAP) and E. coli maltosebinding protein (MBP) and to evaluate its immunoreactivity and immunogenicity.METHODS: Neutrophil-activating protein gene of H pylori (HP-napA) was subcloned from the recombinant plasmid pNEB-napA, and fused to MalE gene of expressing vector pMAL-c2x. The recombinant plasmid pMAL-c2x-napA was confirmed by restriction enzyme digestion, and then transformed into E. coli TB1. Fusion protein rMBP-NAP was induced by IPTG and identified by SDS-PAGE analysis.Soluble rMBP-NAP was purified by amylose affinity chromatography. Immunoreactivity and immunogenicity of the fusion protein were evaluated by animal experiment,Western blotting with human H pylori anti-sera.RESULTS: E.coli TB1 carrying recombinant plasmid pMAL-c2x-napA was constructed and led to a high efficiency cytosol expression of fusion protein rBMP -NAP when induced by IPTG.The molecular weight of rBMP-NAP was about 57 kD,accounting for 37.55% of the total protein in the sonicated supematant of E. coli TB1 (pMAL-c2x-napA). The purity of the fusion protein after one-step affinity chromatography was 94% and the yield was 100 mg per liter of bacterial culture.The purified fusion protein could be specifically recognized by both human anti-sera from clinical patients with H pylori infection and rabbit sera immunized by rMBP-NAP itself.CONCLUSION: Recombinant protein rMBP-NAP might be a novel antigen for vaccine development against H pylori.

  11. Differential regulation of urease activity in Helicobacter hepaticus and Helicobacter pylori.

    Science.gov (United States)

    Belzer, Clara; Stoof, Jeroen; Beckwith, Catherine S; Kuipers, Ernst J; Kusters, Johannes G; van Vliet, Arnoud H M

    2005-12-01

    Helicobacter hepaticus is a pathogen of rodents, which causes diverse enteric and hepatic inflammatory diseases and malignancies. The urease enzyme is an important colonization factor of gastric Helicobacter species like Helicobacter pylori, but little is known about the role and regulation of urease in enterohepatic Helicobacter species. Here it is reported that urease activity of H. hepaticus does not contribute to acid resistance, and that it is nickel-responsive at the post-translational level. H. hepaticus strain ATCC 51449 did not grow or survive at pH 3.0, and supplementation with urea or NiCl2 did not abrogate this acid sensitivity. Furthermore, urease enzyme activity of H. hepaticus was acid-independent, which contrasts with the acid-induced urease system of H. pylori. Nickel supplementation of Brucella medium resulted in a tenfold increase in urease activity in both H. hepaticus and H. pylori, but the maximum level of urease activity in H. hepaticus was still three- to fivefold lower when compared to H. pylori in the same conditions. The increase in urease activity of H. hepaticus was not associated with elevation of urease mRNA or protein levels. Inhibition of protein synthesis by chloramphenicol did not affect nickel-responsive induction of urease activity in H. hepaticus, and confirmed that nickel induction occurs at the post-translational level, probably by activation of preformed apo-enzyme. In conclusion, both the role of the urease enzyme and the regulation of urease activity differ between the enterohepatic pathogen H. hepaticus and the gastric pathogen H. pylori.

  12. Total pepsin activity and gastrin in sera as markers of eradication of Helicobacter pylori

    NARCIS (Netherlands)

    Khoshkholgh, M.; Saberi-Firoozi, M.; Fattahi, M.; Siavoshi, F.; Khatibian, M.; Vahedi, H.; Mikaeli, J.; Ansari, R.; Alizadeh, B.; Malekzadeh, R.; Massarrat, S.

    1994-01-01

    The measurement of total pepsin activity by colorimetry, and gastrin by radioimmunoassay method was performed on the sera of 100 patients (80 with duodenal ulcer and 20 with non-ulcer dyspepsia) before and 4 weeks after the end of antibacterial treatment for eradication of Helicobacter pylori. While

  13. Cytotoxic isolates of Helicobacter pylori from Peptic Ulcer Diseases decrease K+-dependent ATPase Activity in HeLa cells

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    Archana Ayyagari

    2003-11-01

    Full Text Available Abstract Background Helicobacter pylori is a Gram negative bacterium that plays a central role in the etiology of chronic gastritis and peptic ulcer diseases. However, not all H. pylori positive cases develop advanced disease. This discriminatory behavior has been attributed to the difference in virulence of the bacteria. Among all virulence factors, cytotoxin released by H. pylori is the most important factor. In this work, we studied variation in H. pylori isolates from Indian dyspeptic patients on the basis of cytotoxin production and associated changes in K+-dependent ATPase (one of its targets enzyme activity in HeLa cells. Methods The patients were retrospectively grouped on the basis of endoscopic and histopathological observation as having gastritis or peptic ulcer. The HeLa cells were incubated with the broth culture filtrates (BCFs of H. pylori isolates from patients of both groups and observed for the cytopathic effects: morphological changes and viability. In addition, the K+-dependent ATPase activity was measured in HeLa cells extracts. Results The cytotoxin production was observed in 3/7 (gastritis and 4/4 (peptic ulcer H. pylori isolates. The BCFs of cytotoxin producing H. pylori strains reduced the ATPase activity of HeLa cells to 40% of that measured with non-cytotoxin producing H. pylori strains (1.33 μmole Pi/mg protein and 3.36 μmole Pi/mg protein, respectively, p Conclusions Our results suggest that the isolation of cytotoxic H. pylori is more common in severe form of acid peptic diseases (peptic ulcer than in gastritis patients from India. Also the cytotoxin released by H. pylori impairs the ion-transporting ATPase and is a measure of cytotoxicity.

  14. Inhibitory Activities of Palmatine from Coptis chinensis Against Helicobactor pylori and Gastric Damage.

    Science.gov (United States)

    Jung, Joohee; Choi, Jae Sue; Jeong, Choon-Sik

    2014-03-01

    Helicobacter pylori (H. pylori) is the most important factor of gastric disease in clinical practice. Moreover, smoking, stress and a poor diet may be additive factors for gastric damage. With these factors, increasing infection of H. pylori triggers gastritis, gastric ulcers and gastric cancer. To develop a new protective agent, we are concerned with plant-derived extract. The extract of Coptis chinensis (C. chinensis) and its constituents were investigated to assess their protective activities against gastric damage. The C. chinensis extract showed a scavenging effect against 2, 2-diphenyl-1-picrylhydrazyl (DPPH) and superoxide radicals, inhibition of H. pylori colonization and antiulcerogenic activities in rat. In particular, palmatine derived from C. chinensis was found to be the novel protective agent. It is better than the C. chinensis extract, berberine, a well-known constituent of C. chinensis. We suggest that palmatine from the root cortex of C. chinensis may be a good candidate for the development of new pharmaceuticals to prevent gastric disease.

  15. One-step chromatographic purification of Helicobacter pylori neutrophil-activating protein expressed in Bacillus subtilis.

    Directory of Open Access Journals (Sweden)

    Kuo-Shun Shih

    Full Text Available Helicobacter pylori neutrophil-activating protein (HP-NAP, a major virulence factor of Helicobacter pylori (H. pylori, is capable of activating human neutrophils to produce reactive oxygen species (ROS and secrete inammatory mediators. HP-NAP is a vaccine candidate, a possible drug target, and a potential in vitro diagnostic marker for H. pylori infection. HP-NAP has also been shown to be a novel therapeutic agent for the treatment of allergic asthma and bladder cancer. Hence, an efficient way to obtain pure HP-NAP needs to be developed. In this study, one-step anion-exchange chromatography in negative mode was applied to purify the recombinant HP-NAP expressed in Bacillus subtilis (B. subtilis. This purification technique was based on the binding of host cell proteins and/or impurities other than HP-NAP to DEAE Sephadex resins. At pH 8.0, almost no other proteins except HP-NAP passed through the DEAE Sephadex column. More than 60% of the total HP-NAP with purity higher than 91% was recovered in the flow-through fraction from this single-step DEAE Sephadex chromatography. The purified recombinant HP-NAP was further demonstrated to be a multimeric protein with a secondary structure of α-helix and capable of activating human neutrophils to stimulate ROS production. Thus, this one-step negative chromatography using DEAE Sephadex resin can efficiently yield functional HP-NAP from B. subtilis in its native form with high purity. HP-NAP purified by this method could be further utilized for the development of new drugs, vaccines, and diagnostics for H. pylori infection.

  16. Antigenic proteins of Helicobacter pylori of potential diagnostic value.

    Science.gov (United States)

    Khalilpour, Akbar; Santhanam, Amutha; Wei, Lee Chun; Saadatnia, Geita; Velusamy, Nagarajan; Osman, Sabariah; Mohamad, Ahmad Munir; Noordin, Rahmah

    2013-01-01

    Helicobacter pylori antigen was prepared from an isolate from a patient with a duodenal ulcer. Serum samples were obtained from culture-positive H. pylori infected patients with duodenal ulcers, gastric ulcers and gastritis (n=30). As controls, three kinds of sera without detectable H. pylori IgG antibodies were used: 30 from healthy individuals without history of gastric disorders, 30 from patients who were seen in the endoscopy clinic but were H. pylori culture negative and 30 from people with other diseases. OFF-GEL electrophoresis, SDS-PAGE and Western blots of individual serum samples were used to identify protein bands with good sensitivity and specificity when probed with the above sera and HRP-conjugated anti-human IgG. Four H. pylori protein bands showed good (≥ 70%) sensitivity and high specificity (98-100%) towards anti-Helicobacter IgG antibody in culture- positive patients sera and control sera, respectively. The identities of the antigenic proteins were elucidated by mass spectrometry. The relative molecular weights and the identities of the proteins, based on MALDI TOF/ TOF, were as follows: CagI (25 kDa), urease G accessory protein (25 kDa), UreB (63 kDa) and proline/pyrroline- 5-carboxylate dehydrogenase (118 KDa). These identified proteins, singly and/or in combinations, may be useful for diagnosis of H. pylori infection in patients.

  17. Antibacterial activities of almond skins on cagA-positive and-negative clinical isolates of Helicobacter pylori

    Science.gov (United States)

    2013-01-01

    Background Helicobacter pylori is known to be a gastric pathogen of humans. Eradication regimens for H. pylori infection have some side effects, compliance problems, relapses, and antibiotic resistance. Therefore, the need for alternative therapies for H. pylori infections is of special interest. We have previously shown that polyphenols from almond skins are active against a range of food-borne pathogens. The aim of this study was to evaluate the antibacterial effects of natural almond skins before and after simulated human digestion and the pure flavonoid compounds epicatechin, naringenin and protocatechuic acid against H. pylori. Results H. pylori strains were isolated from gastric biopsy samples following standard microbiology procedures. Also, cagA and vacA genes were identified using PCR. Susceptibility studies on 34 strains of H. pylori, including two reference strains (ATCC 43504, ATCC 49503), were performed by the standard agar dilution method. Natural almond skin was the most effective compound against H. pylori (MIC range, 64 to 128 μg/ml), followed by natural skin post gastric digestion (MIC range, 128 to 512 μg/ml), and natural almond skin post gastric plus duodenal digestion (MIC range, 256 to 512 μg/ml). Amongst the pure flavonoid compounds, protocatechuic acid showed the greatest activity (MIC range, 128 to 512 μg/ml) against H. pylori strains. Conclusions Polyphenols from almond skins were effective in vitro against H. pylori, irrespective of genotype status and could therefore be used in combination with antibiotics as a novel strategy for antibiotic resistance. PMID:23659287

  18. Construction of an oral recombinant DNA vaccine from H pylori neutrophil activating protein and its immunogenicity

    Institute of Scientific and Technical Information of China (English)

    Bo Sun; Zhao-Shen Li; Zhen-Xing Tu; Guo-Ming Xu; Yi-Qi Du

    2006-01-01

    AIM: To construct a live attenuated Salmonella typhimurium (S.typhimurium) strain harboring the H pylori neutrophil activating protein (HP-NAP) gene as an oral recombinant DNA vaccine, and to evaluate its immunogenicity.METHODS: By genetic engineering methods, the genomic DNA of H pylori was extracted as a template. The total length of the HP-NAP gene was amplified by polymerase chain reaction (PCR) and cloned into pBT vector for sequencing and BLAST analysis, then subcloned into a eukaryotic expression vector pIRES followed by PCR identification and restriction enzyme digestion. The identified recombinant plasmid pIRES-NAP was transfected into COS-7 cells for target fusion protein expression, and its antigenicity was detected by Western blotting. Then the recombinant plasmid was transformed into a live attenuated S. typhimurium strain SL7207 as an oral vaccine strain, and its immunogenicity was evaluated with animal experiments.RESULTS: A 435 bp product was cloned using high homology with HP-NAP gene in GenBank (more than 98%). With identification by PCR and restriction enzyme digestion, a recompinant eukaryotic expression plasmid pIRES-NAP containing the HP-NAP gene of H pylori was successfully constructed. The expressed target protein had a specific reaction with H pylor(i) whole cell antibody and showed a single strip result detected by Western blotting. Oral immunization of mice with recombinant DNA vaccine strain SL7207 (pIRES-NAP) also induced a specific immune response.CONCLUSION: The successful construction of HP-NAP oral DNA vaccine with good immunogenicity may help to further investigate its immunoprotection effects and develop vaccine against H pylori infection.

  19. Coordinate increase of telomerase activity and c-Myc expression in Helicobacter pylori-associated gastric diseases

    Institute of Scientific and Technical Information of China (English)

    Guo-Xin Zhang; Yan-Hong Gu; Zhi-Quan Zhao; Shun-Fu Xu; Hong-Ji Zhang; Hong-Di Wang; Bo Hao

    2004-01-01

    AIM: To detect the telomerase activity and c-Myc expression in gastric diseases and to examine the relation between these values and Helicobacter pylori (H pylori) as a risk factor for gastric cancer.METHODS: One hundred and seventy-one gastric samples were studied to detect telomerase activity using a telomerase polymerase chain reaction enzyme linked immunosorbent assay (PCR-ELTSA), and c-Myc expression using immunohistochemistry.RESULTS: The telomerase activity and c-Myc expression were higher in cancers (87.69% and 61.54%) than in noncancerous tissues. They were higher in chronic atrophic gastritis with severe intestinal metaplasia (52.38% and 47.62%) than in chronic atrophic gastritis with mild intestinal metaplasia (13.33% and 16.67%). Tn chronic atrophic gastritis with severe intestinal metaplasia, the telomerase activity and c-Myc expression were higher in cases with -H pylori infection (67.86% and 67.86%) than in those without infection (21.43%and 7.14%). c-Myc expression was higher in gastric cancer with H pylori infection (77.27%) than in that without infection (28.57%). The telomerase activity and c-Nyc expression were coordinately up-regulated in H pylori infected gastric cancer and chronic atrophic gastritis with severe intestinal metaplasia.CONCLUSION: H pylori infection may influence both telomerase activity and c-Myc expression in gastric diseases,especially in chronic atrophic gastritis.

  20. The synthesis, structure and activity evaluation of pyrogallol and catechol derivatives as Helicobacter pylori urease inhibitors.

    Science.gov (United States)

    Xiao, Zhu-Ping; Ma, Tao-Wu; Fu, Wei-Chang; Peng, Xiao-Chun; Zhang, Ai-Hua; Zhu, Hai-Liang

    2010-11-01

    Some pyrogallol and catechol derivatives were synthesized, and their urease inhibitory activity was evaluated by using acetohydroxamic acid (AHA), a well known Helicobacter pylori urease inhibitor, as positive control. The assay results indicate that many compounds have showed potential inhibitory activity against H. pylori urease. 4-(4-Hydroxyphenethyl)phen-1,2-diol (2a) was found to be the most potent urease inhibitor with IC(50)s of 1.5±0.2 μM for extracted fraction and 4.2±0.3 μM for intact cell, at least 10 times and 20 times lower than those of AHA (IC(50) of 17.2±0.9 μM, 100.6±13 μM), respectively. This finding indicate that 2a would be a potential urease inhibitor deserves further research. Molecular dockings of 2a into H. pylori urease active site were performed for understanding the good activity observed.

  1. Efficacy of Probiotic Supplementation Therapy for Helicobacter pylori Eradication: A Meta-Analysis of Randomized Controlled Trials

    Science.gov (United States)

    Deng, Jiaqi; Yan, Qiong; Yang, Chun; Xia, Guodong; Zhou, Xian

    2016-01-01

    Background Traditional Helicobacter pylori (H. pylori) eradication therapies have shown efficacies below 80% in several studies, and their use has been accompanied by antibiotic-related side effects. Some recent studies have reported that supplementing standard therapies with probiotics can improve the efficacy and tolerability of Helicobacter pylori eradication therapy. Objective To assess the effects of probiotic supplementation on the eradication rates and therapy-related adverse event rates of anti-Helicobacter pylori regimens. Methods We searched PubMed, Medline, the Cochrane Central Registry of Controlled Trials and the Chinese Biomedical Database for eligible randomized controlled trials published through July, 2015. Review Manager 5.3 was used for all statistical analyses. Results Thirteen randomized controlled trials involving a total of 2306 patients were included in our analysis. Intent-to-treat (ITT) analysis performed using a fixed-effects model (test for heterogeneity I2 = 45%) showed that the pooled relative risk (RR) of eradication was significantly higher in the probiotic supplementation group than in the control group [RR 1.15, 95% confidence interval (CI): 1.10–1.20, Ppylori eradication rates. However, supplementation with Lactobacillus alone did not significantly decrease the overall incidence of side effects (RR = 0.61, 95% CI: 0.11–3.51, P = 0.58). Our study also showed that probiotic supplementation before, during or after H. pylori eradication therapy improved eradication rates, regardless of supplementation duration. Furthermore, probiotic supplementation during H. pylori treatment reduced the incidence of side effects. Conclusion Probiotic supplementation during anti-Helicobacter pylori treatment may be effective for improving H. pylori eradication rates, minimizing the incidence of therapy-related adverse events and alleviating most disease-related clinical symptoms. However, our results should be interpreted with caution because of

  2. The Importance of Toll-like Receptors in NF-κB Signaling Pathway Activation by Helicobacter pylori Infection and the Regulators of this Response.

    Science.gov (United States)

    Hu, Yi; Liu, Jian-Ping; Zhu, Yin; Lu, Nong-Hua

    2016-10-01

    Helicobacter pylori (H. pylori) is a common pathogenic bacterium in the stomach that infects almost half of the population worldwide and is closely related to gastric diseases and some extragastric diseases, including iron-deficiency anemia and idiopathic thrombocytopenic purpura. Both the Maastricht IV/Florence consensus report and the Kyoto global consensus report have proposed the eradication of H. pylori to prevent gastric cancer as H.pylori has been shown to be a major cause of gastric carcinogenesis. The interactions between H. pylori and host receptors induce the release of the proinflammatory cytokines by activating proinflammatory signaling pathways such as nuclear factor kappa B (NF-κB), which plays a central role in inflammation, immune response, and carcinogenesis. Among these receptors, Toll-like receptors (TLRs) are classical pattern recognition receptors in the recognition of H. pylori and the mediation of the host inflammatory and immune responses to H. pylori. TLR polymorphisms also contribute to the clinical consequences of H. pylori infection. In this review, we focus on the functions of TLRs in the NF-κB signaling pathway activated by H. pylori, the regulators modulating this response, and the functions of TLR polymorphisms in H.pylori-related diseases.

  3. Helicobacter pylori in colorectal neoplasms: is there an aetiological relationship?

    Directory of Open Access Journals (Sweden)

    Tharakan Joseph

    2007-05-01

    Full Text Available Abstract Background This pilot study was carried out to determine whether Helicobacter pylori can be detected in normal colon or in association with colorectal neoplasia. Methods Paraffin processed colonic tissue blocks of normal colonic mucosa (n = 60, and patients diagnosed as adenoma (n = 60, and adenocarcinoma (n = 60 were retrieved from our archive; the adenoma group included tubular (n = 20, tubulovillous (n = 20 and villous adenomas (n = 20. 4 μm sections were stained by immunohistochemical methods using anti-Helicobacter pylori antibodies (polyclonal NCL-HPp and monoclonal NCL-C-jejuni. Results Significant numbers of Helicobacter pylori were identified in tubular adenomas (OR = 11.13; 95%CI = 1.62–76.70, tubulovillous adenomas (OR = 10.45; 95%CI = 1.52–71.52 and adenocarcinomas (OR = 8.13; 95%CI = 1.40–46.99 compared to controls: there was no association in numbers of Helicobacter pylori and villous adenomas (OR = 2.95; 95%CI = 0.29–9.96. Conclusion We conclude that although, in this pilot study, there appears to be an association in the prevalence of Helicobacter pylori with some, but not all, colorectal neoplasms, we can not infer causality from these results. These findings need to be further substantiated with a prospective study and the use of molecular biological techniques to determine a causal association.

  4. Azithromycin in a triple therapy for H. pylori eradication in active duodenal ulcer

    Institute of Scientific and Technical Information of China (English)

    Vladimir T. Ivashkin; Tatiana L. Lapina; Oksana Yu. Bondarenko; Olga A. Sklanskaya; Petr Ya. Grigoriev; Yuri V. Vasiliev; Emilia P. Yakovenko; Pavel V. Gulyaev; Valeri I. Fedchenko

    2002-01-01

    AIM: To assess and compare the efficacy and safety of twotriple regimes: A) metronidazole, amoxicillin and omeprazole,which is still widely used in Russia, and B) azithromycin,amoxicillin and omeprazole in healing active duodenal ulcerand H.pylori eradication. METHODS: 100 patients with active duodenal ulcer wereincluded in the open, multicentre, randomized study withcomparative groups. Patients were randomly assigned toone of the following one-week triple regimes: A)metronidazole 500 mg bid, amoxicillin 1 g bid and omeprazole20 mg bid (OAM, n=50) and B) azithromycin 1 g od for thefirst 3 days (total dose 3 g), amoxicillin 1 g bid andomeprazole 20 mg bid (OAA, n=50). Omeprazole 20 mg odwas given after the eradication course as a monotherapyfor three weeks. The control endoscopy was performed 8weeks after the entry. H. pylori infection was determined inthe entry of the study and four weeks after the cessation oftreatment by means of histology and CLO-test.RESULTS: 97 patients completed the study according tothe protocol (1 patient of the OAM group did not come tothe control endoscopy, 2 patients of the OAA group stoppedthe treatment because of mild allergic urticaria). Duodenalulcers were healed in 48 patients of the OAM group (96 %;CI 90.5-100 %) and in 46 patients of the OAA group (92 %;CI 89.5-94.5 %) (p=ns). H. pylori infection was eradicatedin 15 out of 50 patients with OAM (30 %; CI 17-43 %) andin 36 out of 50 patients treated with OAA (72 %; CI 59-85 %)(P<0.001)-ITT analysis.CONCLUSION: The triple therapy with omeprazole,amoxicillin and metronidazole failed to eradicate H. pylori inthe majority of patients, which is an essential argument towithdraw this regimen out of the national recommendations.Macrolide with amoxicillin are preferable to achieve highereradication rates. Azithromycin (1 g od for the first 3 days)can be considered as a successful component of the triplePPI-based regimen.

  5. Neutrophil-activating protein (HP-NAP) versus ferritin (Pfr): comparison of synthesis in Helicobacter pylori.

    Science.gov (United States)

    Dundon, W G; Polenghi, A; Del Guidice, G; Rappuoli, R; Montecucco, C

    2001-05-15

    We recently reported that the neutrophil-activating protein (HP-NAP) of Helicobacter pylori is capable of binding iron in vitro. To more fully understand the relationship between iron and HP-NAP the synthesis of HP-NAP was compared to that of Pfr, another iron-binding protein of H. pylori. Synthesis of HP-NAP and Pfr in growing cultures of H. pylori was analysed under iron depletion and iron, copper, nickel and zinc overload. The synthesis of HP-NAP and Pfr in H. pylori was also analysed under conditions of varying pH and oxidative stress. In addition, recombinant HP-NAP and Pfr were produced in Escherichia coli to assess the contribution of the two proteins to increased survival of E. coli under heavy metal overload. Our data reveal that both HP-NAP and Pfr accumulate in the stationary phase of growth. HP-NAP synthesis is not regulated by iron depletion or overload or by the presence of copper, nickel or zinc in liquid medium and it does not confer resistance to these metals when produced in E. coli. Except for an increase in the synthesis of Pfr at pH 5.7 neither the pH or oxidative stress conditions investigated had an affect on the synthesis of either protein. An increase in Pfr synthesis was observed under iron overload and a decrease was observed under conditions of copper, nickel and zinc overload confirming previous reports. Recombinant Pfr, as well as conferring resistance to iron and copper as previously reported, also conferred resistance to zinc overload when produced in E. coli.

  6. Helicobacter pylori

    Science.gov (United States)

    ... Old Feeding Your 1- to 2-Year-Old Helicobacter pylori KidsHealth > For Parents > Helicobacter pylori Print A A A What's in this article? ... Diagnosis Treatment Prevention When to Call the Doctor Helicobacter pylori ( H. pylori ) bacteria are a common cause of ...

  7. IRAK-M expression limits dendritic cell activation and proinflammatory cytokine production in response to Helicobacter pylori.

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    Jessica Shiu

    Full Text Available Helicobacter pylori (H. pylori infects the gastric mucosa and persists for the life of the host. Bacterial persistence may be due to the induction of regulatory T cells (Tregs whichmay have protective effects against other diseases such as asthma. It has been shown that H. pylori modulates the T cell response through dendritic cell reprogramming but the molecular pathways involved are relatively unknown. The goal of this study was to identify critical elements of dendritic cell (DC activation and evaluate potential influence on immune activation. Microarray analysis was used to demonstrate limited gene expression changes in H. pylori stimulated bone marrow derived DCs (BMDCs compared to the BMDCs stimulated with E. coli. IRAK-M, a negative regulator of TLR signaling, was upregulated and we selectedit for investigation of its role in modulating the DC and T cell responses. IRAK-M(-/- and wild type BMDC were compared for their response to H. pylori. Cells lacking IRAK-M produced significantly greater amounts of proinflammatory MIP-2 and reduced amounts of immunomodulatory IL-10 than wild type BMDC. IRAK-M(-/- cells also demonstrated increased MHC II expression upon activation. However, IRAK-M(-/- BMDCs were comparable to wild type BMDCs in inducing T-helper 17 (TH17 and Treg responses as demonstrated in vitro using BMDC CD4+ T cells co-culture assays,and in vivo though the adoptive transfer of CD4(+ FoxP3-GFP T cells into H. pylori infected IRAK-M(-/- mice. These results suggest that H. pylori infection leads to the upregulation of anti-inflammatory molecules like IRAK-M and that IRAK-M has a direct impact on innate functions in DCs such as cytokine and costimulation molecule upregulation but may not affect T cell skewing.

  8. Compound 13, an α1-selective small molecule activator of AMPK, inhibits Helicobacter pylori-induced oxidative stresses and gastric epithelial cell apoptosis

    Energy Technology Data Exchange (ETDEWEB)

    Zhao, Hangyong; Zhu, Huanghuang; Lin, Zhou; Lin, Gang; Lv, Guoqiang, E-mail: lvguoqiangwuxivip@163.com

    2015-08-07

    Half of the world's population experiences Helicobacter pylori (H. pylori) infection, which is a main cause of gastritis, duodenal and gastric ulcer, and gastric cancers. In the current study, we investigated the potential role of compound 13 (C13), a novel α1-selective small molecule activator of AMP-activated protein kinase (AMPK), against H. pylori-induced cytotoxicity in cultured gastric epithelial cells (GECs). We found that C13 induced significant AMPK activation, evidenced by phosphorylation of AMPKα1 and ACC (acetyl-CoA carboxylase), in both primary and transformed GECs. Treatment of C13 inhibited H. pylori-induced GEC apoptosis. AMPK activation was required for C13-mediated GEC protection. Inhibition of AMPK kinase activity by the AMPK inhibitor Compound C, or silencing AMPKα1 expression by targeted-shRNAs, alleviated C13-induced GEC protective activities against H. pylori. Significantly, C13 inhibited H. pylori-induced reactive oxygen species (ROS) production in GECs. C13 induced AMPK-dependent expression of anti-oxidant gene heme oxygenase (HO-1) in GECs. Zinc protoporphyrin (ZnPP) and tin protoporphyrin (SnPP), two HO-1 inhibitors, not only suppressed C13-mediated ROS scavenging activity, but also alleviated its activity in GECs against H. pylori. Together, these results indicate that C13 inhibits H. pylori-induced ROS production and GEC apoptosis through activating AMPK–HO–1 signaling. - Highlights: • We synthesized compound 13 (C13), a α1-selective small molecule AMPK activator. • C13-induced AMPK activation requires α1 subunit in gastric epithelial cells (GECs). • C13 enhances Helicobacter pylori-induced pro-survival AMPK activation to inhibit GEC apoptosis. • C13 inhibits H. pylori-induced reactive oxygen species (ROS) production in GECs. • AMPK-heme oxygenase (HO-1) activation is required for C13-mediated anti-oxidant activity.

  9. Active Peptic Ulcer Disease in Patients with Hepatitis C Virus-Related Cirrhosis: The Role of Helicobacter pylori Infection and Portal Hypertensive Gastropathy

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    Maria Dore

    2004-01-01

    Full Text Available BACKGROUND & AIM: The relationship between Helicobacter pylori infection and peptic ulcer disease in cirrhosis remains controversial. The purpose of the present study was to investigate the role of H pylori infection and portal hypertension gastropathy in the prevalence of active peptic ulcer among dyspeptic patients with compensated hepatitis C virus (HCV-related cirrhosis.

  10. Helicobacter pylori CagA disrupts epithelial patterning by activating myosin light chain.

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    Jonathan B Muyskens

    Full Text Available Helicobacter pylori infection is a leading cause of ulcers and gastric cancer. We show that expression of the H. pylori virulence factor CagA in a model Drosophila melanogaster epithelium induces morphological disruptions including ectopic furrowing. We find that CagA alters the distribution and increases the levels of activated myosin regulatory light chain (MLC, a key regulator of epithelial integrity. Reducing MLC activity suppresses CagA-induced disruptions. A CagA mutant lacking EPIYA motifs (CagA(EPISA induces less epithelial disruption and is not targeted to apical foci like wild-type CagA. In a cell culture model in which CagA(EPISA and CagA have equivalent subcellular localization, CagA(EPISA is equally potent in activating MLC. Therefore, in our transgenic system, CagA is targeted by EPIYA motifs to a specific apical region of the epithelium where it efficiently activates MLC to disrupt epithelial integrity.

  11. Potential implications of Helicobacter pylori-related neutrophil-activating protein

    Institute of Scientific and Technical Information of China (English)

    Jannis Kountouras; Ioannis Venizelos; Christos Zavos; Georgia Deretzi; Emmanuel Gavalas; Dimitrios Chatzopoulos; Panagiotis Katsinelos; Elena Tsiaousi; Stergios Gagalis; Stergios A Polyzos

    2012-01-01

    Helicobacter pylori (H. pylori) virulence factors promote the release of various chemoattractants/inflammatory mediators, including mainly the neutrophilattractant chemokine interleukin-8 and neutrophilactivating protein (NAP), involved in H. pylori-induced gastric pathologies. Co-administration of Chios mastic gum (CMG), which inhibits H. pylori NAP, with an H. pylori eradication regimen might add clinical benefits against H. pylori-related gastric pathologies, but possibly not CMG as main therapy. Although H. pylori NAP and other H. pylori-related cytotoxins [i.e., vaculating cytotoxin (VacA)] appear to play a major role in generating and maintaining the H. pylori-associated gastric inflammatory response and H. pylori NAP is a promising vaccine candidate against H. pylori infection (H. pylori-I), concerns regarding its potential drawbacks, particularly neurogenic ones, due to possible crossmimicry, should be considered. Possible cross-mimicry between H. pylori NAP and/or bacterial aquaporin (AQP) and neural tissues may be associated with the anti-AQP-4 antibody-related neural damage in multiple sclerosis (MS)/neuromyelitis optica patients. Moreover, the sequence homology found between H. pylori VacA and human Na+/K+-ATPase A subunit suggests that antibodies to VacA involve ion channels in abaxonal Schwann cell plasmalemma resulting in demyelination in some patients. A series of factors have been implicated in inducing blood-brain barrier (BBB) disruption, including inflammatory mediators (e.g., cytokines and chemokines induced by H. pylori-I) and oxidative stress. BBB disruption permits access of AQP4-specific antibodies and T lymphocytes to the central nervous system, thereby playing a major role in multiple sclerosis pathogenesis. Relative studies show a strong association between H. pylori-I and MS. H. pylori-I induces humoral and cellular immune responses that, owing to the sharing of homologous epitopes (molecular mimicry), cross-react with components of

  12. Natural Diversity in the N Terminus of the Mature Vacuolating Cytotoxin of Helicobacter pylori Determines Cytotoxin Activity

    OpenAIRE

    Letley, D. P.; Atherton, J C

    2000-01-01

    Naturally occurring noncytotoxic vacA type s2 strains of Helicobacter pylori have a 12-residue extension to the vacuolating cytotoxin (VacA) compared with cytotoxic type s1 strains. We show that adding the region encoding this extension to type s1 vacA completely abolishes vacuolating cytotoxin activity but has no effect on VacA production.

  13. Antimicrobial activity of Sapindus mukorossi and Rheum emodi extracts against H pylori: In vitro and in vivo studies

    Science.gov (United States)

    Ibrahim, Mohammed; Khan, Aleem A; Tiwari, Santosh K; Habeeb, Mohammed Aejaz; Khaja, MN; Habibullah, CM

    2006-01-01

    AIM: To evaluate the antibacterial activity of Sapindus mukorossi (S. mukorossi) and Rheum emodi (R. emodi). METHODS: Powders of S. mukorossi and R. emodi were extracted successively with petroleum ether, benzene, chloroform and ethanol and were concentrated in vacuum. The disk diffusion method was used for in vitro studies and in vivo studies were performed on male Wister rats. Thirty resistant clinical isolates of H pylori, as determined by their antibiotic sensitivity patterns by E-test, along with two Gram +ve (S. aureus, B. subtilis) and two Gram -ve (E. coli, P. vugaris) organisms were screened for their susceptibility patterns against these extracts. RESULTS: In our screening, all 30 resistant isolates and the other four organisms (two Gram +ve S. aureus, B. subtilis and two Gram -ve, E. coli, P. vugaris) were sensitive to the test compounds. It was found that ethanol and chloroform extracts of S. mukorossi and ethanol and benzene extracts of R. emodi inhibited H pylori at very low concentrations. In the in vitro study, the isolates showed a considerable zone of inhibition at very low concentrations (10 μg/mL) for both the extracts. In the in vivo study, the H pylori infection was cleared with minimal doses of extracts of S. mukorossi (2.5 mg/mL) and R. emodi (3.0 mg/mL) given orally for seven days. CONCLUSION: We can conclude from this study that the extracts of S. mukorossi and R. emodi inhibited the growth of pylori in vitro and, in in vivo studies, the H pylori infection cleared within seven days at very low concentrations. We also found that H pylori did not acquire resistance against these herbal extracts even after 10 consecutive passages. PMID:17131475

  14. Antimicrobial activity of Sapindus mukorossi and Rheum emodi extracts against H pylori: In vitro and in vivo studies

    Institute of Scientific and Technical Information of China (English)

    Mohammed Ibrahim; Aleem A Khan; Santosh K Tiwari; Mohammed Aejaz Habeeb; MN Khaja; CM Habibullah

    2006-01-01

    AIM: To evaluate the antibacterial activity of Sapindus mukorossi (S. mukorossi) and Rheum emodi (R. emodi).METHODS: Powders of S. mukorossi and R. emodi were extracted successively with petroleum ether,benzene, chloroform and ethanol and were concentrated in vacuum. The disk diffusion method was used for in vitro studies and in vivo studies were performed on male Wister rats. Thirty resistant clinical isolates of H pylori,as determined by their antibiotic sensitivity patterns by E-test, along with two Gram +ve (S. aureus, B. subtilis)and two Gram -ve (E. coli, P. vugaris) organisms were screened for their susceptibility patterns against these extracts.RESULTS: In our screening, all 30 resistant isolates and the other four organisms (two Gram +ye S. aureus,B. subtilis and two Gram -ve, E. coli, P. vugaris) were sensitive to the test compounds. It was found that ethanol and chloroform extracts of S. mukorossi and ethanol and benzene extracts of R. emodi inhibited H pylori at very low concentrations. In the in vitro study,the isolates showed a considerable zone of inhibition at very low concentrations (10 μg/mL) for both the extracts. In the in vivo study, the H pylori infection was cleared with minimal doses of extracts of S. mukorossi (2.5 mg/mL) and R. emodi(3.0 mg/mL) given orally for seven days.CONCLUSION: We can conclude from this study that the extracts of S. mukorossi and R. emodi inhibited the growth of pylori in vitro and, in in vivo studies, the H pylori infection cleared within seven days at very low concentrations. We also found that H pylori did not acquire resistance against these herbal extracts even after 10 consecutive passages.

  15. Prediction of extracellular proteases of the human pathogen Helicobacter pylori reveals proteolytic activity of the Hp1018/19 protein HtrA.

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    Martin Löwer

    Full Text Available Exported proteases of Helicobacter pylori (H. pylori are potentially involved in pathogen-associated disorders leading to gastric inflammation and neoplasia. By comprehensive sequence screening of the H. pylori proteome for predicted secreted proteases, we retrieved several candidate genes. We detected caseinolytic activities of several such proteases, which are released independently from the H. pylori type IV secretion system encoded by the cag pathogenicity island (cagPAI. Among these, we found the predicted serine protease HtrA (Hp1019, which was previously identified in the bacterial secretome of H. pylori. Importantly, we further found that the H. pylori genes hp1018 and hp1019 represent a single gene likely coding for an exported protein. Here, we directly verified proteolytic activity of HtrA in vitro and identified the HtrA protease in zymograms by mass spectrometry. Overexpressed and purified HtrA exhibited pronounced proteolytic activity, which is inactivated after mutation of Ser205 to alanine in the predicted active center of HtrA. These data demonstrate that H. pylori secretes HtrA as an active protease, which might represent a novel candidate target for therapeutic intervention strategies.

  16. STUDY OF DIAGNOSTIC TESTS FOR HELICOBACTER PYLORI INFECTION

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    Rajeswari

    2015-12-01

    Full Text Available Helicobacter pylori is the causative agent of most cases of gastritis and peptic ulcer. The diagnosis of H. pylori is an essential element in the management of many common gastrointestinal pathologies. AIMS 1. Comparison of invasive and non-invasive tests to choose the appropriate test for the diagnosis of H. pylori infection. 2. Validation of the comparison of the different diagnostic tests. METHOD Blood and antral biopsy specimens from 100 acid peptic disease patients and blood samples from 10 control subjects were collected. Biopsies were used for Rapid Urease Test (RUT, culture and Gram’s stain by conventional method. Serology using Euroimmun Anti Helicobacter pylori IgG ELISA was done. The efficacy of these tests was determined by calculating the sensitivity, specificity, positive predictive value, negative predictive value and accuracy using culture as gold standard. RESULTS Of the 100 cases 14% were culture positive, 18% Gram stain positive, 36% Rapid urease test positive and 42% were positive for Serology IgG antibodies for H. pylori. Maximum percentage of positivity was in peptic ulcer cases (52.9% followed by Gastritis cases (23.6% and Dyspepsia cases (14.2%. Among the 100 cases of study group, 42(42% were positive by serological test IgG ELISA for H. pylori, whereas 3(30% were positive out of 10 in control group. RUT, IgG Serology showed 100% sensitivity and negative predictive value and Gram stain showed highest specificity (90.1%. CONCLUSION RUT+Gram’s stain+IgG Serology showed highest Sensitivity, Specificity, Positive predictive value, Negative predictive value and Accuracy. IgG Serology indicates a marker for infection. It can be used as a primary diagnostic procedure.

  17. Lactobacilli inhibit interleukin-8 production induced by Helicobacter pylori lipopolysaccharide-activated Toll-like receptor 4

    Institute of Scientific and Technical Information of China (English)

    Chao Zhou; Feng-Zhen Ma; Xue-Jie Deng; Hong Yuan; Hong-Sheng Ma

    2008-01-01

    AIM: To investigate the effect of Lactobacillus bulgaricus (LBG) on the Toll-like receptor 4 (TLR4) pathway and interleukin-8 (IL-8) production in SGC-7901 cells treated with Helicobacter pyloriSydney strain 1 lipopolysaccharide (H pyloriSS1-LPS).METHODS: SGC-7901 cells were treated with H pyIoriSS1-LPS in the presence or absence of pretreatment for 1 h with viable LBG or supematant recovered from LBG culture MRS broth (LBG-s). Cellular lysates were prepared for Western blot with anti-TLR4,anti-transforming growth factor β-activated kinase 1 (TAK1), anti-phospho-TAK1, anti-nuclear factor κB (NF-κB), anti-p38 mitogen-activated protein kinase (p38MAPK), and anti-phospho-p38MAPK antibodies.The amount of IL-8 in cell culture medium was measured by ELISA.RESULTS: H pyloriSS1-LPS up-regulated the expression of TLR4, stimulated the phosphorylation of TAK1, subsequently enhanced the activation of NFκB and the phosphorylation of p38MAPK in a timedependent manner, leading to augmentation of IL-8 production in SGC-7901 cells. Viable LBG or LBG-s pretreatment attenuated the expression of TLR4,inhibited the phosphorylation of TAK1 and p38MAPK,prevented the activation of NF-κB, and consequently blocked IL-8 production.CONCLUSION: H pyloriSS1-LPS induces IL-8production through activating TLR4 signaling in SGC-7901 cells and viable LBG or LBG-s prevents H pyloriSS1-LPS-mediated IL-8 production via inhibition of the TLR4 pathway.

  18. Ca2+/calmodulin-dependent kinase II contributes to inhibitor of nuclear factor-kappa B kinase complex activation in Helicobacter pylori infection.

    Science.gov (United States)

    Maubach, Gunter; Sokolova, Olga; Wolfien, Markus; Rothkötter, Hermann-Josef; Naumann, Michael

    2013-09-15

    Helicobacter pylori, a class I carcinogen, induces a proinflammatory response by activating the transcription factor nuclear factor-kappa B (NF-κB) in gastric epithelial cells. This inflammatory condition could lead to chronic gastritis, which is epidemiologically and biologically linked to the development of gastric cancer. So far, there exists no clear knowledge on how H. pylori induces the NF-κB-mediated inflammatory response. In our study, we investigated the role of Ca(2+) /calmodulin-dependent kinase II (CAMKII), calmodulin, protein kinases C (PKCs) and the CARMA3-Bcl10-MALT1 (CBM) complex in conjunction with H. pylori-induced activation of NF-κB via the inhibitor of nuclear factor-kappa B kinase (IKK) complex. We use specific inhibitors and/or RNA interference to assess the contribution of these components. Our results show that CAMKII and calmodulin contribute to IKK complex activation and thus to the induction of NF-κB in response to H. pylori infection, but not in response to TNF-α. Thus, our findings are specific for H. pylori infected cells. Neither the PKCs α, δ, θ, nor the CBM complex itself is involved in the activation of NF-κB by H. pylori. The contribution of CAMKII and calmodulin, but not PKCs/CBM to the induction of an inflammatory response by H. pylori infection augment the understanding of the molecular mechanism involved and provide potential new disease markers for the diagnosis of gastric inflammatory diseases including gastric cancer.

  19. [Evaluation of infection by Helicobacter pylori in HIV positive patients trough enzyme immunoassay and specific amplification of DNA].

    Science.gov (United States)

    Gutiérrez, Sandra; Chacón-Petrola, María; Flores, María; Pinto, Angela; Pacheco, Mariela

    2005-03-01

    The objective of this work was to assess the effectiveness of detection of specific antibodies anti-Helicobacter pylori (H. pylori) by ELISA and amplification of specific DNA by polimerase chain reaction (PCR) as diagnostic methods of infection of H. pylori in HIV positive patients. Twenty two patients with HIV infection were studied, with ages between 26 to 35 years, 17 masculine, 55% with gastrointestinal symptoms, controlled in the Unit of Immunology, CHET. Inclusion approaches: older than 18 years, with confirmed diagnosis of HIV infection (ELISA and WB), lymphocyte subpopulation and good general conditions. Consent in writing was obtained. Exclusion approaches: previous diagnosis of H. pylori infection or treatment with antibiotics in the three previous months to their inclusion. The quantification of IgG anti H. pylori was carried out by Enzyme Immunoassay methods (ELISA). Biopsy of gastric mucosa was obtained by superior endoscopic study. The amplification of DNA for H. pylori was performed by PCR (Wizard SV Genomik and PCR Ready-Promega). In the statistical analysis was used the test of Fisher, with a level of significance of 5% (0.05). In 15 patients of the total group, antibodies anti H. pylori were confirmed, without statistical association with the presence or not of digestives symptoms, neither with the number of lymphocytes CD4 + in peripheral blood. Also 15 patients were positives by PCR for H. pylori DNA, 73.3% of them presented levels of CD4+ above 200 cells. There was not statistical association between the positivity of this method and levels of lymphocytes CD4+. In 12 of the 15 patients with positive results by PCR, antibodies anti H. pylori were evidenced, and among the 7 patients with negative serology to H. pylori, PCR was positive in three of them. In conclusion, serology is an effective method for the diagnose of H. pylori infection in VIH+ patients, but its negativity doesn't discard the infection for this bacillus.

  20. Helicobacter pylori-induced activation of β-catenin involves low density lipoprotein receptor-related protein 6 and Dishevelled

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    Lendeckel Uwe

    2010-02-01

    Full Text Available Abstract Background The human microbial pathogen Helicobacter pylori resides in the stomach of about fifty percent of the world's population and represents a risk factor for chronic gastritis, peptic ulcers and, in rare cases, gastric cancer. Alterations of the Wnt/β-catenin signaling pathway have been described in almost every human cancer disease, due to the regulation of target genes being involved in cell cycle control, differentiation, cell migration or stem cell control. Our study aimed to elucidate the role of proximal Wnt signaling components low density lipoprotein receptor-related protein 6 (LRP6 and Dishevelled (Dvl in the activation of β-catenin early after infection of gastric epithelial cells with H. pylori. Results Infection of gastric epithelial NCI-N87 cells with H. pylori induces rapid phosphorylation of the Wnt/β-catenin pathway co-receptor LRP6 independent of the cytotoxin-associated gene A (CagA or vacuolating cytotoxin A (VacA. However, bacteria lacking a functional type 4 secretion system (T4SS failed to induce LRP6 phosphorylation. Further, we identified proteins of the Dvl family, namely Dvl2 and Dvl3, which are involved in LRP6 phosphorylation. H. pylori-induced nuclear accumulation of β-catenin and its transcriptional activation, and expression of Wnt target genes are strongly reduced in stable knockdown cell lines deficient for LRP6, Dvl2 or Dvl3. Conclusion We analysed the H. pylori-induced activation of Wnt-signaling factors and demonstrate for the first time that the canonical Wnt-signaling proteins LRP6 and Dvl2 and Dvl3 are involved in the regulation of β-catenin.

  1. Epithelial cell ADAM17 activation by Helicobacter pylori: role of ADAM17 C-terminus and Threonine-735 phosphorylation.

    Science.gov (United States)

    McClurg, Urszula L; Danjo, Kazuma; King, Harry O; Scott, Gina B; Robinson, Philip A; Crabtree, Jean E

    2015-03-01

    Helicobacter pylori transactivates the epidermal growth factor receptor (EGFR) on gastric epithelial cells via a signalling cascade involving a disintegrin and metalloprotease 17 (ADAM17) cleavage of membrane bound heparin binding-epidermal growth factor (HB-EGF). The effects of H. pylori on ADAM17 C-terminus in epithelial cells have been examined. Total cellular ADAM17 and surface expression of ADAM17 were significantly increased by H. pylori in AGS gastric epithelial cells. These changes were associated with ADAM17 C-terminal phosphorylation at T375 and S791. AGS cells lacking the ADAM17 C-terminal domain induced significantly attenuated cleavage of HB-EGF and were also unable to upregulate HB-EGF and EGFR transcripts to the same extent as cells expressing full length ADAM17. In mitotic unstimulated AGS and ADAM17 over-expressing AGS cells, ADAM17 was highly T735 phosphorylated indicating ADAM17 T735 phosphorylation is modified during the cell cycle. In conclusion, H. pylori induced ADAM17 C-terminal T735 and/or S791 phosphorylation in gastric epithelial cells are likely to be an important trigger inducing ADAM17 activation and shedding of HB-EGF leading to EGFR transactivation. ADAM17 over-expression in gastric cancer represents a potential target for therapeutic intervention.

  2. Arginase 2 deletion leads to enhanced M1 macrophage activation and upregulated polyamine metabolism in response to Helicobacter pylori infection.

    Science.gov (United States)

    Hardbower, Dana M; Asim, Mohammad; Murray-Stewart, Tracy; Casero, Robert A; Verriere, Thomas; Lewis, Nuruddeen D; Chaturvedi, Rupesh; Piazuelo, M Blanca; Wilson, Keith T

    2016-10-01

    We reported that arginase 2 (ARG2) deletion results in increased gastritis and decreased bacterial burden during Helicobacter pylori infection in mice. Our studies implicated a potential role for inducible nitric oxide (NO) synthase (NOS2), as Arg2 (-/-) mice exhibited increased NOS2 levels in gastric macrophages, and NO can kill H. pylori. We now bred Arg2 (-/-) to Nos2 (-/-) mice, and infected them with H. pylori. Compared to wild-type mice, both Arg2 (-/-) and Arg2 (-/-) ;Nos2 (-/-) mice exhibited increased gastritis and decreased colonization, the latter indicating that the effect of ARG2 deletion on bacterial burden was not mediated by NO. While Arg2 (-/-) mice demonstrated enhanced M1 macrophage activation, Nos2 (-/-) and Arg2 (-/-) ;Nos2 (-/-) mice did not demonstrate these changes, but exhibited increased CXCL1 and CXCL2 responses. There was an increased expression of the Th1/Th17 cytokines, interferon gamma and interleukin 17, in gastric tissues and splenic T-cells from Arg2 (-/-), but not Nos2 (-/-) or Arg2 (-/-) ;Nos2 (-/-) mice. Gastric tissues from infected Arg2 (-/-) mice demonstrated increased expression of arginase 1, ornithine decarboxylase, adenosylmethionine decarboxylase 1, spermidine/spermine N (1)-acetyltransferase 1, and spermine oxidase, along with increased spermine levels. These data indicate that ARG2 deletion results in compensatory upregulation of gastric polyamine synthesis and catabolism during H. pylori infection, which may contribute to increased gastric inflammation and associated decreased bacterial load. Overall, the finding of this study is that ARG2 contributes to the immune evasion of H. pylori by restricting M1 macrophage activation and polyamine metabolism.

  3. [Clinical significance of Helicobacter pylori in children with idiopathic thrombocytopenic purpura].

    Science.gov (United States)

    Tang, Ying; Wang, Shu-Chun; Wang, Lu-Juan; Liu, Yong; Wang, Hai-Ying; Wang, Zhan-Ju

    2013-04-01

    This study was aimed to investigate the clinic significance of helicobacter pylori (HP) in children with idiopathic thrombocytopenic purpura (ITP). The infection of HP in 92 ITP children was determined by (13) C-Urea Breath Test, the same test was also performed on 66 healthy children. The 68 children infected with HP were randomly divided into 2 groups: single drug group treated only with corticosteroid and; combined drug group treated with corticosteroid and anti-helicobacter pylori treatment. The results showed that 68 patients infected with HP were found in 92 ITP children (74.7%), 26 patients infected with HP were observed in 66 healthy children (39.4%), which was lower than that in ITP children (74.7%, P helicobacter pylori therapy, the total effective rate and cure rate of ITP patients increased respectively from 73.5% to 94.1%, and the total recurrence rate (17.0%) was much lower than single drug group (47.1%, P helicobacter pylori group was higher than that in the single drug group (P helicobacter pylori therapy would help to improve the therapeutic efficacy and reduce the recurrence of ITP children.

  4. Helicobacter pylori CagA triggers expression of the bactericidal lectin REG3γ via gastric STAT3 activation.

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    Kai Syin Lee

    Full Text Available BACKGROUND: Most of what is known about the Helicobacter pylori (H. pylori cytotoxin, CagA, pertains to a much-vaunted role as a determinant of gastric inflammation and cancer. Little attention has been devoted to potential roles of CagA in the majority of H. pylori infected individuals not showing oncogenic progression, particularly in relation to host tolerance. Regenerating islet-derived (REG3γ encodes a secreted C-type lectin that exerts direct bactericidal activity against Gram-positive bacteria in the intestine. Here, we extend this paradigm of lectin-mediated innate immunity, showing that REG3γ expression is triggered by CagA in the H. pylori-infected stomach. METHODOLOGY/PRINCIPAL FINDINGS: In human gastric mucosal tissues, REG3γ expression was significantly increased in CagA-positive, compared to CagA-negative H. pylori infected individuals. Using transfected CagA-inducible gastric MKN28 cells, we recapitulated REG3γ induction in vitro, also showing that tyrosine phosphorylated, not unphosphorylated CagA triggers REG3γ transcription. In concert with induced REG3γ, pro-inflammatory signalling downstream of the gp130 cytokine co-receptor via the signal transducer and activator of transcription (STAT3 and transcription of two cognate ligands, interleukin(IL-11 and IL-6, were significantly increased. Exogenous IL-11, but not IL-6, directly stimulated STAT3 activation and REG3γ transcription. STAT3 siRNA knockdown or IL-11 receptor blockade respectively abrogated or subdued CagA-dependent REG3γ mRNA induction, thus demonstrating a requirement for uncompromised signalling via the IL-11/STAT3 pathway. Inhibition of the gp130-related SHP2-(Ras-ERK pathway did not affect CagA-dependent REG3γ induction, but strengthened STAT3 activation as well as augmenting transcription of mucosal innate immune regulators, IL-6, IL-8 and interferon-response factor (IRF1. CONCLUSIONS/SIGNIFICANCE: Our results support a model of CagA-directed REG3

  5. Biological activity of the virulence factor cagA of Helicobacter pylori

    Institute of Scientific and Technical Information of China (English)

    朱永良; 郑树; 钱可大; 方平楚

    2004-01-01

    Background China is one of the countries with the highest incidence of H. Pylori and more than 9090 isolates possessed the cagA gene. This study was to evaluate the biological activity of the H.pylori virulence factor cagA isolated from Chinese patients. Methods cagA DNA fragments were amplified from the genomic DNA and subsequently cloned into the mammalian expression vector for cell transfection and DNA sequencing. cagA protein, phosphorylated-tyrosine cagA and the complex of cagA precipitated with SHP-2 were identified respectively by western blot in the crude cell lysate from conditionally immortalized gastric epithelial cells at 48 hours after transfection with cagA DNA. In addition, the ability of induction of scattering phenotype was examined after transient expression of cagA in AGS cells. Results The C-terminal half of cagA contained only one repeated sequence and three tandem five-amino-acid motifs glutamic acid-proline-isoleucine-tyrosine-alanine (EPIYA). Moreover, the amino acid sequence of D2 region in repeated sequence was aspartic acid-phenylanaline-aspartic acid (D-F-D) which was significantly distinguished from the three repeated sequences and aspartic acid-aspartic adid-leucine (D-D-L) in the western standard strain NCTC11637. Western blot revealed that cagA became phosphorylated in tyrosine site and bound with SHP-2 after transient expression of cagA DNA in gastric epithelial cells. Transient expression of cagA in AGS cells showed that cagA was able to induce the elongation phenotype although to a lesser extent than western strains. Conclusions cagA perturbs cell signaling pathways by binding with SHP-2. However, significant difference exists in amino acid sequence and biological function of cagA in Chinese compared with those of western countries.

  6. Linked color imaging improves endoscopic diagnosis of active Helicobacter pylori infection

    Science.gov (United States)

    Dohi, Osamu; Yagi, Nobuaki; Onozawa, Yuriko; Kimura-Tsuchiya, Reiko; Majima, Atsushi; Kitaichi, Tomoko; Horii, Yusuke; Suzuki, Kentaro; Tomie, Akira; Okayama, Tetsuya; Yoshida, Naohisa; Kamada, Kazuhiro; Katada, Kazuhiro; Uchiyama, Kazuhiko; Ishikawa, Takeshi; Takagi, Tomohisa; Handa, Osamu; Konishi, Hideyuki; Naito, Yuji; Itoh, Yoshito

    2016-01-01

    Background and study aims: Linked color imaging (LCI) is a new image-enhanced endoscopy technique using a laser light source to enhance slight differences in mucosal color. The aim of this study was to compare the usefulness of LCI and conventional white light imaging (WLI) endoscopy for diagnosing Helicobacter pylori (H. pylori). Patients and methods: We retrospectively analyzed images from 60 patients examined with WLI and LCI endoscopy between October 2013 and May 2014. Thirty patients had H. pylori infections, and other thirty patients tested negative for H. pylori after eradication therapy. Four endoscopists evaluated the 2 types of images to determine which was better at facilitating a diagnosis of H. pylori infection. Results: H. pylori infection was identified with LCI by enhancing the red appearance of the fundic gland mucosa. The accuracy, sensitivity, and specificity for diagnosing H. pylori infection using WLI were 74.2 %, 81.7 %, and 66.7 %, respectively, while those for LCI were 85.8 %, 93.3 %, and 78.3 %, respectively. Thus, the accuracy and sensitivity for LCI were significantly higher than those for WLI (P = 0.002 and P = 0.011, respectively). The kappa values for the inter- and intraobserver variability among the 4 endoscopists were higher for LCI than for WLI. Conclusions: H. pylori infection can be identified by enhancing endoscopic images of the diffuse redness of the fundic gland using LCI. LCI is a novel image-enhanced endoscopy and is more useful for diagnosing H. pylori infection than is WLI. PMID:27556101

  7. Synthesis, structure-activity relationship analysis and kinetics study of reductive derivatives of flavonoids as Helicobacter pylori urease inhibitors.

    Science.gov (United States)

    Xiao, Zhu-Ping; Peng, Zhi-Yun; Dong, Jing-Jun; He, Juan; Ouyang, Hui; Feng, Yu-Ting; Lu, Chun-Lei; Lin, Wan-Qiang; Wang, Jin-Xiang; Xiang, Yin-Ping; Zhu, Hai-Liang

    2013-05-01

    In a continuing study for discovering urease inhibitors based on flavonoids, nineteen reductive derivatives of flavonoids were synthesized and evaluated against Helicobacter pylori urease. Analysis of structure-activity relationship disclosed that 4-deoxy analogues are more potent than other reductive products. Out of them, 4',7,8-trihydroxyl-2-isoflavene (13) was found to be the most active with IC50 of 0.85 μM, being over 20-fold more potent than the commercial available urease inhibitor, acetohydroxamic acid (AHA). Kinetics study revealed that 13 is a competitive inhibitor of H. pylori urease with a Ki value of 0.641 μM, which is well matched with the results of molecular docking. Biological evaluation and mechanism study of 13 suggest that it is a good candidate for discovering novel anti-gastritis and anti-gastric ulcer agent.

  8. Sequence and apoptotic activity of VacA cytotoxin cloned from a Helicobacter pylori Thai clinical isolate.

    Science.gov (United States)

    Junaid, Muhammad; Al-Gubare, Sarbast; Yousef, Muhammad; Ubol, Mathukorn Na; Leetachewa, Somphob; Muanprasat, Chatchai; Angsuthanasombat, Chanan; Chaicumpa, Wanpen; Ali, Niaz; Katzenmeier, Gerd

    2014-01-01

    The vacuolating cytotoxin VacA produced by Helicobacter pylori induces the formation of large cytoplasmic vacuoles in host gastric epithelial cells as well as a release of cytochrome C from mitochondria resulting in cell apoptosis. Considerable sequence diversity in VacA relating to different degrees of disease severity is observed with clinical samples from a multitude of geographic places. In this study we describe expression in Escherichia coli, purification to homogeneity and in vitro assay of its apoptotic activity of a VacA toxin from a H. pylori isolate of a Thai patient with gastrointestinal lymphoma. Sequencing revealed that the deduced amino acid sequence of the cloned Thai isolate VacA is similar to H. pylori s1/m2 type strains. The percent sequence similarity to the model strain 60190 was lower due to the presence of extra amino acids in the mid (m) region. The purified VacA toxin exhibited significant apoptotic activity on both T84 and MDCK epithelial cell lines, as revealed by DAPI staining, whereby the observed activity was significantly higher on MDCK cells. These findings could relate to a modulation of VacA activity on host cells in the Thai isolate-VacA toxin that may differ from those of the model strain.

  9. Sequence and Apoptotic Activity of VacA Cytotoxin Cloned from a Helicobacter pylori Thai Clinical Isolate

    Directory of Open Access Journals (Sweden)

    Muhammad Junaid

    2014-01-01

    Full Text Available The vacuolating cytotoxin VacA produced by Helicobacter pylori induces the formation of large cytoplasmic vacuoles in host gastric epithelial cells as well as a release of cytochrome C from mitochondria resulting in cell apoptosis. Considerable sequence diversity in VacA relating to different degrees of disease severity is observed with clinical samples from a multitude of geographic places. In this study we describe expression in Escherichia coli, purification to homogeneity and in vitro assay of its apoptotic activity of a VacA toxin from a H. pylori isolate of a Thai patient with gastrointestinal lymphoma. Sequencing revealed that the deduced amino acid sequence of the cloned Thai isolate VacA is similar to H. pylori s1/m2 type strains. The percent sequence similarity to the model strain 60190 was lower due to the presence of extra amino acids in the mid (m region. The purified VacA toxin exhibited significant apoptotic activity on both T84 and MDCK epithelial cell lines, as revealed by DAPI staining, whereby the observed activity was significantly higher on MDCK cells. These findings could relate to a modulation of VacA activity on host cells in the Thai isolate-VacA toxin that may differ from those of the model strain.

  10. Helicobacter pylori promotes invasion and metastasis of gastric cancer cells through activation of AP-1 and up-regulation of CACUL1.

    Science.gov (United States)

    Kong, Ying; Ma, Li-qing; Bai, Pei-song; Da, Rong; Sun, Hong; Qi, Xiao-gai; Ma, Jie-qun; Zhao, Ru-ming; Chen, Nan-zheng; Nan, Ke-jun

    2013-11-01

    Infection with Helicobacter pylori is important in the development and progression of gastric cancer. However, the mechanisms that regulate this activation in gastric tumors remain elusive. CACUL1 has been cloned and identified as a novel gene that is expressed in many types of cancer and is involved in cell cycle regulation and tumor growth. The current study aimed to examine the expression of CACUL1 in gastric cancer samples and analyze its correlation with H. pylori infection. We found that CACUL1 was highly expressed in gastric cancer tissues and negatively correlated with gastric cancer differentiation and TNM stage. In addition, CACUL1 expression was high in H. pylori-infected tissues compared with H. pylori non-infected tissue. We found that H. pylori could up-regulate CACUL1 expression through activating protein 1. The up-regulation of CACUL1 expression could promote matrix metalloproteinase 9 and Slug expression to increase invasion and metastasis of tumor cells. These results suggested that H. pylori-triggered CACUL1 production occurred in an activating protein 1-dependent manner and regulated matrix metalloproteinase 9 and Slug expression to affect the invasion and metastasis of tumor cells. Therefore, CACUL1 is a potential therapeutic target for the treatment of aggressive gastric cancer.

  11. Helicobacter pylori induces Snail expression through ROS-mediated activation of Erk and inactivation of GSK-3β in human gastric cancer cells.

    Science.gov (United States)

    Ngo, Hoang-Kieu-Chi; Lee, Hee Geum; Piao, Juan-Yu; Zhong, Xiancai; Lee, Ha-Na; Han, Hyeong-Jun; Kim, Wonki; Kim, Do-Hee; Cha, Young-Nam; Na, Hye-Kyung; Surh, Young-Joon

    2016-12-01

    Helicobacter pylori (H. pylori) infection has been known to be implicated in human gastric carcinogenesis. Snail, the zinc-finger transcription factor known as a key inducer of changes in the cell shape and morphogenetic movement, is aberrantly overexpressed and correlates with lymph node metastasis in gastric cancer. In the present study, we investigated whether H. pylori could induce Snail activation to provoke these changes. Using a cell scatter assay, we noticed that human gastric cancer AGS cells infected with H. pylori underwent morphological changes as well as disruption of cell-cell interaction, which was then reversed by silencing of Snail by use of small interfering RNA (siRNA). In addition, infection with H. pylori resulted in an increased intracellular level of Snail in gastric cancer cells, which was abrogated in the presence of U0126 and LY294002, inhibitors of MEK/Erk and PI3K/Akt pathways, respectively. Cycloheximide pulse-chase experiments coupled with immunocytochemical analysis revealed that the induction of Snail by H. pylori was regulated at multiple levels, including increased transcription of Snail mRNA, inhibition of protein degradation, and enhancement of nuclear translocation of Snail. Pre-treatment of AGS cells with N-acetylcysteine, a well-known reactive oxygen species (ROS) scavenger, attenuated the H. pylori-induced activation of Erk, its binding to Snail promoter, inactivation of GSK-3β, and accumulation of Snail. Collectively, these findings suggest that the upregulation of Snail expression induced by H. pylori and transformation to a spindle-like shape as a consequence in gastric cancer cells are attributable to ROS-mediated activation of Erk and the inhibition of GSK-3β signaling. © 2016 Wiley Periodicals, Inc.

  12. Helicobacter pylori

    OpenAIRE

    BATESON, M

    2000-01-01

    Helicobacter pylori infection is a major cause of peptic ulcer disease, and its detection and eradication are now an important part of gastroenterology. Effective regimes are available which will eliminate the organism in about 90% of cases in developed countries.


Keywords: Helicobacter pylori

  13. Detection and evaluation of antibodies against neutrophil-activating protein of Helicobacter pylori in patients with gastric cancer

    Institute of Scientific and Technical Information of China (English)

    Min Long; Jun Luo; Yan Li; Fang-Yin Zeng; Ming Li

    2009-01-01

    AIM: To detect and evaluate the antibodies against Helicobacter pylori ( H pylori) neutrophil-activating protein (HP-NAP) in patients with gastric cancer and other gastroduodenal diseases.METHODS: Recombinant HP-NAP was prepared from a prokaryotic expression system in Escherichia coli. Serum positivity and level of HP-NAP-specific antibodies in sera from 43 patients with gastric cancer, 28 with chronic gastritis, 28 with peptic ulcer, and 89 healthy controls were measured by rHP-NAP-based ELISA. rHP-NAP-stimulated production of interleukin-8 (IL-8) and growth-related oncogene (GROα) cytokines in the culture supernatant of SGC7901 gastric epithelial cells was also detected. RESULTS: The serum positivity and mean absorbance value of HP-NAP-specific antibodies in the gastric cancer group (97.7% and 1.01 ± 0.24) were significantly higher than those in the chronic gastritis group (85.7% and 0.89 ± 0.14, P < 0.005) and healthy control group (27.7% and 0.65 ± 0.18, P < 0.001). The sensitivity and specificity of ELISA for the detection of HP-NAP-specific antibodies were 95.5% and 91.5%, respectively. HP-NAP could slightly upregulate IL-8 production in gastric epithelial cell lines but had no effect on GROα production. CONCLUSION: Infection with virulent H pylori strains secreting HP-NAP is associated with severe gastroduodenal diseases, and HP-NAP may play a role in the development of gastric carcinoma. rHP-NAPbased ELISA can be used as a new method to detect H pylori infection. The direct effect of HP-NAP on gastric epithelial cells may be limited, but HP-NAP may contribute to inflammatory response or carcinogenesis by activating neutrophils.

  14. Development of gastric cancer in nonatrophic stomach with highly active inflammation identified by serum levels of pepsinogen and Helicobacter pylori antibody together with endoscopic rugal hyperplastic gastritis.

    Science.gov (United States)

    Watanabe, Mika; Kato, Jun; Inoue, Izumi; Yoshimura, Noriko; Yoshida, Takeichi; Mukoubayashi, Chizu; Deguchi, Hisanobu; Enomoto, Shotaro; Ueda, Kazuki; Maekita, Takao; Iguchi, Mikitaka; Tamai, Hideyuki; Utsunomiya, Hirotoshi; Yamamichi, Nobutake; Fujishiro, Mitsuhiro; Iwane, Masataka; Tekeshita, Tatsuya; Mohara, Osamu; Ushijima, Toshikazu; Ichinose, Masao

    2012-12-01

    This study aimed to elucidate groups at high risk of developing cancer among patients with serologically identified Helicobacter pylori infection and nonatrophic stomach. Annual endoscopy was performed for a mean of 5.4 years in 496 asymptomatic middle-aged men who were H. pylori antibody-positive and pepsinogen (PG) test-negative. Subjects were stratified according to the activity of H. pylori-associated gastritis measured by serum levels of PG and H. pylori antibody, and/or by endoscopic findings of rugal hyperplastic gastritis (RHG), and cancer development was investigated. During the study period, seven cases of cancer developed in the cohort (incidence rate, 261/100,000 person-years), with 85.7% developing in the group showing a PGI/II ratio ≤ 3.0, reflecting active inflammation-based high PGII levels. Cancer incidence was significantly higher in this group (750/100,000 person-years) than in groups with less active gastritis. Furthermore, cancer incidence for this group was significantly higher in the subgroup with high H. pylori antibody titers than in the low-titer subgroup. Meanwhile, endoscopic findings revealed that 11.7% of subjects showed RHG reflecting localized highly active inflammation, and cancer risk was significantly higher in patients with RHG than in patients without. Combining the two serum tests and endoscopic examination for RHG allowed identification of subjects with more active gastritis and higher cancer risk. No cancer development was observed in these high-risk subjects after H. pylori eradication. Subjects with highly active gastritis identified by the two serological tests and endoscopic RHG constitute a group at high risk of cancer development with H. pylori-infected nonatrophic stomach.

  15. α-Lipoic Acid Inhibits Helicobacter pylori-Induced Oncogene Expression and Hyperproliferation by Suppressing the Activation of NADPH Oxidase in Gastric Epithelial Cells

    Directory of Open Access Journals (Sweden)

    Eunyoung Byun

    2014-01-01

    Full Text Available Hyperproliferation and oncogene expression are observed in the mucosa of Helicobacter pylori- (H. pylori- infected patients with gastritis or adenocarcinoma. Expression of oncogenes such as β-catenin and c-myc is related to oxidative stress. α-Lipoic acid (α-LA, a naturally occurring thiol compound, acts as an antioxidant and has an anticancer effect. The aim of this study is to investigate the effect of α-LA on H. pylori-induced hyperproliferation and oncogene expression in gastric epithelial AGS cells by determining cell proliferation (viable cell numbers, thymidine incorporation, levels of reactive oxygen species (ROS, NADPH oxidase activation (enzyme activity, subcellular levels of NADPH oxidase subunits, activation of redox-sensitive transcription factors (NF-κB, AP-1, expression of oncogenes (β-catenin, c-myc, and nuclear localization of β-catenin. Furthermore, we examined whether NADPH oxidase mediates oncogene expression and hyperproliferation in H. pylori-infected AGS cells using treatment of diphenyleneiodonium (DPI, an inhibitor of NADPH oxidase. As a result, α-LA inhibited the activation of NADPH oxidase and, thus, reduced ROS production, resulting in inhibition on activation of NF-κB and AP-1, induction of oncogenes, nuclear translocation of β-catenin, and hyperproliferation in H. pylori-infected AGS cells. DPI inhibited H. pylori-induced activation of NF-κB and AP-1, oncogene expression and hyperproliferation by reducing ROS levels in AGS cells. In conclusion, we propose that inhibiting NADPH oxidase by α-LA could prevent oncogene expression and hyperproliferation occurring in H. pylori-infected gastric epithelial cells.

  16. Structural and mechanistic insights into Helicobacter pylori NikR activation

    Science.gov (United States)

    Bahlawane, C.; Dian, C.; Muller, C.; Round, A.; Fauquant, C.; Schauer, K.; de Reuse, H.; Terradot, L.; Michaud-Soret, I.

    2010-01-01

    NikR is a transcriptional metalloregulator central in the mandatory response to acidity of Helicobacter pylori that controls the expression of numerous genes by binding to specific promoter regions. NikR/DNA interactions were proposed to rely on protein activation by Ni(II) binding to high-affinity (HA) and possibly secondary external (X) sites. We describe a biochemical characterization of HpNikR mutants that shows that the HA sites are essential but not sufficient for DNA binding, while the secondary external (X) sites and residues from the HpNikR dimer–dimer interface are important for DNA binding. We show that a second metal is necessary for HpNikR/DNA binding, but only to some promoters. Small-angle X-ray scattering shows that HpNikR adopts a defined conformation in solution, resembling the cis-conformation and suggests that nickel does not trigger large conformational changes in HpNikR. The crystal structures of selected mutants identify the effects of each mutation on HpNikR structure. This study unravels key structural features from which we derive a model for HpNikR activation where: (i) HA sites and an hydrogen bond network are required for DNA binding and (ii) metallation of a unique secondary external site (X) modulates HpNikR DNA binding to low-affinity promoters by disruption of a salt bridge. PMID:20089510

  17. Curcumin suppresses gastric NF-κB activation and macromolecular leakage in Helicobacter pylori-infected rats

    Institute of Scientific and Technical Information of China (English)

    Kawiya; Sintara; Duangporn; Thong-Ngam; Suthiluk; Patumraj; Naruemon; Klaikeaw; Tanittha; Chatsuwan

    2010-01-01

    AIM:To investigate whether curcumin could attenuate nuclear factor(NF)-κB p65 expression and macromolecular leakage in the gastric mucosa of Helicobacter pylori(H.pylori)-infected rats.METHODS:Twenty-five male Sprague-Dawley rats were equally divided into five groups:control rats(Control),control rats supplemented with 600 mg/kg curcumin,H.pylori-infected rats(Hp),H.pylori-infected rats supplemented with 200 mg/kg curcumin(Hp + curIn H.pylori-infected groups,rats were inoculated with H.pylori suspension twi...

  18. Helicobacter pylori activates the TLR2/NLRP3/caspase-1/IL-18 axis to induce regulatory T-cells, establish persistent infection and promote tolerance to allergens.

    Science.gov (United States)

    Koch, Katrin N; Müller, Anne

    2015-01-01

    The Gram-negative bacterium Helicobacter pylori is both a normal constituent of the human gastric microbiota as well as a pathogen tightly associated with severe gastric disorders. The ability of H. pylori to activate the inflammasome and caspase-1 in antigen-presenting and other cells, and the resulting processing and release of caspase-1-dependent cytokines, impacts both the immunomodulatory and pathogenic activities of H. pylori. This article summarizes recent insights by us and others on the bacterial and host prerequisites of inflammasome activation. H. pylori predominantly activates the NLRP3 inflammasome through a process that requires TLR2-dependent licensing. We identified the urease enzyme, a colonization determinant known to be required for acid adaptation, as critically required for activation of the TLR2/NLRP3/caspase-1 axis. The phenotypes of urease mutants, as well as mouse strains defective for TLR2 or NLRP3, are discussed with respect to their ability to support persistent colonization, immune tolerance and immunity to H. pylori.

  19. Aqueous and Organic Solvent-Extracts of Selected South African Medicinal Plants Possess Antimicrobial Activity against Drug-Resistant Strains of Helicobacter pylori: Inhibitory and Bactericidal Potential

    Directory of Open Access Journals (Sweden)

    Collise Njume

    2011-09-01

    Full Text Available The aim of this study was to identify sources of cheap starting materials for the synthesis of new drugs against Helicobacter pylori. Solvent-extracts of selected medicinal plants; Combretum molle, Sclerocarya birrea, Garcinia kola, Alepidea amatymbica and a single Strychnos species were investigated against 30 clinical strains of H. pylori alongside a reference control strain (NCTC 11638 using standard microbiological techniques. Metronidazole and amoxicillin were included in these experiments as positive control antibiotics. All the plants demonstrated anti-H. pylori activity with zone diameters of inhibition between 0 and 38 mm and 50% minimum inhibitory concentration (MIC50 values ranging from 0.06 to 5.0 mg/mL. MIC50 values for amoxicillin and metronidazole ranged from 0.001 to 0.63 mg/mL and 0.004 to 5.0 mg/mL respectively. The acetone extracts of C. molle and S. birrea exhibited a remarkable bactericidal activity against H. pylori killing more than 50% of the strains within 18 h at 4× MIC and complete elimination of the organisms within 24 h. Their antimicrobial activity was comparable to the control antibiotics. However, the activity of the ethanol extract of G. kola was lower than amoxicillin (P < 0.05 as opposed to metronidazole (P > 0.05. These results demonstrate that S. birrea, C. molle and G. kola may represent good sources of compounds with anti-H. pylori activity.

  20. Helicobacter pylori neutrophil-activating protein: A potential Treg modulator suppressing allergic asthma?

    Directory of Open Access Journals (Sweden)

    Anjna eSehrawat

    2015-06-01

    Full Text Available The ultimate aim of immunology is to kill the pathogen without being harmful to the host. But what if eliminating the pathogen in itself is discomforting for the host? One such emerging case is of Helicobacter pylori. Modern medicine, infantile vaccination and ultra-hygienic conditions have led to progressive disappearance of H. pylori in different parts of the world. However, the adversities caused by H. pylori’s absence are much larger than those caused by its presence. Asthma is rising as an epidemic in last few decades and several reports suggest an inverse-relationship between H. pylori’s persistence and early-life onset asthma. Regulatory T cells play an important role in both the cases. This is further supported by experiments on mouse-models. Hence, need of the hour is to discern the relationship between H. pylori and its host and eliminating its negative impacts without disturbing our indigenous microbiota. To resolve whether H. pylori is a pathogen or an amphibiont is another important side. This review explores the biological basis of H. pylori-induced priming of immune system offering resistance to childhood-onset asthma. HP-NAP-Tregs interaction has been predicted using molecular docking and dynamic simulation.

  1. A novel insight into the oxidoreductase activity of Helicobacter pylori HP0231 protein.

    Directory of Open Access Journals (Sweden)

    Paula Roszczenko

    Full Text Available BACKGROUND: The formation of a disulfide bond between two cysteine residues stabilizes protein structure. Although we now have a good understanding of the Escherichia coli disulfide formation system, the machineries at work in other bacteria, including pathogens, are poorly characterized. Thus, the objective of this work was to improve our understanding of the disulfide formation machinery of Helicobacter pylori, a leading cause of ulcers and a risk factor for stomach cancer worldwide. METHODS AND RESULTS: The protein HP0231 from H. pylori, a structural counterpart of E. coli DsbG, is the focus of this research. Its function was clarified by using a combination of biochemical, microbiological and genetic approaches. In particular, we determined the biochemical properties of HP0231 as well as its redox state in H. pylori cells. CONCLUSION: Altogether our results show that HP0231 is an oxidoreductase that catalyzes disulfide bond formation in the periplasm. We propose to call it HpDsbA.

  2. HELICOBACTER PYLORI

    Science.gov (United States)

    Helicobacter pylori is a pathogenic bacteria which inhabits the human stomach and upper gastrointestinal tract. This encyclopedic entry summarizes the potential role of this organism as a waterborne pathogen. Information is provided on the physiology and morphology of this bacter...

  3. Active infection with Helicobacter pylori in an asymptomatic population of middle aged to elderly people

    DEFF Research Database (Denmark)

    Rothenbacher, D; Bode, G; Peschke, F

    1998-01-01

    The study objective was to investigate prevalence and determinants of current Helicobacter pylori infection in an asymptomatic population of middle-aged to elderly people. A cross-sectional study was conducted among 337 participants of a general education programme of the University of Ulm aged 50...

  4. Lactobacillus plantarum B7 inhibits Helicobacter pylori growth and attenuates gastric inflammation

    Institute of Scientific and Technical Information of China (English)

    Chompoonut Sunanliganon; Duangporn Thong-Ngam; Somying Tumwasorn; Naruemon Klaikeaw

    2012-01-01

    AIM:To determine the anti-Helicobacter property of Lactobacillus plantarum B7 (L.plantarum) B7 supernatants in vitro and the protective effects of L.plantarum B7 on serum tumor necrosis factor-alpha (TNF-α),gastric malondialdehyde (MDA) level,apoptosis,and histopathology in Helicobacter pylori (H.pylorl)-induced gastric inflammation in rats.METHODS:In vitro,the inhibition of H,pylori growth was examined using L.plantarum B7 supernatants at pH 4 and pH 7 and at the concentration of 1×,5× and 10× on plates inoculated with H.pylori.The inhibitory effect of H.pylori was interpreted by the size of the inhibition zone.In vitro,male Sprague-Dawley rats were randomly divided into four groups including group 1 (control group),group 2 (H.pylori infected group),group 3 (H.pylori infected with L.plantarum B7 10é CFUs/mL treated group) and group 4 (H.pylori infected with L.plantarum B7 1010 CFUs/mL treated group).One week after H.pylori inoculation,L.plantarum B7 106 CFUs/mL or 1010 CFUs/mL were fed once daily to group 3 and group 4,respectively,for one week.Blood and gastric samples were collected at the end of the study.RESULTS:In vitro,at intact pH 4,mean inhibitory zone diameters of 8.5 mm and 13 mm were noted at concentrations of 5× and 10× of L.plantarum B7supernatant disks,respectively.At adjusted pH 7,L.plantarum B7 supernatants at concentrations of 5 × and 10× yielded mean inhibitory zone diameters of 6.5 mm and 11 mm,respectively.In the in vitro study,in group 2,stomach histopathology revealed mild to moderate H.pylori colonization and inflammation.The level of gastric MDA and epithelial cell apoptosis were significantly increased compared with group 1.The serum TNF-α level was significant decreased in group 3compared with group 2 (P < 0.05).In addition,L.plantarum B7 treatments resulted in a significant improvement in stomach pathology,and decreased gastric MDA level and apoptotic epithelial cells.CONCLUSION:L.plantarum B7 supernatant inhibits H.pylori

  5. Is a 7-day Helicobater pylori treatment enough for eradication and inactivation of gastric inflammatory activity?

    Institute of Scientific and Technical Information of China (English)

    Carlos Robles-lara; Carlos Robles-Medranda; Manuel Moncayo; Byron Landivar; Johnny Parrales

    2008-01-01

    AIM- To compare the efficacy of a 7-d vs 10-d triple therapy regarding H pylori eradication, endoscopic findings and histological gastric inflammatory inactivation in the Ecuadorian population. METHODS: 136 patients with dyspepsia and H pylori infection were randomized in 2 groups (68 per group): group 1, 7-d therapy; group 2, t0-d therapy. Both groups received the same medication and daily dosage: omeprazole 20 mg bid, clarithromycin 500 mg bid and amoxicillin I g bid. Endoscopy was performed for histological assessment and H pylori infection status before and 8 wk after treatment. RESULTS: H pylori was eradicated in 68% of group 1 vs 83. 8% of group 2 for the intention-to-treat analysis (ITT) (P = 0. 03; OR = 2. 48; 95% CI, 1. 1-5. 8), and 68% in group 1 vs 88% in group 2 for the per-protocol analysis (PP) (P = 0. 008; OR = 3. 66; 95% CI, 1. 4-10). Endoscopic gastric mucosa normalization was observed in 56. 9% in group 1 vs 61. 2% in group 2 for ITT, with similar results for the PP, the difference being statistically not significant. The rate of inflammatory inactivation was 69% in group 1 vs 88. 7% in group 2 for ITT (P = 0. 007;OR = 3. 00; 95% CI, 1. 2-7. 5), and 69% in group 1 vs96% in group 2 for PP (P = 0. 0002; OR = 7. 25; 95% CI, 2-26). CONCLUSION: In this Ecuadorian population, the 10-d therapy was more effective than the 7-d therapy for H pylori eradication as well as for gastric mucosa inflammatory inactivation.

  6. A case of severe pseudomembranous colitis diagnosed by colonoscopy after Helicobacter pylori eradication.

    Science.gov (United States)

    Sato, Satoshi; Chinda, Daisuke; Yamai, Kiyonori; Satake, Ryu; Soma, Yasushi; Shimoyama, Tadashi; Fukuda, Shinsaku

    2014-06-01

    A 65-year-old male was admitted for hemorrhagic gastric ulcer. Since anti-Helicobacter pylori-immunoglobulin G antibody tested positive, eradication therapy was administered using rabeprazole, amoxicillin, and clarithromycin. During hospitalization, colonoscopy showed normal colonic mucosa except for a polyp of the sigmoid colon. He was discharged 4 days after finishing eradication therapy, but fever up and diarrhea appeared on the following day. After re-admission, colonoscopy revealed multiple yellowish-white, small circular membranous elevations, and a diagnosis of pseudomembranous colitis was made. He was successfully treated by oral administration of vancomycin. Concomitant use of antibiotics and a proton pump inhibitor for a hospitalized patient is a risk for pseudomembranous colitis. However, H. pylori eradication therapy should be started at re-introduction of oral feeding in cases of bleeding ulcers because rebleeding can be mortal in patients in 'poor general condition'. Physicians should consider pseudomembranous colitis as a diagnosis for the patients with diarrhea and high fever following H. pylori eradication therapy.

  7. Helicobacter pylori Test

    Science.gov (United States)

    ... urease test (RUT) for H. pylori Formal name: Helicobacter pylori Related tests: Gastrin At a Glance Test Sample ... else I should know? How is it used? Helicobacter pylori testing is used to diagnose an infection due ...

  8. [Helicobacter pylori and Arteriosclerosis].

    Science.gov (United States)

    Matsui, Teruaki

    2011-03-01

    Helicobacter pylori (H. pylori) infection-related diseases are known to include gastritis, gastric and duodenal ulcer, gastric cancer, gastric MALT lymphoma, idiopathic thrombocytopenic purpura, iron-deficient anemia, urticaria, reflux esophagitis, and some lifestyle-related diseases. It is indicated that homocysteine involved with arteriosclerosis induces lifestyle-related diseases. Homocysteine is decomposed to methionine and cysteine (useful substances) in the liver, through the involvement of vitamin B₁₂ (VB₁₂) and folic acid. However, deficiency of VB₁₂ and folic acid induces an increase in unmetabolized homocysteine stimulating active oxygen and promoting arteriosclerosis. VB₁₂ and folic acid are activated by the intrinsic factors of gastric parietal cells and gastric acid. The question of whether homocysteine, as a trigger of arteriosclerosis, was influenced by H. pylori infection was investigated. H. pylori infection induces atrophy of the gastric mucosa, and the function of parietal cells decreases with the atrophy to inactivate its intrinsic factor. The inactivation of the intrinsic factor causes a deficiency of VB₁₂ and folic acid to increase homocysteine's chances of triggering arteriosclerosis. The significance and usefulness of H. pylori eradication therapy was evaluated for its ability to prevent arteriosclerosis that induces lifestyle-related diseases. Persons with positive and negative results of H. pylori infection were divided into a group of those aged 65 years or more (early and late elderly) and a group of those under 65 years of age, and assessed for gastric juice. For twenty-five persons from each group who underwent gastrointestinal endoscopy, the degree of atrophy of the gastric mucosa was observed. Blood homocysteine was measured as a novel index of arteriosclerosis, as well as VB₁₂ and folic acid that affect the metabolism of homocysteine, and then activated by gastric acid and intrinsic factors. Their

  9. Enzyme-ligand interactions that drive active site rearrangements in the Helicobacter pylori 5´-methylthioadenosine/S-adenosylhomocysteine nucleosidase

    Energy Technology Data Exchange (ETDEWEB)

    Ronning, Donald R; Iacopelli, Natalie M; Mishra, Vidhi [Toledo

    2012-03-15

    The bacterial enzyme 5'-methylthioadenosine/S-adenosylhomocysteine nucleosidase (MTAN) plays a central role in three essential metabolic pathways in bacteria: methionine salvage, purine salvage, and polyamine biosynthesis. Recently, its role in the pathway that leads to the production of autoinducer II, an important component in quorum-sensing, has garnered much interest. Because of this variety of roles, MTAN is an attractive target for developing new classes of inhibitors that influence bacterial virulence and biofilm formation. To gain insight toward the development of new classes of MTAN inhibitors, the interactions between the Helicobacter pylori-encoded MTAN and its substrates and substrate analogs were probed using X-ray crystallography. The structures of MTAN, an MTAN-Formycin A complex, and an adenine bound form were solved by molecular replacement and refined to 1.7, 1.8, and 1.6 Å, respectively. The ribose-binding site in the MTAN and MTAN-adenine cocrystal structures contain a tris[hydroxymethyl]aminomethane molecule that stabilizes the closed form of the enzyme and displaces a nucleophilic water molecule necessary for catalysis. This research gives insight to the interactions between MTAN and bound ligands that promote closing of the enzyme active site and highlights the potential for designing new classes of MTAN inhibitors using a link/grow or ligand assembly development strategy based on the described H. pylori MTAN crystal structures.

  10. Structures and Metal-Binding Properties of Helicobacter pylori Neutrophil-Activating Protein with a Di-Nuclear Ferroxidase Center

    Directory of Open Access Journals (Sweden)

    Hideshi Yokoyama

    2014-06-01

    Full Text Available Helicobacter pylori causes severe diseases, such as chronic gastritis, peptic ulcers, and stomach cancers. H. pylori neutrophil-activating protein (HP-NAP is an iron storage protein that forms a dodecameric shell, promotes the adhesion of neutrophils to endothelial cells, and induces the production of reactive oxygen radicals. HP-NAP belongs to the DNA-protecting proteins under starved conditions (Dps family, which has significant structural similarities to the dodecameric ferritin family. The crystal structures of the apo form and metal-ion bound forms, such as iron, zinc, and cadmium, of HP-NAP have been determined. This review focused on the structures and metal-binding properties of HP-NAP. These metal ions bind at the di-nuclear ferroxidase center (FOC by different coordinating patterns. In comparison with the apo structure, metal loading causes a series of conformational changes in conserved residues among HP-NAP and Dps proteins (Trp26, Asp52, and Glu56 at the FOC. HP-NAP forms a spherical dodecamer with 23 symmetry including two kinds of pores. Metal ions have been identified around one of the pores; therefore, the negatively-charged pore is suitable for the passage of metal ions.

  11. Pathogenesis of Helicobacter pylori infection.

    Science.gov (United States)

    Hofman, Paul; Waidner, Barbara; Hofman, Véronique; Bereswill, Stefan; Brest, Patrick; Kist, Manfred

    2004-01-01

    Research in the last year has provided new insights into the function of the the cag-associated type IV secretion system and the vacuolating toxin VacA. A quite new aspect was disclosed by the finding that Helicobacter pylori in Mongolian gerbils colonizes a very distinct topology in the gastric mucous layer, obviously providing optimal conditions for long-term survival. Further research activities focused on H. pylori ammonia and metal metabolism as well as on bacterial stress defence mechanisms. Differential expression of approximately 7% of the bacterial genome was found at low pH suggesting that H. pylori has evolved a multitude of acid-adaptive mechanisms. VacA was shown to interrupt phagosome maturation in macrophage cell lines as well as to modulate and interfere with T lymphocyte immunological functions. Gastric mucosa as well as the H. pylori-infected epithelial cell line AGS strongly express IL-8 receptor A and B, which might contribute to the augmentation of the inflammatory response. Accumulating evidence implicates genetic variation in the inflammatory response to H. pylori in the etiology of the increased risk of gastric cancer after H. pylori infection. The chronic imbalance between apoptosis and cell proliferation is the first step of gastric carcinogenesis. In this regard, it was demonstrated that coexpression of two H. pylori proteins, CagA and HspB, in AGS cells, caused an increase in E2F transcription factor, cyclin D3, and phosphorylated retinoblastoma protein. Taken together, we now have a better understanding of the role of different virulence factors of H. pylori. There is still a lot to be learned, but the promising discoveries summarized here, demonstrate that the investigation of the bacterial survival strategies will give novel insights into pathogenesis and disease development.

  12. Concurrent proinflammatory and apoptotic activity of a Helicobacter pylori protein (HP986 points to its role in chronic persistence.

    Directory of Open Access Journals (Sweden)

    Ayesha Alvi

    Full Text Available Helicobacter pylori induces cytokine mediated changes in gastroduodenal pathophysiology, wherein, the activated macrophages at the sub-mucosal space play a central role in mounting innate immune response against the antigens. The bacterium gains niche through persistent inflammation and local immune-suppression causing peptic ulcer disease or chronic gastritis; the latter being a significant risk factor for the development of gastric adenocarcinoma. What favors persistence of H. pylori in the gastric niches is not clearly understood. We report detailed characterization of a functionally unknown gene (HP986, which was detected in patient isolates associated with peptic ulcer and gastric carcinoma. Expression and purification of recombinant HP986 (rHP986 revealed a novel, ∼29 kDa protein in biologically active form which associates with significant levels of humoral immune responses in diseased individuals (p<0.001. Also, it induced significant levels of TNF-α and Interleukin-8 in cultured human macrophages concurrent to the translocation of nuclear transcription factor-κB (NF-κB. Further, the rHP986 induced apoptosis of cultured macrophages through a Fas mediated pathway. Dissection of the underlying signaling mechanism revealed that rHP986 induces both TNFR1 and Fas expression to lead to apoptosis. We further demonstrated interaction of HP986 with TNFR1 through computational and experimental approaches. Independent proinflammatory and apoptotic responses triggered by rHP986 as shown in this study point to its role, possibly as a survival strategy to gain niche through inflammation and to counter the activated macrophages to avoid clearance.

  13. Helicobacter pylori Couples Motility and Diffusion to Actively Create a Heterogeneous Complex Medium in Gastric Mucus

    Science.gov (United States)

    Fu, Henry; Mirbagheri, Seyed Amir

    2016-11-01

    Helicobacter pylori swims through mucus gel by generating ammonia that locally neutralizes the acidic gastric environment, turning nearby gel into a fluid pocket. The size of the fluid zone is important for determining the physics of the motility: in a large zone swimming occurs as in a fluid through hydrodynamic principles, while in a very small zone the motility could be strongly influenced by nonhydrodynamic cell-mucus interactions including chemistry and adhesion. We calculate the size of the fluid pocket. We model how swimming depends on the de-gelation range using a Taylor sheet swimming through a layer of Newtonian fluid bounded by a Brinkman fluid. Then, we model how the de-gelation range depends on the swimming speed by considering the advection-diffusion of ammonia exuded from a translating sphere. Self-consistency between both models determines the values of the swimming speed and the de-gelation range. We find that H. pylori swims through mucus as if unconfined, in a large pocket of Newtonian fluid. Funded by National Science Foundation award CBET-1252182.

  14. Helicobacter pylori Couples Motility and Diffusion to Actively Create a Heterogeneous Complex Medium in Gastric Mucus

    Science.gov (United States)

    Mirbagheri, Seyed Amir; Fu, Henry Chien

    2016-05-01

    Helicobacter pylori swims through mucus gel by generating ammonia that locally neutralizes the acidic gastric environment, turning nearby gel into a fluid pocket. The size of the fluid zone is important for determining the physics of the motility: in a large zone swimming occurs as in a fluid through hydrodynamic principles, while in a very small zone the motility could be strongly influenced by nonhydrodynamic cell-mucus interactions including chemistry and adhesion. Here, we calculate the size of the fluid pocket. We model how swimming depends on the de-gelation range using a Taylor sheet swimming through a layer of Newtonian fluid bounded by a Brinkman fluid. Then, we model how the de-gelation range depends on the swimming speed by considering the advection-diffusion of ammonia exuded from a translating sphere. Self-consistency between both models determines the values of the swimming speed and the de-gelation range. We find that H. pylori swims through mucus as if unconfined, in a large pocket of Newtonian fluid.

  15. Curcumin alleviates matrix metalloproteinase-3 and -9 activities during eradication of Helicobacter pylori infection in cultured cells and mice.

    Directory of Open Access Journals (Sweden)

    Parag Kundu

    Full Text Available Current therapy-regimens against Helicobacter pylori (Hp infections have considerable failure rates and adverse side effects that urge the quest for an effective alternative therapy. We have shown that curcumin is capable of eradicating Hp-infection in mice. Here we examine the mechanism by which curcumin protects Hp infection in cultured cells and mice. Since, MMP-3 and -9 are inflammatory molecules associated to the pathogenesis of Hp-infection, we investigated the role of curcumin on inflammatory MMPs as well as proinflammatory molecules. Curcumin dose dependently suppressed MMP-3 and -9 expression in Hp infected human gastric epithelial (AGS cells. Consistently, Hp-eradication by curcumin-therapy involved significant downregulation of MMP-3 and -9 activities and expression in both cytotoxic associated gene (cag(+ve and cag(-ve Hp-infected mouse gastric tissues. Moreover, we demonstrate that the conventional triple therapy (TT alleviated MMP-3 and -9 activities less efficiently than curcumin and curcumin's action on MMPs was linked to decreased pro-inflammatory molecules and activator protein-1 activation in Hp-infected gastric tissues. Although both curcumin and TT were associated with MMP-3 and -9 downregulation during Hp-eradication, but unlike TT, curcumin enhanced peroxisome proliferator-activated receptor-γ and inhibitor of kappa B-α. These data indicate that curcumin-mediated healing of Hp-infection involves regulation of MMP-3 and -9 activities.

  16. Ghrelin and Helicobacter pylori infection

    Institute of Scientific and Technical Information of China (English)

    Hiroyuki Osawa

    2008-01-01

    Ghrelin is primarily secreted from the stomach and has been implicated in the coordination of eating behavior and weight regulation. Ghrelin also plays an essential role in the mechanism of gastric mucosal defense. Thus, it is important to clarify which diseases primar-ily influence changes in plasma ghrelin concentrations. Helicobacter pylori(H pylori infection is involved in the pathogenesis of gastritis, gastric and duodenal ulcer, gastric carcinoma, and mucosa-associated lym-phoid tissue lymphorna. H pylori eradication is related to body weight change. Compared, H pylori infected and negative subjects with normal body mass index, plasma ghrelin concentration, gastric ghrelin mRNA, and the number of ghrelin producing cells in gastric mucosa are significantly lower in Hpylori injected sub-jects than in H pylori-negative controls. Plasma ghrelin concentration decreases with the progression of gastric atrophy. Impaired gastric ghrelin production in associa-tion with atrophic gastritis induced by Hpylori infection accounts for the decrease in plasma ghrelin concentra-tion. However, the ratio of plasma acylated ghrelin to total ghrelin levels is higher in patients with chronic atrophic gastritis than in healthy subjects. This may re-sult from the compensatory increase in plasma active ghrelin concentration in response to gastric atrophy. After H pylori eradication, gastric preproghrelin mRNA expression is increased nearly 4-fold in most cases. However, changes in plasma ghrelin concentrations be-fore and after H pylori cure are not associated with the gastric ghrelin production. Plasma ghrelin changes are inversely correlated with both body weight change and initial plasma ghrelin levels.

  17. Molecular docking, kinetics study, and structure-activity relationship analysis of quercetin and its analogous as Helicobacter pylori urease inhibitors.

    Science.gov (United States)

    Xiao, Zhu-Ping; Wang, Xu-Dong; Peng, Zhi-Yun; Huang, Shen; Yang, Pan; Li, Qing-Shan; Zhou, Li-Hu; Hu, Xiao-Jun; Wu, Li-Jun; Zhou, Yin; Zhu, Hai-Liang

    2012-10-24

    It was disclosed in our group for the first time that the flavonoids in Lonicera japonica Thunb. are related to its therapy for gastric ulcer. Based on this finding, 20 flavonoids were selected for Helicobacter pylori urease inhibitory activity evaluation, and quercetin showed excellent potency with IC(50) of 11.2 ± 0.9 μM. Structure-activity relationship analysis revealed that removal of the 5-, 3-, or 3'-OH in quercetin led to a sharp decrease in activity. Thus, 3- and 5-OH as well as 3',4'-dihydroxyl groups are believed to be the key structural characteristics for active compounds, which was supported by the molecular docking study. Meanwhile, the results obtained from molecular docking and enzymatic kinetics research strongly suggested that quercetin is a noncompetitive urease inhibitor, indicating that quercetin may be able to tolerate extensive structural modification irrespective of the shape of the active site cavity and could be used as a lead candidate for the development of novel urease inhibitors.

  18. Helicobacter pylori therapy:Present and future

    Institute of Scientific and Technical Information of China (English)

    Vincenzo; De; Francesco; Enzo; Ierardi; Cesare; Hassan; Angelo; Zullo

    2012-01-01

    Helicobacter pylori(H.pylori) plays a crucial role in the pathogenesis of chronic active gastritis,peptic ulcer and gastric mucosa-associated lymphoid tissue-lymphoma,and is also involved in carcinogenesis of the stomach.H.pylori treatment still remains a challenge for physicians,since no current first-line therapy is able to cure the infection in all treated patients.Several factors may help in the eradication of therapy failure.We reviewed both bacterial and host factors involved in therapeutic management of the H.pylori infection.In addition,we evaluated data on the most successful therapy regimens-sequential and concomitant therapies-currently available for H.pylori eradication.

  19. Helicobacter pylori: From Infection to Cure

    Directory of Open Access Journals (Sweden)

    ABR Thomson

    1996-01-01

    Full Text Available Over 380 abstracts, presentations and posters of recent advances were highlighted at the European and International Helicobacter pylori meeting held July 7 to 9, 1995 in Edinburgh, Scotland. New advances abound, with major interest focusing on the simple, safe, inexpensive new `gold standard’ for H pylori eradication therapy: a single week of tid omeprazole 20 mg, metronidazole 400 mg and clarithromycin 250 mg, or omeprazole 20 mg, amoxicillin 1000 mg and clarithromycin 500 mg. To avoid false negative results, two biopsies must be taken from the antrum and two from the gastric body at least four weeks after completion of eradication therapy, and ideally should be supplemented with at least one further H pylori test such as a biopsy for urease activity or culture, or a urea breath test. While most patients with a gastric or duodenal ulcer (DU who do not consume nonsteroidal anti-inflammatory drugs are infected with H pylori, the association is much less apparent in those with a DU who present with an upper gastrointestinal hemorrhage. H pylori eradication for nonulcer dyspepsia is not widely recommended, and the patient with a DU given effective H pylori eradication who presents with dyspepsia likely has erosive esophagitis rather than recurrent DU or H pylori. Gastroenterologists are at increased risk of H pylori infection, particularly older gastroenterologists who are very busy endoscopists.

  20. Helicobacter pylori eradication for preventing gastric cancer.

    Science.gov (United States)

    Lu, Bin; Li, Meng

    2014-05-21

    Helicobacter pylori (H. pylori) infection is a major risk factor for gastric cancer (GC) development, which is one of the most challenging malignant diseases worldwide with limited treatments. In the multistep pathogenesis of GC, H. pylori infection slowly induces chronic active gastritis, which progresses through the premalignant stages of atrophic gastritis, intestinal metaplasia, and dysplasia, and then finally to GC. Although eradication of H. pylori is a reasonable approach for the prevention of GC, there have been some contradictory reports, with only some long-term follow-up data showing efficacy of this approach. The inconsistencies are likely due to the insufficient number of participants, relatively short follow-up periods, poor quality of study designs, and the degree and extent of preneoplastic changes at the time of H. pylori eradication. This review analyzes recent high-quality studies to resolve the discrepancies regarding the eradication of H. pylori for GC prevention. The relationship between H. pylori eradication and GC/precancerous lesions/metachronous GC is examined, and the cost-effectiveness of this strategy in the prevention of GC is assessed. Although it is assumed that eradication of H. pylori has the potential to prevent GC, the feasibility and appropriate timing of this strategy for cancer prevention remain to be determined. As a result, additional well-designed trials with longer follow-up periods are needed to clarify this issue.

  1. Helicobacter pylori Induced Phosphatidylinositol-3-OH Kinase/mTOR Activation Increases Hypoxia Inducible Factor-1α to Promote Loss of Cyclin D1 and G0/G1 Cell Cycle Arrest in Human Gastric Cells

    Science.gov (United States)

    Canales, Jimena; Valenzuela, Manuel; Bravo, Jimena; Cerda-Opazo, Paulina; Jorquera, Carla; Toledo, Héctor; Bravo, Denisse; Quest, Andrew F. G.

    2017-01-01

    Helicobacter pylori (H. pylori) is a human gastric pathogen that has been linked to the development of several gastric pathologies, such as gastritis, peptic ulcer, and gastric cancer. In the gastric epithelium, the bacterium modifies many signaling pathways, resulting in contradictory responses that favor both proliferation and apoptosis. Consistent with such observations, H. pylori activates routes associated with cell cycle progression and cell cycle arrest. H. pylori infection also induces the hypoxia-induced factor HIF-1α, a transcription factor known to promote expression of genes that permit metabolic adaptation to the hypoxic environment in tumors and angiogenesis. Recently, however, also roles for HIF-1α in the repair of damaged DNA and inhibition of gene expression were described. Here, we investigated signaling pathways induced by H. pylori in gastric cells that favor HIF-1α expression and the consequences thereof in infected cells. Our results revealed that H. pylori promoted PI3K/mTOR-dependent HIF-1α induction, HIF-1α translocation to the nucleus, and activity as a transcription factor as evidenced using a reporter assay. Surprisingly, however, transcription of known HIF-1α effector genes evaluated by qPCR analysis, revealed either no change (LDHA and GAPDH), statistically insignificant increases SLC2A1 (GLUT-1) or greatly enhance transcription (VEGFA), but in an HIF-1α-independent manner, as quantified by PCR analysis in cells with shRNA-mediated silencing of HIF-1α. Instead, HIF-1α knockdown facilitated G1/S progression and increased Cyclin D1 protein half-life, via a post-translational pathway. Taken together, these findings link H. pylori-induced PI3K-mTOR activation to HIF-1α induced G0/G1 cell cycle arrest by a Cyclin D1-dependent mechanism. Thus, HIF-1α is identified here as a mediator between survival and cell cycle arrest signaling activated by H. pylori infection.

  2. Regulation of RKIP function by Helicobacter pylori in gastric cancer.

    Directory of Open Access Journals (Sweden)

    Erika L Moen

    Full Text Available Helicobacter pylori (H. pylori is a gram-negative, spiral-shaped bacterium that infects more than half of the world's population and is a major cause of gastric adenocarcinoma. The mechanisms that link H. pylori infection to gastric carcinogenesis are not well understood. In the present study, we report that the Raf-kinase inhibitor protein (RKIP has a role in the induction of apoptosis by H. pylori in gastric epithelial cells. Western blot and luciferase transcription reporter assays demonstrate that the pathogenicity island of H. pylori rapidly phosphorylates RKIP, which then localizes to the nucleus where it activates its own transcription and induces apoptosis. Forced overexpression of RKIP enhances apoptosis in H. pylori-infected cells, whereas RKIP RNA inhibition suppresses the induction of apoptosis by H. pylori infection. While inducing the phosphorylation of RKIP, H. pylori simultaneously targets non-phosphorylated RKIP for proteasome-mediated degradation. The increase in RKIP transcription and phosphorylation is abrogated by mutating RKIP serine 153 to valine, demonstrating that regulation of RKIP activity by H. pylori is dependent upon RKIP's S153 residue. In addition, H. pylori infection increases the expression of Snail, a transcriptional repressor of RKIP. Our results suggest that H. pylori utilizes a tumor suppressor protein, RKIP, to promote apoptosis in gastric cancer cells.

  3. The neutrophil-activating Dps protein of Helicobacter pylori, HP-NAP, adopts a mechanism different from Escherichia coli Dps to bind and condense DNA.

    Science.gov (United States)

    Ceci, Pierpaolo; Mangiarotti, Laura; Rivetti, Claudio; Chiancone, Emilia

    2007-01-01

    The Helicobacter pylori neutrophil-activating protein (HP-NAP), a member of the Dps family, is a fundamental virulence factor involved in H.pylori-associated disease. Dps proteins protect bacterial DNA from oxidizing radicals generated by the Fenton reaction and also from various other damaging agents. DNA protection has a chemical component based on the highly conserved ferroxidase activity of Dps proteins, and a physical one based on the capacity of those Dps proteins that contain a positively charged N-terminus to bind and condense DNA. HP-NAP does not possess a positively charged N-terminus but, unlike the other members of the family, is characterized by a positively charged protein surface. To establish whether this distinctive property could be exploited to bind DNA, gel shift, fluorescence quenching and atomic force microscopy (AFM) experiments were performed over the pH range 6.5-8.5. HP-NAP does not self-aggregate in contrast to Escherichia coli Dps, but is able to bind and even condense DNA at slightly acid pH values. The DNA condensation capacity acts in concert with the ferritin-like activity and could be used to advantage by H.pylori to survive during host-infection and other stress challenges. A model for DNA binding/condensation is proposed that accounts for all the experimental observations.

  4. Validation of low activity {sup 14}C-urea breath test in diagnosis of ``Helicobacter pylori``in humans

    Energy Technology Data Exchange (ETDEWEB)

    Bielanski, W.; Konturek, S.J.; Dobrzanka, M.J.; Plonka, M.; Sito, E.; Stachura, J. [Uniwersytet Jagiellonski, Cracow (Poland); Hoffman, S.R.; Marshall, B.J. [Tri-Med Specialtis, Charlottenville, VA (United States)

    1996-12-31

    Etiologic role for ``Helicobacter pylori`` (HP) seems to be well established in gastric pathology. The high urease activity of HP can be used to detect this bacterium by non-invasive urea breath tests (UBT). We validated the low activity version of the test in which 37 kBq {sup 14}C-urea is given orally in capsule. With the cut off value {>=} 1.66 Bq (100 DPM) as positive, UBT results correlated highly significant with combined results for invasive methods, i.e. CLO-test + Histology score. The reproducibility of the test was 100%. The results obtained for the breath test performed locally were almost identical with that read at remote laboratory. The data found for fasting and fed states of subjects agreed in 87%. When {sup 14}C-urea was confined in the mouth of both HP positive and HP negative patients UBT showed the presence of urease activity in the mouth cavity. (author). 21 refs, 2 figs, 1 tab.

  5. H. pylori Infection

    Science.gov (United States)

    ... think you may have a high risk of stomach cancer, talk to your doctor. Together you can decide whether you may benefit from H. pylori screening. References H. pylori and peptic ulcers. National Institute ...

  6. Helicobacter Pylori Infections

    Science.gov (United States)

    Helicobacter pylori (H. pylori) is a type of bacteria that causes infection in the stomach. It is found in about two-thirds of ... or stool to see if it contains H. pylori. The best treatment is a combination of antibiotics ...

  7. Epithelial cell kinetics of the gastric mucosa during Helicobacter pylori infection

    DEFF Research Database (Denmark)

    Holck, Susanne; Holm, I.L.; Holck, P.P.

    2007-01-01

    Helicobacter pylori is an important pathogen in major gastroduodenal diseases, including inflammation with ulceration and gastric malignancies. Alterations in H. pylori associated cell turnover in gastric epithelial cells are examined in relation to inflammatory activity, bacteria load...

  8. The Helicobacter pylori UreI Protein Is Not Involved in Urease Activity but Is Essential for Bacterial Survival In Vivo

    OpenAIRE

    Skouloubris, Stéphane; Thiberge, Jean-Michel; Labigne, Agnès; De Reuse, Hilde

    1998-01-01

    We produced defined isogenic Helicobacter pylori ureI mutants to investigate the function of UreI, the product of one of the genes of the urease cluster. The insertion of a cat cassette had a strong polar effect on the expression of the downstream urease genes, resulting in very weak urease activity. Urease activity, measured in vitro, was normal in a strain in which ureI was almost completely deleted and replaced with a nonpolar cassette. In contrast to previous reports, we thus found that t...

  9. Challenges in Diagnosis of H. Pylori Infection in Children

    OpenAIRE

    M Sobhani Shahmirzadi

    2014-01-01

    H. pylori infection is usually acquired in early childhood. Its role in gastrointestinal and extra intestinal complaints and serious consequences in adulthood make it as challenging issues. Despite different clinical presentations, in most children, the presence of H. pylori infection does not lead to clinically apparent disease, even when it causes chronic active gastritis. Some of most important recommendations for managing H. pylori infection in children based on Guidelines from ESPGHAN an...

  10. Helicobacter pylori infection: New pathogenetic and clinical aspects

    OpenAIRE

    Hagymási, Krisztina; Tulassay, Zsolt

    2014-01-01

    Helicobacter pylori (H. pylori) infects more than half of the world’s human population, but only 1% to 3% of infected people consequently develop gastric adenocarcinomas. The clinical outcome of the infection is determined by host genetic predisposition, bacterial virulence factors, and environmental factors. The association between H. pylori infection and chronic active gastritis, peptic ulcer disease, gastric cell carcinoma, and B cell mucosa-associated lymphoid tissue lymphoma has been wel...

  11. Functional and evolutionary analyses of Helicobacter pylori HP0231 (DsbK) protein with strong oxidative and chaperone activity characterized by a highly diverged dimerization domain.

    Science.gov (United States)

    Bocian-Ostrzycka, Katarzyna M; Łasica, Anna M; Dunin-Horkawicz, Stanisław; Grzeszczuk, Magdalena J; Drabik, Karolina; Dobosz, Aneta M; Godlewska, Renata; Nowak, Elżbieta; Collet, Jean-Francois; Jagusztyn-Krynicka, Elżbieta K

    2015-01-01

    Helicobacter pylori does not encode the classical DsbA/DsbB oxidoreductases that are crucial for oxidative folding of extracytoplasmic proteins. Instead, this microorganism encodes an untypical two proteins playing a role in disulfide bond formation - periplasmic HP0231, which structure resembles that of EcDsbC/DsbG, and its redox partner, a membrane protein HpDsbI (HP0595) with a β-propeller structure. The aim of presented work was to assess relations between HP0231 structure and function. We showed that HP0231 is most closely related evolutionarily to the catalytic domain of DsbG, even though it possesses a catalytic motif typical for canonical DsbA proteins. Similarly, the highly diverged N-terminal dimerization domain is homologous to the dimerization domain of DsbG. To better understand the functioning of this atypical oxidoreductase, we examined its activity using in vivo and in vitro experiments. We found that HP0231 exhibits oxidizing and chaperone activities but no isomerizing activity, even though H. pylori does not contain a classical DsbC. We also show that HP0231 is not involved in the introduction of disulfide bonds into HcpC (Helicobacter cysteine-rich protein C), a protein involved in the modulation of the H. pylori interaction with its host. Additionally, we also constructed a truncated version of HP0231 lacking the dimerization domain, denoted HP0231m, and showed that it acts in Escherichia coli cells in a DsbB-dependent manner. In contrast, HP0231m and classical monomeric EcDsbA (E. coli DsbA protein) were both unable to complement the lack of HP0231 in H. pylori cells, though they exist in oxidized forms. HP0231m is inactive in the insulin reduction assay and possesses high chaperone activity, in contrast to EcDsbA. In conclusion, HP0231 combines oxidative functions characteristic of DsbA proteins and chaperone activity characteristic of DsbC/DsbG, and it lacks isomerization activity.

  12. Functional and evolutionary analyses of Helicobacter pylori HP0231 (DsbK protein with strong oxidative and chaperone activity characterized by a highly diverged dimerization domain

    Directory of Open Access Journals (Sweden)

    Katarzyna Marta Bocian-Ostrzycka

    2015-10-01

    Full Text Available Helicobacter pylori does not encode the classical DsbA/DsbB oxidoreductases that are crucial for oxidative folding of extracytoplasmic proteins. Instead, this microorganism encodes an untypical two proteins playing a role in disulfide bond formation – periplasmic HP0231, which structure resembles that of EcDsbC/DsbG, and its redox partner, a membrane protein HpDsbI (HP0595 with a -propeller structure. The aim of presented work was to assess relations between HP0231 structure and function.We showed that HP0231 is most closely related evolutionarily to the catalytic domain of DsbG, even though it possesses a catalytic motif typical for canonical DsbA proteins. Similarly, the highly diverged N-terminal dimerization domain is homologous to the dimerization domain of DsbG. To better understand the functioning of this atypical oxidoreductase, we examined its activity using in vivo and in vitro experiments. We found that HP0231 exhibits oxidizing and chaperone activities but no isomerizing activity, even though H. pylori does not contain a classical DsbC. We also show that HP0231 is not involved in the introduction of disulfide bonds into HcpC (Helicobacter cysteine-rich protein C, a protein involved in the modulation of the H. pylori interaction with its host. Additionally, we also constructed a truncated version of HP0231 lacking the dimerization domain, denoted HP0231m, and showed that it acts in E. coli cells in a DsbB-dependent manner. In contrast, HP0231m and classical monomeric EcDsbA (Escherichia coli DsbA protein were both unable to complement the lack of HP0231 in H. pylori cells, though they exist in oxidized forms. HP0231m is inactive in the insulin reduction assay and possesses high chaperone activity, in contrast to EcDsbA. In conclusion, HP0231 combines oxidative functions characteristic of DsbA proteins and chaperone activity characteristic of DsbC/DsbG, and it lacks isomerization activity.

  13. Helicobacter pylori CagA Suppresses Apoptosis through Activation of AKT in a Nontransformed Epithelial Cell Model of Glandular Acini Formation

    Directory of Open Access Journals (Sweden)

    Gabriela Vallejo-Flores

    2015-01-01

    Full Text Available H. pylori infection is the most important environmental risk to develop gastric cancer, mainly through its virulence factor CagA. In vitro models of CagA function have demonstrated a phosphoprotein activity targeting multiple cellular signaling pathways, while cagA transgenic mice develop carcinomas of the gastrointestinal tract, supporting oncogenic functions. However, it is still not completely clear how CagA alters cellular processes associated with carcinogenic events. In this study, we evaluated the capacity of H. pylori CagA positive and negative strains to alter nontransformed MCF-10A glandular acini formation. We found that CagA positive strains inhibited lumen formation arguing for an evasion of apoptosis activity of central acini cells. In agreement, CagA positive strains induced a cell survival activity that correlated with phosphorylation of AKT and of proapoptotic proteins BIM and BAD. Anoikis is a specific type of apoptosis characterized by AKT and BIM activation and it is the mechanism responsible for lumen formation of MCF-10A acini in vitro and mammary glands in vivo. Anoikis resistance is also a common mechanism of invading tumor cells. Our data support that CagA positive strains signaling function targets the AKT and BIM signaling pathway and this could contribute to its oncogenic activity through anoikis evasion.

  14. Helicobacter pylori CagA Suppresses Apoptosis through Activation of AKT in a Nontransformed Epithelial Cell Model of Glandular Acini Formation

    Science.gov (United States)

    Vallejo-Flores, Gabriela; Torres, Javier; Sandoval-Montes, Claudia; Arévalo-Romero, Haruki; Meza, Isaura; Camorlinga-Ponce, Margarita; Torres-Morales, Julián; Chávez-Rueda, Adriana Karina; Legorreta-Haquet, María Victoria; Fuentes-Pananá, Ezequiel M.

    2015-01-01

    H. pylori infection is the most important environmental risk to develop gastric cancer, mainly through its virulence factor CagA. In vitro models of CagA function have demonstrated a phosphoprotein activity targeting multiple cellular signaling pathways, while cagA transgenic mice develop carcinomas of the gastrointestinal tract, supporting oncogenic functions. However, it is still not completely clear how CagA alters cellular processes associated with carcinogenic events. In this study, we evaluated the capacity of H. pylori CagA positive and negative strains to alter nontransformed MCF-10A glandular acini formation. We found that CagA positive strains inhibited lumen formation arguing for an evasion of apoptosis activity of central acini cells. In agreement, CagA positive strains induced a cell survival activity that correlated with phosphorylation of AKT and of proapoptotic proteins BIM and BAD. Anoikis is a specific type of apoptosis characterized by AKT and BIM activation and it is the mechanism responsible for lumen formation of MCF-10A acini in vitro and mammary glands in vivo. Anoikis resistance is also a common mechanism of invading tumor cells. Our data support that CagA positive strains signaling function targets the AKT and BIM signaling pathway and this could contribute to its oncogenic activity through anoikis evasion. PMID:26557697

  15. The nickel-responsive regulator NikR controls activation and repression of gene transcription in Helicobacter pylori.

    NARCIS (Netherlands)

    F.D.J. Ernst (Florian); E.J. Kuipers (Ernst); A. Heijens (Angela); R. Sarwari (Roya); J. Stoof (Jeroen); C.W. Penn (Charles); J.G. Kusters (Johannes); A.H.M. van Vliet (Arnoud)

    2005-01-01

    textabstractThe NikR protein is a nickel-dependent regulatory protein which is a member of the ribbon-helix-helix family of transcriptional regulators. The gastric pathogen Helicobacter pylori expresses a NikR ortholog, which was previously shown to mediate regulation of metal metabolism and urease

  16. The prevalence and related symptomatology of Helicobacter pylori in children with recurrent abdominal pain

    DEFF Research Database (Denmark)

    Wewer, Anne Vibeke; Andersen, L P; Pærregaard, Anders

    1998-01-01

    in 46/66 by culture and histology. The presence of H. pylori was significantly associated with active or inactive chronic gastritis. The presence of H. pylori was associated with both parents being born in a country with a high prevalence and a low social class. Helicobacter pylori-positive children had...

  17. Pathogenesis of helicobacter pylori infection: Bacterium and host relationship

    Directory of Open Access Journals (Sweden)

    Sokić-Milutinović Aleksandra

    2004-01-01

    Full Text Available Helicobacter pylori (H. pylori colonizes the gastric mucosa of a half of the mankind. Duodenal ulcer is found in 15-25%, t gastric ulcer in 13%, while gastric adenocarcinoma develops in 1% of all infected individuals. Pathogenesis of H. pylori infection is related to the virulence factors of the bacterium, environmental (dietary habits, hygiene, stress and host factors (age, sex, blood type. Colonization of the gastric mucosa is related to the motility of the bacterium, presence of lipopolysacharide (LPS and various bacterial enzymes. Gastric mucosal injury is the result of H. pylori LPS, vacuolization cytotoxin (vacA, cytotoxin associated protein (cagA, heat shock proteins and factors responsible for neutrophil chemotaxis and activity. H. pylori colonizes the gastric mucosa and zones of ectopic gastric epithelium. H. pylori infection is transmitted via oral-oral, fecal-oral and iatrogenic way (during endoscopy. Higher prevalence of the infection is associated with lower socioeconomic level, lack of drinking water, and living in a community. Acute H. pylori gastritis is superficial pangastritis progressing into the chronic phase after 7-10 days. Gastric mucosal atrophy and intestinal metaplasia can develop during the course of H. pylori infection. Clearly defined factors that influence the outcome of H. pylori infection include bacterial strain, distribution of gastritis, acid secretion and gastric mucosal atrophy.

  18. Pre-treatment urea breath test results predict the efficacy of Helicobacter pylori eradication therapy in patients with active duodenal ulcers

    Institute of Scientific and Technical Information of China (English)

    Yung-Chih Lai; Jyh-Chin Yang; Shih-Hung Huang

    2004-01-01

    AIM: To evaluate the association of pre-treatment 13C-urea breath test (UBT) results with H pyloridensity and efficacy of eradication therapy in patients with active duodenal ulcers.METHODS: One hundred and seventeen consecutive outpatients with active duodenal ulcer and H pyloriinfection were recruited. H pylori density was histologically graded according to the Sydney system. Each patient received lansoprazole (30 mg b.i.d.), clarithromycin (500 mg b.i.d.) and amoxicillin (1 g b.i.d.) for 1 week. According to pre-treatment UBT values, patients were allocated into low (<16%o),intermediate (16-35%o), and high (>35%o) UBT groups.RESULTS: A significant correlation was found between pre-treatment UBT results andHpyloridensity (P<0.001).H pylorieradication rates were 94.9%, 94.4% and 81.6%in the low, intermediate and high UBT groups, respectively (per protocol analysis, P=0.11). When patients were assigned into two groups (UBT results ≤35%o and >35%o),the eradication rates were 94.7% and 81.6%, respectively (P=0.04).CONCLUSION: The intragastric bacterial load of H pylori can be evaluated by UBT, and high pre-treatment UBT results can predict an adverse outcome of eradication therapy.

  19. Crystal structure of Helicobacter pylori neutrophil-activating protein with a di-nuclear ferroxidase center in a zinc or cadmium-bound form

    Energy Technology Data Exchange (ETDEWEB)

    Yokoyama, Hideshi, E-mail: h-yokoya@u-shizuoka-ken.ac.jp [School of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, Suruga-ku, Shizuoka 422-8526 (Japan); Tsuruta, Osamu; Akao, Naoya; Fujii, Satoshi [School of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, Suruga-ku, Shizuoka 422-8526 (Japan)

    2012-06-15

    Highlights: Black-Right-Pointing-Pointer Structures of a metal-bound Helicobacter pylori neutrophil-activating protein were determined. Black-Right-Pointing-Pointer Two zinc ions were tetrahedrally coordinated by ferroxidase center (FOC) residues. Black-Right-Pointing-Pointer Two cadmium ions were coordinated in a trigonal-bipyramidal and octahedral manner. Black-Right-Pointing-Pointer The second metal ion was more weakly coordinated than the first at the FOC. Black-Right-Pointing-Pointer A zinc ion was found in one negatively-charged pore suitable as an ion path. -- Abstract: Helicobacter pylori neutrophil-activating protein (HP-NAP) is a Dps-like iron storage protein forming a dodecameric shell, and promotes adhesion of neutrophils to endothelial cells. The crystal structure of HP-NAP in a Zn{sup 2+}- or Cd{sup 2+}-bound form reveals the binding of two zinc or two cadmium ions and their bridged water molecule at the ferroxidase center (FOC). The two zinc ions are coordinated in a tetrahedral manner to the conserved residues among HP-NAP and Dps proteins. The two cadmium ions are coordinated in a trigonal-bipyramidal and distorted octahedral manner. In both structures, the second ion is more weakly coordinated than the first. Another zinc ion is found inside of the negatively-charged threefold-related pore, which is suitable for metal ions to pass through.

  20. Immune response to H pylori

    Institute of Scientific and Technical Information of China (English)

    Giovanni Suarez; Victor E Reyes; Ellen J Beswick

    2006-01-01

    The gastric mucosa separates the underlying tissue from the vast array of antigens that traffic through the stomach lumen. While the extreme pH of this environment is essential in aiding the activation of enzymes and food digestion, it also renders the gastric epithelium free from bacterial colonization, with the exception of one important human pathogen, H pylori. This bacterium has developed mechanisms to survive the harsh environment of the stomach, actively move through the mucosal layer,attach to the epithelium, evade immune responses, and achieve persistent colonization. While a hallmark of this infection is a marked inflammatory response with the infiltration of various immune cells into the infected gastric mucosa, the host immune response is unable to clear the infection and may actually contribute to the associated pathogenesis. Here, we review the host responses involved during infection with H pylori and how they are influenced by this bacterium.

  1. Helicobacter pylori in out-patients of a general practitioner

    DEFF Research Database (Denmark)

    Rothenbacher, D; Bode, G; Winz, T

    1997-01-01

    Data on prevalence and determinants of Helicobacter pylori infection in well-defined populations are scarce. We investigated the prevalence and determinants of active H. pylori infection in a population of out-patients attending a general practitioner in Southern Germany. Infection status...

  2. Molecular Mechanisms of Antibiotic Resistance in Helicobacter pylori

    NARCIS (Netherlands)

    M.M. Gerrits (Monique)

    2004-01-01

    textabstractAn estimated 4 to 5 million individuals in the Netherlands are actively infected with Helicobacter pylori. Eradication of this bacterium becomes more difficult as the prevalence of antibiotic resistance is increasing worldwide. Most H. pylori infections are now diagnosed by non-invasi

  3. Epithelial cell kinetics of the gastric mucosa during Helicobacter pylori infection

    DEFF Research Database (Denmark)

    Holck, Susanne; Holm, I.L.; Holck, P.P.

    2007-01-01

    Helicobacter pylori is an important pathogen in major gastroduodenal diseases, including inflammation with ulceration and gastric malignancies. Alterations in H. pylori associated cell turnover in gastric epithelial cells are examined in relation to inflammatory activity, bacteria load...... and cytokines which may improve knowledge concerning the outcome of gastric diseases caused by H. pylori. Antral biopsies from 42 dyspeptic patients including 27 H. pylori-positive and 15 H. pylori-negative patients were tested for apoptotic activity by the TUNEL assay, and immuno-histochemically for p53...... and the proliferative marker Ki-67. H. pylori infection, bacteria load and inflammatory activity were associated with increased cell turnover as judged by enhanced activities of TUNEL, p53 and Ki-67. Only p53 was significantly correlated to IFN-gamma, IL-8 and IL-10. The H. pylori-positive state was furthermore...

  4. Helicobacter pylori Activates HMGB1 Expression and Recruits RAGE into Lipid Rafts to Promote Inflammation in Gastric Epithelial Cells

    OpenAIRE

    Lin, Hwai-Jeng; Hsu, Fang-Yu; Chen, Wei-Wei; Lee, Che-Hsin; Lin, Ying-Ju; Yi-Ywan M Chen; Chen, Chih-Jung; Huang, Mei-Zi; Kao, Min-Chuan; Chen, Yu-An; Lai, Hsin-Chih; Lai, Chih-Ho

    2016-01-01

    Helicobacter pylori infection is associated with several gastrointestinal disorders in the human population worldwide. High-mobility group box 1 (HMGB1), a ubiquitous nuclear protein, mediates various inflammation functions. The interaction between HMGB1 and receptor for advanced glycation end-products (RAGE) triggers nuclear factor (NF)-κB expression, which in turn stimulates the release of proinflammatory cytokines, such as interleukin (IL)-8, and enhances the inflammatory response. However...

  5. Treatment of Helicobacter pylori

    Institute of Scientific and Technical Information of China (English)

    Adam Harris

    2001-01-01

    @@ INTRODUCTION Using an evidence-based approach this review discusses the current treatment of Helicobacter pylori infection in patients with peptic ulcer disease, functional (non-ulcer)dyspepsia or gastro-oesophageal reflux disease (GORD).It also briefly addresses the potential role of eradication of H . pylori in preventing gastric cancer .

  6. Helicobacter pylori lipopolysaccharide:Biological activities in vitro and in vivo, pathological correlation to human chronic gastritis and peptic ulcer

    Institute of Scientific and Technical Information of China (English)

    Yi-Hui Luo; Jie Yan; Ya-Fei Mao

    2004-01-01

    AIM: To determine the biological activity of Helicobacter pylori (Hpylori) lipopolysaccharide (H-LPS) and understand pathological correlation between H-LPS and human chronic gastritis and peptic ulcer.METHODS: H-LPS of a clinical Hpylori strain and LPS of Escherichia coli strain O55:B5 (E-LPS) were extracted by phenol-water method. Biological activities of H-LPS and E-LPS were detected by limulus lysate assay, pyrogen assay,blood pressure test and PBMC induction test in rabbits,cytotoxicity test in NIH 3T3 fibroblast cells and lethality test in NIH mice. By using self-prepared rabbit anti-H-LPS serum as the first antibody and commercial HRP-labeled sheep anti-rabbit sera as the second antibody, H-LPS in biopsy specimens from 126 patients with chronic gastritis (68 cases) or gastric ulcer (58 cases) were examined by immunohistochemistry.RESULTS: Fibroblast cytotoxicity and mouse lethality of H-LPS were weaker than those of E-LPS. But the ability of coagulating limulus lysate of the two LPSs was similar (+/0.5 ng/mL). At 0.5 h after H-LPS injection, the blood pressures of the 3 rabbits rapidly declined. At 1.0 h after H-LPS injection, the blood pressures in 2 of the 3 rabbits fell to zero causing death of the 2 animals. For the other one rabbit in the same group, its blood pressure gradually elevated. At 0.5 h after E-LPS injection, the blood pressures of the three rabbits also quickly declined and then maintained at low level for approximately 1.0 h. At 0.5 h after injection with H-LPS or E-LPS, PBMC numbers of the rabbits showed a remarkable increase. The total positivity rate of H-LPS from 126 biopsy specimens was 60.3%(76/126). H-LPS positivity rate in the biopsy specimens from chronic gastritis (50/68, 73.5%) was significantly higher than that from gastric ulcer (26/58, 44.8%) (X2=10.77,P<0.01). H-LPS positivity rates in biopsy specimens from chronic superficial gastritis (38/48, 79.2%) and chronic active gastritis (9/10, 90.0%) were significantly higher than

  7. Association of NOD1 and NOD2 genes polymorphisms with Helicobacter pylori related gastric cancer in a Chinese population

    Institute of Scientific and Technical Information of China (English)

    Peng Wang; Zhao-Shan Zhang; Chun-Jie Liu; Li Zhang; Jian-Ming Jiang; Dan Ma; Hao-Xia Tao; Sheng-Ling Yuan; Yan-Chun Wang; Ling-Chun Wang; Hao Liang

    2012-01-01

    AIM:To investigate the association between the tag single nucleotide polymorphisms (TagSNPs) of NOD1 and NOD2 and the risk of developing gastric cancer.METHODS:We conducted a hospital-based case-control study including 296 incident gastric cancer patients and 160 gastritis controls.Eight TagSNPs in the NOD1 and NOD2 genes were selected from the Hapmap database using the haploview software and genotyped by the Sequenom MassArray system.The serum levels of anti-Helicobacter pylori (H.pylori) IgG were measured by enzyme-linked immunosorbent assay to indicate H.pylori infection.The odds ratios (OR) and 95% confidence intervals (CI) were calculated by unconditional logistic regression,including sex and age as confounding factors.RESULTS:The NOD1 rs2907749 GG genotype showed a decreased risk for gastric cancer (OR 0.50,95% CI:0.26-0.95,P =0.04) while the rs7789045 TT genotype showed an increased risk (OR 2.14,95% CI:1.20-3.82,P =0.01).An elevated susceptibility to gastric cancer was observed in the subjects with H.pylori infection and the NaOD1 rs7789045 TT genotype (OR 2.05,95% CI:1.07-3.94,P =0.03) or the NOD2 rs7205423 GC genotype (OR 2.52,95% CI:1.05-6.04,P =0.04).Haplotype analysis suggested that the distribution of AGT (rs2907749,rs2075820 and rs7789045) in NOD1 between the cases and control groups was significantly different (P corrected:0.04),and the diplotype AGT/AGT was associated with an elevated gastric cancer risk (OR 1.98,95%CI:1.04-3.79,P =0.04).The association of the NOD1 rs7789045 Tr genotype and the diplotype AGT/AGT was significant with H.pylori-related diffuse-type gastric cancer (OR 3.00,95% CI:1.38-6.53,P =0.01; OR 4.02,95% CI:1.61-10.05,P < 0.01,respectively).CONCLUSION:Genetic polymorphisms in NOD1 and NOD2 may interact with H.pylori infection and may play important roles in promoting the development of gastric cancer in the Chinese population.

  8. An Overview of the Relationship Between Helicobacter Pylori Infection and Otolaryngology Head and Neck Surgery Diseases%幽门螺旋杆菌感染与耳鼻咽喉头颈外科疾病关系研究综述

    Institute of Scientific and Technical Information of China (English)

    杜芬

    2012-01-01

    Helicobacter pylori is closely related to diseases like chronic gastritis and peptic ulcer, but recent studies show that there is also some connection with certain diseases concerning otolaryngology head and neck surgery. This paper begins with the de scription about helicobacter pylori biology, diagnosis, epidemiology and anti helicobacter pylori treatment and comprehensively states the relationship between helicobacter pylori and diseases concerning otolaryngology head and neck surgery in the hope providing a new perspective for the research of diseases connected with otolaryngology head and neck surgery.%幽门螺旋杆菌与慢性胃炎及消化性溃疡密切相关,但最近研究发现与某些耳鼻咽喉头颈外科疾病亦有一定关系。本文从阐述幽门螺旋杆菌的生物学性状、诊断技术、流行病学及抗幽门螺旋杆菌治疗入手,综述了幽门螺旋杆菌与耳鼻咽喉头颈外科疾病的关系,为从系统因素出发研究耳鼻咽喉头颈外科疾病提供新思路。

  9. Helicobacter pylori arginase mutant colonizes arginase Ⅱ knockout mice

    Institute of Scientific and Technical Information of China (English)

    Songhee H Kim; Melanie L Langford; Jean-Luc Boucher; Traci L Testerman; David J McGee

    2011-01-01

    AIM: To investigate the role of host and bacterial argi-nases in the colonization of mice by Helicobacter pylori (H. Pylori).METHODS: H. Pylori produces a very powerful urease that hydrolyzes urea to carbon dioxide and ammonium, which neutralizes acid. Urease is absolutely essential to H. Pylori pathogenesis; therefore, the urea substrate must be in ample supply for urease to work efficiently. The urea substrate is most likely provided by arginase activity, which hydrolyzes L-arginine to L-ornithine and urea. Previous work has demonstrated that H. Pylori arginase is surprisingly not required for colonization of wild-type mice. Hence, another in vivo source of the critical urea substrate must exist. We hypothesized that the urea source was provided by host arginase Ⅱ, since this enzyme is expressed in the stomach, and H. Pylori has previously been shown to induce the expres-sion of murine gastric arginase Ⅱ. To test this hypoth-esis, wild-type and arginase (rocF) mutant H. Pylori strain SS1 were inoculated into arginase Ⅱ knockout mice. RESULTS: Surprisingly, both the wild-type and rocF mutant bacteria still colonized arginase Ⅱ knock-out mice. Moreover, feeding arginase Ⅱ knockout mice the host arginase inhibitor S-(2-boronoethyl)-L-cysteine (BEC), while inhibiting > 50% of the host arginase Ⅰactivity in several tissues, did not block the ability of the rocF mutant H. Pylori to colonize. In con-trast, BEC poorly inhibited H. Pylori arginase activity. CONCLUSION: The in vivo source for the essential urea utilized by H. Pylori urease is neither bacterial arginase nor host arginase Ⅱ; instead, either residual host arginase Ⅰor agmatinase is probably responsible.

  10. NOD1-Mediated Mucosal Host Defense against Helicobacter pylori

    Directory of Open Access Journals (Sweden)

    Tomohiro Watanabe

    2010-01-01

    Full Text Available Infection of the stomach with Helicobacter pylori is an important risk factor for gastritis, peptic ulcer, and gastric carcinoma. Although it has been well established that persistent colonization by H. pylori is associated with adaptive Th1 responses, the innate immune responses leading to these Th1 responses are poorly defined. Recent studies have shown that the activation of nucleotide-binding oligomerization domain 1 (NOD1 in gastric epithelial cells plays an important role in innate immune responses against H. pylori. The detection of H. pylori-derived ligands by cytosolic NOD1 induces several host defense factors, including antimicrobial peptides, cytokines, and chemokines. In this paper, we review the molecular mechanisms by which NOD1 contributes to mucosal host defense against H. pylori infection of the stomach.

  11. Helicobacter pylori-related chronic gastritis as a risk factor for colonic neoplasms.

    Science.gov (United States)

    Inoue, Izumi; Kato, Jun; Tamai, Hideyuki; Iguchi, Mikitaka; Maekita, Takao; Yoshimura, Noriko; Ichinose, Masao

    2014-02-14

    To summarize the current views and insights on associations between Helicobacter pylori (H. pylori)-related chronic gastritis and colorectal neoplasm, we reviewed recent studies to clarify whether H. pylori infection/H. pylori-related chronic gastritis is associated with an elevated risk of colorectal neoplasm. Recent studies based on large databases with careful control for confounding variables have clearly demonstrated an increased risk of colorectal neoplasm associated with H. pylori infection. The correlation between H. pylori-related chronic atrophic gastritis (CAG) and colorectal neoplasm has only been examined in a limited number of studies. A recent large study using a national histopathological database, and our study based on the stage of H. pylori-related chronic gastritis as determined by serum levels of H. pylori antibody titer and pepsinogen, indicated that H. pylori-related CAG confers an increased risk of colorectal neoplasm, and more extensive atrophic gastritis will probably be associated with even higher risk of neoplasm. In addition, our study suggested that the activity of H. pylori-related chronic gastritis is correlated with colorectal neoplasm risk. H. pylori-related chronic gastritis could be involved in an increased risk of colorectal neoplasm that appears to be enhanced by the progression of gastric atrophy and the presence of active inflammation.

  12. Crystal structure of TNF-α-inducing protein from Helicobacter pylori in active form reveals the intrinsic molecular flexibility for unique DNA-binding.

    Directory of Open Access Journals (Sweden)

    Mingming Gao

    Full Text Available Tipα (TNF-α-inducing protein from Helicobacter pylori is a carcinogenic effector. Studies on this protein revealed that a homodimer linked by a pair of intermolecular disulfide bridges (Cys25-Cys25 and Cys27-Cys27 was absolutely necessary for its biological functions. The activities of Tipα would be abolished when both disulfide bridges were disrupted. The crystal structures of Tipα reported to date, however, were based on inactive, monomeric mutants with their N-terminal, including residues Cys25 and Cys27, truncated. Here we report the crystal structure of H. pylori Tipα protein, TipαN(25, at 2.2Å resolution, in which Cys25 and Cys27 form a pair of inter-chain disulfide bridges linking an active dimer. The disulfide bridges exhibit structural flexibility in the present structure. A series of structure-based mutagenesis, biochemical assays and molecular dynamic simulations on DNA-Tipα interactions reveal that Tipα utilizes the dimeric interface as the DNA-binding site and that residues His60, Arg77 and Arg81 located at the interface are crucial for DNA binding. Tipα could bind to one ssDNA, two ssDNA or one dsDNA in experiments, respectively, in the native or mutant states. The unique DNA-binding activities of Tipα indicate that the intrinsic flexible nature of disulfide bridges could endow certain elasticity to the Tipα dimer for its unique bioactivities. The results shed light on the possible structural mechanism for the functional performances of Tipα.

  13. Synthesis, physicochemical characterization, DFT calculation and biological activities of Fe(III) and Co(II)-omeprazole complexes. Potential application in the Helicobacter pylori eradication

    Science.gov (United States)

    Russo, Marcos G.; Vega Hissi, Esteban G.; Rizzi, Alberto C.; Brondino, Carlos D.; Salinas Ibañez, Ángel G.; Vega, Alba E.; Silva, Humberto J.; Mercader, Roberto; Narda, Griselda E.

    2014-03-01

    The reaction between the antiulcer agent omeprazole (OMZ) with Fe(III) and Co(II) ions was studied, observing a high ability to form metal complexes. The isolated microcrystalline solid complexes were characterized by elemental analysis, X-ray powder diffraction (XRPD), Scanning Electron Microscopy (SEM), magnetic measurements, thermal study, FTIR, UV-Visible, Mössbauer, electronic paramagnetic resonance (EPR), and DFT calculations. The metal-ligand ratio for both complexes was 1:2 determined by elemental and thermal analysis. FTIR spectroscopy showed that OMZ acts as a neutral bidentate ligand through the pyridinic nitrogen of the benzimidazole ring and the oxygen atom of the sulfoxide group, forming a five-membered ring chelate. Electronic, Mössbauer, and EPR spectra together with magnetic measurements indicate a distorted octahedral geometry around the metal ions, where the coordination sphere is completed by two water molecules. SEM and XRPD were used to characterize the morphology and the crystal nature of the complexes. The most favorable conformation for the Fe(III)-OMZ and Co(II)-OMZ complexes was obtained by DFT calculations by using B3LYP/6-31G(d)&LanL2DZ//B3LYP/3-21G(d)&LanL2DZ basis set. Studies of solubility along with the antibacterial activity against Helicobacter pylori for OMZ and its Co(II) and Fe(III) complexes are also reported. Free OMZ and both metal complexes showed antibacterial activity against H. pylori. Co(II)-OMZ presented a minimal inhibitory concentration ˜32 times lower than that of OMZ and ˜65 lower than Fe(III)-OMZ, revealing its promising potential use for the treatment of gastric pathologies associated with the Gram negative bacteria. The morphological changes observed in the cell membrane of the bacteria after the incubation with the metal-complexes were also analyzed by SEM microscopy. The antimicrobial activity of the complexes was proved by the viability test.

  14. The Expression of VacA in BCF of Helicobacter Pylori and Its Relationship to Vacuolated Effect

    Institute of Scientific and Technical Information of China (English)

    施理; 侯晓华; 易粹琼; 张锦坤

    2002-01-01

    Summary: The vacuolated effect of Helicobacter (H. Pylori) and its relationship to vacuolated cyto toxin antigen (VacA) were investigated by the method of cytotoxic test and SDS-pobyacrylamide gel electrophoresis (SDS-PAGE). Of the 62 clinical isolates, the broth culture filter (BCF) of 43 strains causecl the Vero cell intracytoplasmically vacuolated. H. Pylori strains were divided into H. Pylori (Toxin+) group with vacuolated effect and H. Pylori (Toxin-) group without vacuolated effect. The analysis of the BCF of H. Pylori (Toxin+) and that of H. Pylori (Toxin-) was studied by SDS-PAGE and Scan reader. A kind of protein with 87 ku molecular weight was recognized in the BCF of 30.23 % (13/43) H. Pylori (Toxin+) strains but in none of that of H. Pylori (Toxin-) strains, the difference was statistically significant (P<0. 05). There was a significant and concordant relation ship between OD of the protein band with 87 ku molecular weight and titer of vacuolated activity of H. Pylori(Toxin+) (r=0. 67 and P<0. 05 by linear regression analysis). H. Pylori strains were di-vided into H. Pylori (Toxin+) group with vacuolated effect and H. Pylori (Toxin-) group without vacuolated effect. The vacuolated effect of H. Pylori (Toxin+) was caused by the protein with 87 ku molecular weight (VacA).

  15. Trans-anethole kills Helicobacter pylori in vitro and in vivo

    Institute of Scientific and Technical Information of China (English)

    Yuhong Li; Gang Guo; Xuhu Mao

    2007-01-01

    Objective To determine the ability of trans-anethole to kill Helicobacter pylori(H, pylori) in vitro and the ability to eradicate H. pylori from infected mice. Materials and methods The suscepti bility of H. pyloriATCC11637 to trans-anethole was assessed by broth dilution determination. BALB/c mice were inoculated intragastrically with either a suspension of H. pylori B3 or special broth alone after pretreatment with ethanol and antibiotics. The infection status of H. pylori was confirmed before treatment. Then, mice were administered with either 10mg trans-anethole, 5rag trans-anethole,3mg metronidazole or 200μl salad oil every day for 14 days .Mice were sacrificed either in the 7th day ,15th day or 30 days after the completion of treatment, and the presence of H. pylori in their stomachs were detected via culture or PCR method. Results The MIC and MBC of trans-anethole against H.pylori ATCC 11637 were 39 μg/ml and 78 μg/ml, respectively. On condition of treatment of 10mg trans-anethole, 5mg trans-anethole or 3rag metronidazole, there was a significant reduction in H. pylori infection. Conclusion trans-anethole has good in vitro activity against H. pylori. It can eradicate H. pylori infection from mice.

  16. The Immunomodulator VacA Promotes Immune Tolerance and Persistent Helicobacter pylori Infection through Its Activities on T-Cells and Antigen-Presenting Cells

    Directory of Open Access Journals (Sweden)

    Aleksandra Djekic

    2016-06-01

    Full Text Available VacA is a pore-forming toxin that has long been known to induce vacuolization in gastric epithelial cells and to be linked to gastric disorders caused by H. pylori infection. Its role as a major colonization and persistence determinant of H. pylori is less well-understood. The purpose of this review is to discuss the various target cell types of VacA and its mechanism of action; specifically, we focus on the evidence showing that VacA targets myeloid cells and T-cells to directly and indirectly prevent H. pylori-specific T-cell responses and immune control of the infection. In particular, the ability of VacA-proficient H. pylori to skew T-cell responses towards regulatory T-cells and the effects of Tregs on H. pylori chronicity are highlighted. The by-stander effects of VacA-driven immunomodulation on extragastric diseases are discussed as well.

  17. Helicobacter pylori in pediatrics.

    Science.gov (United States)

    Homan, Matjaž; Hojsak, Iva; Kolaček, Sanja

    2012-09-01

    This review summarizes important pediatric studies published from April 2011 up to March 2012. Proteomics profile of ulcerogenic Helicobacter pylori strains was defined in the most interesting study of the last year. The antigen stool test is becoming the "gold standard" in prevalence studies, and according to the last epidemiologic studies, the prevalence of H. pylori infection in childhood is not decreasing any more in the developed world. The resistance rate of H. pylori strains is high in children. Therefore, among other important issues concerning H. pylori in pediatrics, guidelines published by ESPGHAN and NASPGHAN last year also recommended culture and susceptibility testing before first-line treatment in areas with high or unknown antibiotic resistance rates.

  18. Helicobacter pylori impairs murine dendritic cell responses to infection.

    Directory of Open Access Journals (Sweden)

    Ya-Hui Wang

    Full Text Available BACKGROUND: Helicobacter pylori, a human pathogen associated with chronic gastritis, peptic ulcer and gastric malignancies, is generally viewed as an extracellular microorganism. Here, we show that H. pylori replicates in murine bone marrow derived-dendritic cells (BMDCs within autophagosomes. METHODOLOGY/PRINCIPAL FINDINGS: A 10-fold increase of CFU is found between 2 h and 6 h p.i. in H. pylori-infected BMDCs. Autophagy is induced around the bacterium and participates at late time points of infection for the clearance of intracellular H. pylori. As a consequence of infection, LC3, LAMP1 and MHC class II molecules are retained within the H. pylori-containing vacuoles and export of MHC class II molecules to cell surface is blocked. However, formalin-fixed H. pylori still maintain this inhibitory activity in BMDC derived from wild type mice, but not in from either TLR4 or TLR2-deficient mice, suggesting the involvement of H. pylori-LPS in this process. TNF-alpha, IL-6 and IL-10 expression was also modulated upon infection showing a TLR2-specific dependent IL-10 secretion. No IL-12 was detected favoring the hypothesis of a down modulation of DC functions during H. pylori infection. Furthermore, antigen-specific T cells proliferation was also impaired upon infection. CONCLUSIONS/SIGNIFICANCE: H. pylori can infect and replicate in BMDCs and thereby affects DC-mediated immune responses. The implication of this new finding is discussed for the biological life cycle of H. pylori in the host.

  19. Helicobacter pylori and nonmalignant diseases.

    LENUS (Irish Health Repository)

    Alakkari, Alaa

    2012-02-01

    Research published over the past year has documented the continued decline of Helicobacter pylori-related peptic ulcer disease and increased recognition of non-H. pylori, non-steroidal anti-inflammatory drugs ulcer disease--idiopathic ulcers. Despite reduced prevalence of uncomplicated PUD, rates of ulcer complications and associated mortality remain stubbornly high. The role of H. pylori in functional dyspepsia is unclear, with some authors considering H. pylori-associated nonulcer dyspepsia a distinct organic entity. There is increasing acceptance of an inverse relationship between H. pylori and gastroesophageal reflux disease (GERD), but little understanding of how GERD might be more common\\/severe in H. pylori-negative subjects. Research has focused on factors such as different H. pylori phenotypes, weight gain after H. pylori eradication, and effects on hormones such as ghrelin that control appetite.

  20. 清除幽门螺杆菌感染在帕金森病治疗中的作用%Efficacy of anti-helicobacter pylori in treatment of parkinson disease

    Institute of Scientific and Technical Information of China (English)

    许文芳; 陈育华; 马博; 时鹏; 陈齐鸣; 屈洪党

    2014-01-01

    目的 观察清除幽门螺杆菌(Hp)感染在帕金森病(PD)治疗中的作用.方法 选择60例年龄在40~69岁之间的早期PD患者,病史1~3年,UPDRS评分小于20分,且其血清HP抗体阳性,随机分成2组,对照组30例,男性20人,女性10人,从小剂量开始给予美多芭治疗,每次美多芭0.0625 g,每日2次,逐渐增加剂量,最高量为每次0.25 g,每日3次;观察组30例,男性19人,女性11人,在此基础上加用清除Hp治疗(雷尼替丁0.15g+阿莫西林1.0g+克拉霉素0.5g,每天2次,共7d).采用UPDRS评分量表比较2组患者治疗1个月、3个月后的疗效.结果 对照组患者治疗1个月和3个月后UPDRS评分从11.77分别降至9.43分(P<0.01)和8.73分(P<0.01),治疗3个月UPDRS评分较治疗1个月UPDRS评分差异无统计学意义(P=0.214).观察组患者治疗1个月和3个月后UPDRS评分从12.67分别降至10.30分(P<0.01)和7.77分(P<0.01),治疗3个月UPDRS评分优于治疗1个月UPDRS评分(P<0.01).治疗1个月UPDRS评分观察组较对照组无明显改善(P=0.140);治疗3个月后UPDRS评分观察组较对照组有明显改善(P =0.018).结论 清除Hp感染可提高治疗PD的疗效.

  1. Human immune responses to H. pylori HLA Class II epitopes identified by immunoinformatic methods.

    Directory of Open Access Journals (Sweden)

    Songhua Zhang

    Full Text Available H. pylori persists in the human stomach over decades and promotes several adverse clinical sequelae including gastritis, peptic ulcers and gastric cancer that are linked to the induction and subsequent evasion of chronic gastric inflammation. Emerging evidence indicates that H. pylori infection may also protect against asthma and some other immune-mediated conditions through regulatory T cell effects outside the stomach. To characterize the complexity of the CD4+ T cell response generated during H. pylori infection, computational methods were previously used to generate a panel of 90 predicted epitopes conserved among H. pylori genomes that broadly cover HLA Class II diversity for maximum population coverage. Here, these sequences were tested individually for their ability to induce in vitro responses in peripheral blood mononuclear cells by interferon-γ ELISpot assay. The average number of spot-forming cells/million PBMCs was significantly elevated in H. pylori-infected subjects over uninfected persons. Ten of the 90 peptides stimulated IFN-γ secretion in the H. pylori-infected group only, whereas two out of the 90 peptides elicited a detectable IFN-γ response in the H. pylori-uninfected subjects but no response in the H. pylori-infected group. Cytokine ELISA measurements performed using in vitro PBMC culture supernatants demonstrated significantly higher levels of TNF-α, IL-2, IL-4, IL-6, IL-10, and TGF-β1 in the H. pylori-infected subjects, whereas IL-17A expression was not related to the subjects H. pylori-infection status. Our results indicate that the human T cell responses to these 90 peptides are generally increased in actively H. pylori-infected, compared with H. pylori-naïve, subjects. This information will improve understanding of the complex immune response to H. pylori, aiding rational epitope-driven vaccine design as well as helping identify other H. pylori epitopes with potentially immunoregulatory effects.

  2. Halitosis and Helicobacter pylori infection

    NARCIS (Netherlands)

    Tangerman, A.; Winkel, E. G.; de Laat, L.; van Oijen, A. H.; de Boer, W. A.

    2012-01-01

    There is disagreement about a possible relationship between Helicobacter pylori (H. pylori) infection and objective halitosis, as established by volatile sulfur compounds (VSCs) in the breath. Many studies related to H. pylori used self-reported halitosis, a subjective and unreliable method to detec

  3. Antimicrobial Nanotherapeutics Against Helicobacter pylori Infection

    Science.gov (United States)

    Thamphiwatana, Soracha

    Helicobacter pylori (H. pylori) infection with its vast prevalence is responsible for various gastric diseases including gastritis, peptic ulcers, and gastric malignancy. While effective, current treatment regimens are challenged by a fast-declining eradication rate due to the increasing emergence of H. pylori strains resistant to existing antibiotics. Therefore, there is an urgent need to develop novel antibacterial strategies against H. pylori. The first area of this research, we developed a liposomal nanoformulation of linolenic acid (LipoLLA) and evaluated its bactericidal activity against resistant strains of H. pylori. We found that LipoLLA was effective in killing both spiral and dormant forms of the bacteria via disrupting bacterial membranes. LipoLLA eradicated all strains of the bacteria regardless of their antibiotic resistance status. Furthermore, the bacteria did not develop drug resistance toward LipoLLA. Our findings suggest that LipoLLA is a promising antibacterial nanotherapeutic to treat antibiotic-resistant H. pylori infection. The next step, we investigated the in vivo therapeutic potential of LipoLLA for the treatment of H. pylori infection. In vivo tests further confirmed that LipoLLA was able to kill H. pylori and reduce bacterial load in the mouse stomach. LipoLLA treatment was also shown to reduce the levels of proinflammatory cytokines including interleukin-1beta (IL-1beta), IL-6, and tumor necrosis factor alpha, which were otherwise elevated due to the H. pylori infection. Finally, toxicity test demonstrated excellent biocompatibility of LipoLLA to normal mouse stomach. Collectively, results from this work indicate that LipoLLA is a promising, new, effective, and safe therapeutic agent for the treatment of H. pylori infection. The second area is stimuli-responsive liposomes development. By adsorbing small chitosan-modified gold nanoparticles (AuChi) onto the outer surface of liposomes, we show that at gastric pH the liposomes have

  4. H pylori infection among 1000 southern Iranian dyspeptic patients

    Institute of Scientific and Technical Information of China (English)

    Mahmood Reza Hashemi; Mohammad Rahnavardi; Bavand Bikdeli; Mohsen Dehghani Zahedani

    2006-01-01

    AIS: To describe the frequency of H pylori infection among 1000 southern Iranian dyspeptic patients.METHODS: A prospective study was performed in a referral hospital in south of Iran from 1999 to 2005. One thousand dyspeptic patients (518 males, mean ± SD age of 49.12 ± 12.82 years) consecutively underwent upper gastrointestinal endoscopy. Multiple gastric antral biopsy samples were taken from all patients for rapid ureasetest and histopathologic examination (96.9% satisfactory samples). Patients were considered H pylori-infected if one or both tests were positive.RESULTS: Six hundred and seventy-one patients (67.1%, 95% confidence interval [CI]: 64.2%-70.0%) were H pylori-infected.H pylori positivity was significantly more frequent in patients with peptic ulcer disease (PUD)than in those with non-ulcer dyspepsia (P < 0.001).Male-to-female ratio for duodenal and gastric ulcers was 2.7:1 and 1.5:1, respectively. Moreover, the duodenalto-gastric ulcer ratio was 1.95:1. The frequency of H pylori infection among those with endoscopic diagnosis of gastritis, duodenal ulcer, gastric ulcer, and normal mucosa was 70.1% (398/568), 86.2% (150/174),71.9% (64/89), and 33.5% (54/161), respectively. H pylori infection, male sex, and older age were independently associated with PUD in multivariate analysis.H pylori positivity was associated with chronic gastritis, and chronic active gastritis with odds ratios of 34.21 (95% CI: 12.19%-96.03%) and 81.21 (95% CI:28.85%-228.55%), respectively.CONCLUSION: H pylori and PUD are highly frequent in dyspeptic patients from south of Iran. H pylori is a cardinal risk factor for chronic active or inactive gastritis.

  5. Prominent role of γ-glutamyl-transpeptidase on the growth of Helicobacter pylori

    Institute of Scientific and Technical Information of China (English)

    Min Gong; Bow Ho

    2004-01-01

    AIM: γ-glutamyl transpeptidase (GGT) has been reported as a virulence and colonizing factor of Helicobacter pylori (H pylori). This study examined the effect of GGT on the growth of H pylori.METHODS: Standard H pylori strain NCTC 11637 and 4clinical isolates with different levels of GGT activity as measured by an enzymatic assay were used in this study. Growth inhibition and stimulation studies were carried out by culturing H pylori in brain heart infusion broth supplemented with specific GGT inhibitor (L-serine sodium borate complex, SBC)or enhancer (glutathione together with glycyl-glycine),respectively. The growth profiles of H pyloriwere determined based on viable bacterial count at time interval.RESULTS: Growth was more profuse for H pylori isolates with higher GGT activity than those present with lower GGT activity. However, in the presence of SBC, growth of H pylori was retarded in a dose dependent manner (P = 0.034). In contrast, higher growth rate was observed when GGT activity was enhanced in the presence of glutathione and glycyl-glycine.CONCLUSION: Higher GGT activity provides an advantage to the growth of H pylori in vitro. Inhibition of GGT activity by SBC resulted in growth retardation. The study shows that GGT plays an important role on the growth of H pylori.

  6. Helicobacter pylori and colorectal neoplasia: Is there a causal link?

    Science.gov (United States)

    Papastergiou, Vasilios; Karatapanis, Stylianos; Georgopoulos, Sotirios D

    2016-01-14

    Ever since Helicobacter pylori (H. pylori) was recognized as an infectious cause of gastric cancer, there has been increasing interest in examining its potential role in colorectal carcinogenesis. Data from case-control and cross-sectional studies, mostly relying on hospital-based samples, and several meta-analyses have shown a positive statistical relationship between H. pylori infection and colorectal neoplasia. However, the possibility exists that the results have been influenced by bias, including the improper selection of patients and disparities with respect to potential confounders. While the evidence falls short of a definitive causal link, it appears that infection with H. pylori/H. pylori-related gastritis is associated with an increased, although modest, risk of colorectal adenoma and cancer. The pathogenic mechanisms responsible for this association remain uncertain. H. pylori has been detected in colorectal malignant tissues; however, the possibility that H. pylori is a direct activator of colonic carcinogenesis remains purely hypothetical. On the other hand, experimental data have indicated a series of potential oncogenic interactions between these bacteria and colorectal mucosa, including induction and perpetuation of inflammatory responses, alteration of gut microflora and release of toxins and/or hormonal mediators, such as gastrin, which may contribute to tumor formation.

  7. Nitric oxide synthetase and Helicobacter pylori in patients undergoing appendicectomy.

    LENUS (Irish Health Repository)

    Kell, M R

    2012-02-03

    BACKGROUND: This study was designed to determine whether Helicobacter pylori forms part of the normal microenvironment of the appendix, whether it plays a role in the pathogenesis of acute appendicitis, and whether it is associated with increased expression of inducible nitric oxide synthetase (iNOS) in appendicular macrophages. METHODS: Serology for H. pylori was performed on 51 consecutive patients undergoing emergency appendicectomy. Appendix samples were tested for urease activity, cultured and stained for H. pylori, graded according to the degree of inflammatory infiltrate, and probed immunohistochemically for iNOS expression. RESULTS: The mean age of the patients was 21 (range 7-51) years. Seventeen patients (33 per cent) were seropositive for H. pylori but no evidence of H. pylori was found in any appendix specimen. However, an enhanced inflammatory cell infiltration was observed in seropositive patients (P < 0.04) and the expression of macrophage iNOS in the mucosa of normal and inflamed appendix specimens was increased (P < 0.01). CONCLUSION: H. pylori does not colonize the appendix and is unlikely to be a pathogenic stimulus for appendicitis. Priming effects on mucosal immunology downstream from the foregut may occur after infection with H. pylori.

  8. Eradication of H pylori for the prevention of gastric cancer

    Institute of Scientific and Technical Information of China (English)

    Karolin Trautmann; Manfred Stolte; Stephan Miehlke

    2006-01-01

    Tnfection with H pylori is the most important known etiological factor associated with gastric cancer. While colonization of the gastric mucosa with H pylori results in active and chronic gastritis in virtually all individuals infected, the likelihood of developing gastric cancer depends on environmental, bacterial virulence and host specific factors. The majority of all gastric cancer cases are attributable to H pylori infection and therefore theoretically preventable. There is evidence from animal models that eradication of H pylori at an early time point can prevent gastric cancer development. However, randomized clinical trials exploring the prophylactic effect of H pylori eradication on the incidence of gastric cancer in humans remain sparse and have yielded conflicting results. Better markers for the identification of patientsat risk for H pylori induced gastric malignancy are needed to allow the development of a more efficient public eradication strategy. Meanwhile, screening and treatment of H pylori in first-degree relatives of gastric cancer patients as well as certain high-risk populations might be beneficial.

  9. Helicobacter pylori associated Asian enigma: Does diet deserve distinction?

    Institute of Scientific and Technical Information of China (English)

    Syed Faisal Zaidi

    2016-01-01

    Helicobacter pylori(H. pylori) is one of the most widespread infections in humans worldwide that chronically infects up to 50% of the world’s population. The infection is involved in the pathogenesis of chronic active gastritis, peptic ulcer, mucosa-associated lymphoid tissue lymphoma and gastric cancer, therefore, it has been classified as class Ⅰ definite carcinogen by the World Health Organization. Despite the established etiological role of H. pylori, its actual distribution and association with related diseases is controversial and there is a large intercountry variation especially among Asian countries. H. pylori infection is more frequent in developing countries like India, Pakistan, and Bangladesh as compared to developed Asian countries like Japan, China and South Korea. However, the frequency of gastric cancer is comparatively lower in India, Pakistan, and Bangladesh with that of Japan, China and South Korea. Such phenomenon of clinical diversity, defined as enigma, is judged by genetic variability of the infecting H. pylori strains, differences in the host genetic background in various ethnic groups, and environmental factors such as dietary habits. Most of the studies have so far focused on the bacterial factor while environmental issues, including dietary components, were not given due attention as one of the factors related with H. pylori associated gastric carcinogenesis. The dietary factor has been suggested to play an important role in H. pylori related carcinogenesis, and in this respect several studies have corroborated the intake of various dietary components as modulatory factors for gastric cancer risk. In this review, such studies, from in vitro experiments to clinical trials, are being focused in detail with respect to enigma associated with H. pylori. It may be conceivably concluded from the available evidence that dietary factor can be a game changer in the scenario of Asian enigma, particularly in high risk population infected with

  10. Gastric angiogenesis and Helicobacter pylori infection

    Directory of Open Access Journals (Sweden)

    I. D. Pousa

    Full Text Available The formation of new blood vessels seen in conditions commonly associated with Helicobacter pylori (H. pylori infection, including gastritis, peptic ulcer, and gastric carcinoma, prompts consideration of a potential relationship between mucosal colonization by this organism and the angiogenic process. H. pylori directly or indirectly damages endothelial cells, which induces a number of changes in the microvasculature of the gastric mucosa. In H. pylori-associated conditions, that is, in gastritis, peptic ulcer and gastric carcinoma, there is an increased concentration of angiogenic factors, and subsequently a formation of new blood vessels. However, this early angiogenesis -which is activated to repair the gastric mucosa- is subsequently inhibited in patients with peptic ulcer, and ulcer healing is thus delayed. This may be due to the antiproliferative action of this organism on endothelial cells. While the angiogenic process becomes inhibited in infected patients with peptic ulcer, it remains seemingly active in those with gastritis or gastric cancer. This fact is in support of the notion suggested by various studies that peptic ulcer and gastric cancer are mutually excluding conditions. In the case of gastric cancer, neoangiogenesis would enhance nutrient and oxygen supply to cancer cells, and thus tumor growth and metastatic spread.

  11. Role of γ-glutamyltranspeptidase in the pathogenesis of Helicobacter pylori infection.

    Science.gov (United States)

    Rimbara, Emiko; Mori, Shigetarou; Kim, Hyun; Shibayama, Keigo

    2013-10-01

    γ-Glutamyltranspeptidase and asparaginase have been shown to play important roles in Helicobacter pylori colonization and cell death induced by H. pylori infection. In this study, the association of γ-glutamyltranspeptidase and asparaginase was elucidated by comparing activities of both deamidases in H. pylori strains from patients with chronic gastritis, gastric and duodenal ulcers, and gastric cancer. γ-Glutamyltranspeptidase activities in H. pylori strains from patients with gastric cancer were significantly higher than in those from patients with chronic gastritis or gastric ulcers. There was a wide range of asparaginase activities in H. pylori strains from patients with gastric cancer and these were not significantly than those from patients with other diseases. To identify the contributions of γ-glutamyltranspeptidase and asparaginase to gastric cell inflammation, human gastric epithelial cells (AGS line) were infected with H. pylori wild-type and knockout strains and inflammatory responses evaluated by induction of interleukin-8 (IL-8). IL-8 response was significantly decreased by knockout of the γ-glutamyltranspeptidase-encoding gene but not by knockout of the asparaginase-encoding gene. Additionally, IL-8 induction by infection with the H. pylori wild-type strain was significantly decreased by adding glutamine during infection. These findings indicate that IL-8 induction caused by γ-glutamyltranspeptidase activity in H. pylori is mainly attributable to depletion of glutamine. These data suggest that γ-glutamyltranspeptidase plays a significant role in the chronic inflammation caused by H. pylori infection.

  12. Nickel-Responsive Induction of Urease Expression in Helicobacter pylori Is Mediated at the Transcriptional Level

    OpenAIRE

    van Vliet, Arnoud H. M.; Kuipers, Ernst J; Waidner, Barbara; Davies, Beverly J.; de Vries, Nicolette; Penn, Charles W.; Vandenbroucke-Grauls, Christina M. J. E.; Kist, Manfred; Bereswill, Stefan; Kusters, Johannes G.

    2001-01-01

    The nickel-containing enzyme urease is an essential colonization factor of the gastric pathogen Helicobacter pylori, as it allows the bacterium to survive the acidic conditions in the gastric mucosa. Although urease can represents up to 10% of the total protein content of H. pylori, expression of urease genes is thought to be constitutive. Here it is demonstrated that H. pylori regulates the expression and activity of its urease enzyme as a function of the availability of the cofactor nickel....

  13. Endoscopic gastritis, serum pepsinogen assay, and Helicobacter pylori infection

    OpenAIRE

    Lee, Sun-Young

    2016-01-01

    Endoscopic findings of the background gastric mucosa are important in the Helicobacter pylori-seroprevalent population. It is strongly correlated not only with the risk of gastric cancer, but also with the excretion ability of gastric mucosa cells. In noninfected subjects, common endoscopic findings are regular arrangement of collecting venules, chronic superficial gastritis, and erosive gastritis. In cases of active H. pylori infection, nodularity on the antrum, hemorrhagic spots on the fund...

  14. Molecular Mechanisms of Antibiotic Resistance in Helicobacter pylori

    OpenAIRE

    Gerrits, Monique

    2004-01-01

    textabstractAn estimated 4 to 5 million individuals in the Netherlands are actively infected with Helicobacter pylori. Eradication of this bacterium becomes more difficult as the prevalence of antibiotic resistance is increasing worldwide. Most H. pylori infections are now diagnosed by non-invasive testing (i.e. urea breath test, serology, stool test), and thus data on antibiotic susceptibility are lacking. Furthermore, once the antibiotic susceptibility is assessed using conventional culture...

  15. Structural Studies of FlaA1 from Helicobacter Pylori Reveal the Mechanism for Inverting 4,6-dehydratase Activity

    Energy Technology Data Exchange (ETDEWEB)

    Ishiyama,N.; Creuzenet, C.; Miller, W.; Demendi, M.; Anderson, E.; Harauz, G.; Lam, J.; Berghuis, A.

    2006-01-01

    FlaA1 from the human pathogen Helicobacter pylori is an enzyme involved in saccharide biosynthesis that has been shown to be essential for pathogenicity. Here we present five crystal structures of FlaA1 in the presence of substrate, inhibitors, and bound cofactor, with resolutions ranging from 2.8 to 1.9 {angstrom}. These structures reveal that the enzyme is a novel member of the short-chain dehydrogenase/reductase superfamily. Additional electron microscopy studies show the enzyme to possess a hexameric doughnut-shaped quaternary structure. NMR analyses of 'real time' enzyme-substrate reactions indicate that FlaA1 is a UDP-GlcNAc-inverting 4,6-dehydratase, suggesting that the enzyme catalyzes the first step in the biosynthetic pathway of a pseudaminic acid derivative, which is implicated in protein glycosylation. Guided by evidence from site-directed mutagenesis and computational simulations, a three-step reaction mechanism is proposed that involves Lys-133 functioning as both a catalytic acid and base.

  16. Consequences of Helicobacter pylori infection in children

    Institute of Scientific and Technical Information of China (English)

    Lucia; Pacifico; Caterina; Anania; John; F; Osborn; Flavia; Ferraro; Claudio; Chiesa

    2010-01-01

    Although evidence is emerging that the prevalence of Helicobacter pylori (H. pylori) is declining in all age groups, the understanding of its disease spectrum continues to evolve. If untreated, H. pylori infection is lifelong. Although H. pylori typically colonizes the hu-man stomach for many decades without adverse con-sequences, children infected with H. pylori can manifest gastrointestinal diseases. Controversy persists regarding testing (and treating) for H. pylori infection in children with recurrent a...

  17. Consequences of Helicobacter pylori infection in children

    OpenAIRE

    Pacifico, Lucia; Anania, Caterina; Osborn, John F.; Ferraro, Flavia; Chiesa, Claudio

    2010-01-01

    Although evidence is emerging that the prevalence of Helicobacter pylori (H. pylori) is declining in all age groups, the understanding of its disease spectrum continues to evolve. If untreated, H. pylori infection is lifelong. Although H. pylori typically colonizes the human stomach for many decades without adverse consequences, children infected with H. pylori can manifest gastrointestinal diseases. Controversy persists regarding testing (and treating) for H. pylori infection in children wit...

  18. Association of Helicobacter pylori infection with nodular antritis and follicular gastritis

    Directory of Open Access Journals (Sweden)

    Tomašević Ratko

    2006-01-01

    Full Text Available Introduction. Helicobacter pylori (H. pylori infection is known to be the must common cause of chronic gastritis having some endoscopic and pathologic characteristies as determinated by the Sydney System for Gastritis Classification. The aim of our case report was to point out the relationship between an endoscopic finding of nodular antritis and the presence of H. pylori infection and active chronic gastritis. Case report. Our patient underwent upper gastrointestinal endoscopy for dyspeptic complaints and was diagnosed as having nodular antritis, but also underwent urease test and hystopathologic examination of antral mucosa, to determine the presence and density of H. pylori infection and the presence and severity of gastritis. After a course of anti H. pylori treatment, dyspepsia improved and new biopsy specimens obtained two months and six months afterwards revealed no pathological findings. Conclusion. The case report supported the association of H. pylori infection of lymphoid follicles with nodular gastric mucosis.

  19. Helicobacter pylori Infection Induces Genetic Instability of Nuclear and Mitochondrial DNA in Gastric Cells

    DEFF Research Database (Denmark)

    Machado, Ana Manuel; Figueiredo, Ceu; Touati, Eliette;

    2009-01-01

    Purpose: Helicobacter pylori is a major cause of gastric carcinoma. To investigate a possible link between bacterial infection and genetic instability of the host genome, we examined the effect of H. pylori infection on known cellular repair pathways in vitro and in vivo. Moreover, various types...... of genetic instabilities in the nuclear and mitochondrial DNA (mtDNA) were examined. Experimental Design: We observed the effects of H pylori infection on a gastric cell line (AGS), on C57BL/6 mice, and on individuals with chronic gastritis. In AGS cells, the effect of H pylori infection on base excision...... cells and chronic gastritis tissue were determined by PCR, single-stranded conformation polymorphism, and sequencing. H pylori vacA and cagA genotyping was determined by multiplex PCR and reverse hybridization. Results: Following H pylori infection, the activity and expression of base excision repair...

  20. The prevalence and related symptomatology of Helicobacter pylori in children with recurrent abdominal pain

    DEFF Research Database (Denmark)

    Wewer, Anne Vibeke; Andersen, L P; Pærregaard, Anders;

    1998-01-01

    The aim of the study was to assess and compare the IgG seroprevalence of H. pylori in children with recurrent abdominal pain with healthy children and to investigate the related symptoms. IgG antibodies against low-molecular weight H. pylori antigens were assessed in 438 children with recurrent...... of the abdominal pain, presence of pyrosis, nocturnal pain, relation of pain to meals and bowel irregularities. The seroprevalence was 21% (95% CI: 17-25%) in the children with recurrent abdominal pain and 10% (95% CI: 5-18%) in the healthy controls (p = 0.30). In seropositive children with RAP H. pylori was found...... in 46/66 by culture and histology. The presence of H. pylori was significantly associated with active or inactive chronic gastritis. The presence of H. pylori was associated with both parents being born in a country with a high prevalence and a low social class. Helicobacter pylori-positive children had...

  1. Helicobacter pylori Infection in Pediatrics.

    Science.gov (United States)

    Roma, Eleftheria; Miele, Erasmo

    2015-09-01

    This review includes the main pediatric studies published from April 2014 to March 2015. The host response of Treg cells with increases in FOXP3 and TGF-β1 combined with a reduction in IFN-γ by Teff cells may contribute to Helicobacter pylori susceptibility in children. Genotypic variability in H. pylori strains influences the clinical manifestation of the infection. Helicobacter pylori infection is associated with variables indicative of a crowded environment and poor living conditions, while breast-feeding has a protective effect. Intrafamilial infection, especially from mother to children and from sibling to sibling, is the dominant transmission route. Studies showed conflicting results regarding the association between H. pylori infection and iron deficiency anemia. One study suggests that H. pylori eradication plays a role in the management of chronic immune thrombocytopenic purpura in H. pylori-infected children and adolescents. The prevalence of H. pylori was higher in chronic urticaria patients than in controls and, following H. pylori eradication, urticarial symptoms disappeared. An inverse relationship between H. pylori infection and allergic disease was reported. Antibiotic resistance and insufficient compliance to treatment limit the efficacy of eradication therapy. Sequential therapy had no advantage over standard triple therapy. In countries where H. pylori infection is prevalent, studies focusing on virulence factors and antibiotic susceptibility may provide anticipation of the prognosis and may be helpful to reduce morbidity and mortality.

  2. Extradigestive Manifestation of Helicobacter Pylori Infection in Children and Adolescents

    Directory of Open Access Journals (Sweden)

    Philip M Sherman

    2005-01-01

    Full Text Available Helicobacter pylori infection fulfills each of Koch's postulates as a human pathogen causing chronic active gastritis. Disease consequences that develop in a subset of infected subjects include peptic ulcerations, gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma. More recently, multiple publications have advocated a role for H pylori infection in causing a variety of extraintestinal manifestations. Many of these reports suffer from being case reports or case series without adequate controls. As a result, purported manifestations may simply be coincidental in nature. On the other hand, increasing evidence supports H pylori infection as a cause of sideropenic (refractory iron deficiency anemia. Moderate evidence supports H pylori gastric infection as a cause of some cases of immune thrombocytopenic purpura due to molecular mimicry. Guidelines should be adjusted in accordance with advancing knowledge in the field.

  3. NikR mediates nickel-responsive transcriptional induction of urease expression in Helicobacter pylori

    NARCIS (Netherlands)

    A.H.M. van Vliet (Arnoud); S.W. Poppelaars (Sophie); B.J. Davies; J. Stoof (Jeroen); S. Bereswill (Stefan); M. Kist (Manfred); C.W. Penn (Charles); E.J. Kuipers (Ernst); J.G. Kusters (Johannes)

    2002-01-01

    textabstractThe important human pathogen Helicobacter pylori requires the abundant expression and activity of its urease enzyme for colonization of the gastric mucosa. The transcription, expression, and activity of H. pylori urease were previously demonstrated to be induced by nick

  4. 幽门螺杆菌研究进展%ADVANCES IN RESEARCH OF HELICOBACTER PYLORI

    Institute of Scientific and Technical Information of China (English)

    丁云菲; 李安明

    1999-01-01

    Helicobacter pylori is an important pathogenic microorganism for chronic active gastritis and peptic ulcers, probably causing gastric cancer. With many characteristics, this organism colonizes the surface of the human stomach and worldwide transmits from human to human via the fecal-oral or the oral-oral route. Several kinds of methods are currently available for diagnosis of H.pylori infection and isolation of H.pylori. Some measures of treatment and prevention are necessary to decline the incidence of H.pylori infection and upper gastrointestinal tract disease.

  5. Bactericidal and anti-adhesive properties of culinary and medicinal plants against Helicobacter pylori

    Institute of Scientific and Technical Information of China (English)

    Rachel O'Mahony; Huda Al-Khtheeri; Deepeka Weerasekera; Neluka Fernando; Dino Vaira; John Holton; Christelle Basset

    2005-01-01

    AIM: To investigate the bactericidal and anti-adhesive properties of 25 plants against Helicobacter pylori (H pylori).METHODS: Twenty-five plants were boiled in water to produce aqueous extracts that simulate the effect of cooking. The bactericidal activity of the extracts was assessed by a standard kill-curve with seven strains of H pylori. The anti-adhesive property was assessed by the inhibition of binding of four strains of FITC-labeled H pylori to stomach sections. RESULTS: Of all the plants tested, eight plants, including Bengal quince, nightshade, garlic, dill, black pepper, coriander, fenugreek and black tea, were found to have no bactericidal effect on any of the isolates. Columbo weed, long pepper, parsley, tarragon, nutmeg, yellow-berried nightshade, threadstem carpetweed, sage and cinnamon had bactericidal activities against H pylori, but total inhibition of growth was not achieved in this study. Among the plants that killed H pylori, turmeric was the most efficient, followed by cumin, ginger, chilli, borage, black caraway, oregano and liquorice. Moreover, extracts of turmeric; borage and parsley were able to inhibit the adhesion of H pylori strains to the stomach sections.CONCLUSION: Several plants that were tested in our study had bactericidal and/or anti-adhesive effects on H pylori. Ingestion of the plants with anti-adhesive properties could therefore provide a potent alternative therapy for H pylori infection, which overcomes the problem of resistance associated with current antibiotic treatment.

  6. The antimicrobial effects and metabolomic footprinting of carboxyl-capped bismuth nanoparticles against Helicobacter pylori.

    Science.gov (United States)

    Nazari, P; Dowlatabadi-Bazaz, R; Mofid, M R; Pourmand, M R; Daryani, N E; Faramarzi, M A; Sepehrizadeh, Z; Shahverdi, A R

    2014-01-01

    Organic salts of bismuth are currently used as antimicrobial agents against Helicobacter pylori. This study evaluated the antibacterial effect of elemental bismuth nanoparticles (Bi NPs) using a serial agar dilution method for the first time against different clinical isolates and a standard strain of H. pylori. The Bi NPs were biologically prepared and purified by a recently described method and subjected to further characterization by infrared spectroscopy and anti-H. pylori evaluation. Infrared spectroscopy results showed the presence of carboxyl functional groups on the surface of biogenic Bi NPs. These biogenic nanoparticles showed good antibacterial activity against all tested H. pylori strains. The resulting MICs varied between 60 and 100 μg/ml for clinical isolates of H. pylori and H. pylori (ATCC 26695). The antibacterial effect of bismuth ions was also tested against all test strains. The antimicrobial effect of Bi ions was lower than antimicrobial effect of bismuth in the form of elemental NPs. The effect of Bi NPs on metabolomic footprinting of H. pylori was further evaluated by (1)H NMR spectroscopy. Exposure of H. pylori to an inhibitory concentration of Bi NPs (100 μg/ml) led to release of some metabolites such as acetate, formic acid, glutamate, valine, glycine, and uracil from bacteria into their supernatant. These findings confirm that these nanoparticles interfere with Krebs cycle, nucleotide, and amino acid metabolism and shows anti-H. pylori activity.

  7. Linezolid susceptibility in Helicobacter pylori, including strains with multidrug resistance.

    Science.gov (United States)

    Boyanova, Lyudmila; Evstatiev, Ivailo; Gergova, Galina; Yaneva, Penka; Mitov, Ivan

    2015-12-01

    Only a few studies have evaluated Helicobacter pylori susceptibility to linezolid. The aim of the present study was to assess linezolid susceptibility in H. pylori, including strains with double/multidrug resistance. The susceptibility of 53 H. pylori strains was evaluated by Etest and a breakpoint susceptibility testing method. Helicobacter pylori resistance rates were as follows: amoxicillin, 1.9%; metronidazole, 37.7%; clarithromycin, 17.0%; tetracycline, 1.9%; levofloxacin, 24.5%; and linezolid (>4 mg/L), 39.6%. The linezolid MIC50 value was 31.2-fold higher than that of clarithromycin and 10.5-fold higher than that of levofloxacin; however, 4 of 11 strains with double/multidrug resistance were linezolid-susceptible. The MIC range of the oxazolidinone agent was larger (0.125-64 mg/L) compared with those in the previous two reports. The linezolid resistance rate was 2.2-fold higher in metronidazole-resistant strains and in strains resistant to at least one antibiotic compared with the remaining strains. Briefly, linezolid was less active against H. pylori compared with clarithromycin and levofloxacin, and linezolid resistance was linked to resistance to metronidazole as well as to resistance to at least one antibiotic. However, linezolid activity against some strains with double/multidrug resistance may render the agent appropriate to treat some associated H. pylori infections following in vitro susceptibility testing of the strains. Clinical trials are required to confirm this suggestion.

  8. Probiotic lactobacilli and bifidobacteria in a fermented milk product with added fruit preparation reduce antibiotic associated diarrhea and Helicobacter pylori activity.

    Science.gov (United States)

    de Vrese, Michael; Kristen, Holger; Rautenberg, Peter; Laue, Christiane; Schrezenmeir, Jürgen

    2011-11-01

    To investigate matrix-specifity of probiotic effects and particularly of the reduction of antibiotics-associated diarrhea, a controlled, randomized, double-blind study was performed, in which 88 Helicobacter pylori-infected but otherwise healthy subjects were given for eight weeks either a) a probiotic fruit yoghurt "mild" containing Lactobacillus acidophilus LA-5 plus Bifidobacterium lactis BB-12, n = 30), b) the same product but pasteurized after fermentation (n = 29) or c) milk acidified with lactic acid (control, n = 29). During week five, a Helicobacter eradication therapy was performed. Helicobacter activity was measured via 13C-2-urea breath tests and antibiotic-associated diarrhoea and other gastrointestinal complaints were recorded by validated questionnaires. In intervention group a, b and c the mean number of days with diarrhoea was 4, 10 and 10 (Pantibiotics treatment was -1·4 ± 1·1, -1·2 ± 1·1, 2·6 ± 1·1 points/four weeks (Pprobiotic bacteria but (rather) to components of acidified milk (most probably lactic acid). Fruit-yogurt-like fermented milk products with living probiotic bacteria significantly shorten the duration of antibiotics-associated diarrhoea and improve gastrointestinal complaints. Fruit yogurt-like fermented milk is a matrix suitable for probiotic bacteria.

  9. Infection with Helicobacter pylori is associated with protection against tuberculosis.

    Directory of Open Access Journals (Sweden)

    Sharon Perry

    Full Text Available BACKGROUND: Helicobacter pylori, a lifelong and typically asymptomatic infection of the stomach, profoundly alters gastric immune responses, and may benefit the host in protection against other pathogens. We explored the hypothesis that H. pylori contributes to the control of infection with Mycobacterium tuberculosis. METHODOLOGY/PRINCIPAL FINDINGS: We first examined M. tuberculosis-specific IFN-gamma and H. pylori antibody responses in 339 healthy Northern Californians undergoing routine tuberculin skin testing. Of 97 subjects (29% meeting criteria for latent tuberculosis (TB infection (LTBI, 45 (46% were H. pylori seropositive. Subjects with LTBI who were H. pylori-seropositive had 1.5-fold higher TB antigen-induced IFN-gamma responses (p = 0.04, ANOVA, and a more Th-1 like cytokine profile in peripheral blood mononuclear cells, compared to those who were H. pylori seronegative. To explore an association between H. pylori infection and clinical outcome of TB exposure, we evaluated H. pylori seroprevalence in baseline samples from two high risk TB case-contact cohorts, and from cynomolgus macaques experimentally challenged with M. tuberculosis. Compared to 513 household contacts who did not progress to active disease during a median 24 months follow-up, 120 prevalent TB cases were significantly less likely to be H. pylori infected (AOR: 0.55, 95% CI 0.0.36-0.83, p = 0.005, though seroprevalence was not significantly different from non-progressors in 37 incident TB cases (AOR: 1.35 [95% CI 0.63-2.9] p = 0.44. Cynomolgus macaques with natural H. pylori infection were significantly less likely to progress to TB 6 to 8 months after M. tuberculosis challenge (RR: 0.31 [95% CI 0.12-0.80], p = 0.04. CONCLUSIONS/SIGNIFICANCE: H. pylori infection may induce bystander effects that modify the risk of active TB in humans and non-human primates. That immunity to TB may be enhanced by exposure to other microbial agents may have important implications for

  10. Helicobacter pylori and Hepatitis C virus coinfection in Egyptian patients

    Directory of Open Access Journals (Sweden)

    El-Masry Samir

    2010-01-01

    Full Text Available Introduction: Chronic hepatitis C virus (HCV infection is a leading cause of end-stage liver disease worldwide. It has been shown that Helicobacter pylori (H. pylori plays an important role in chronic gastritis, peptic ulcer disease and gastric malignancies, and its eradication has been advocated. The association between H. pylori infection and liver cirrhosis in patients with hepatitis C virus has been documented in different parts of the world; nevertheless, no conclusive data is available in Egypt. Materials and Methods: In the present study, the status of H. pylori infection was sought in 90 patients with chronic HCV infection and in 66 HCV-free healthy controls. Results: The study showed that the H. pylori positivity was increased significantly (P = 0.03 in the HCV-infected patients when compared to that in healthy controls, where H. pylori infection was found in 50 (55.6% out of 90 of the HCV-infected patients versus 26 (39.4% out of 66 of the healthy controls. In HCV-infected patients, the prevalence of H. pylori infection was increased significantly (P = 0.04 from chronic active hepatitis to cirrhosis. H. pylori infection was present in 6/18 (33.3%, 10/21 (47.6%, 16/27 (59.3%, 18/24 (75.0% patients with chronic active hepatitis, Child-Pugh score A, Child-Pugh score B and Child-Pugh score C, respectively. More importantly, the prevalence of H. pylori infection in HCV-infected patients was increased very significantly (P = 0.003 with increasing Meld (model for end-stage liver disease score. The prevalence of H. pylori was documented in 9/28 (32.1% patients with Meld score ≤10 and in 41/62 (66.1% patients with Meld score> 10. Conclusion: It may be stated that our results collectively reflect a remarkable increase in H. pylori prevalence with advancing hepatic lesions, and the eradication treatment may prove beneficial in those patients with chronic hepatitis C.

  11. Biopatologia do Helicobacter pylori

    Directory of Open Access Journals (Sweden)

    Ladeira Marcelo Sady Plácido

    2003-01-01

    Full Text Available A infecção pelo Helicobacter pylori (H. pylori induz inflamação persistente na mucosa gástrica com diferentes lesões orgânicas em humanos, tais como gastrite crônica, úlcera péptica e câncer gástrico. Os fatores determinantes desses diferentes resultados incluem a intensidade e a distribuição da inflamação induzida pelo H. pylori na mucosa gástrica. Evidências recentes demonstram que cepas do H. pylori apresentam diversidade genotípica, cujos produtos acionam o processo inflamatório por meio de mediadores e citocinas, que podem levar a diferentes graus de resposta inflamatória do hospedeiro, resultando em diferentes destinos patológicos. Cepas H. pylori com a ilha de patogenicidade cag induzem resposta inflamatória mais grave, através da ativação da transcrição de genes, aumentando o risco para desenvolvimento de úlcera péptica e câncer gástrico. O estresse oxidativo e nitrosativo induzido pela inflamação desempenha importante papel na carcinogênese gástrica como mediador da formação ou ativação de cancerígenos, danos no DNA, bem como de alterações da proliferação celular e da apoptose.

  12. Helicobacter pylori eradication using tetracycline and furazolidone versus amoxicillin and azithromycin in lansoprazole based triple therapy: an open randomized clinical trial Erradicação de Helicobacter pylori com o uso de tetraciclina e furazolidona versus amoxicilina e azitromicina em terapia tríplice com lansoprazol

    Directory of Open Access Journals (Sweden)

    Laura Cidrão Frota

    2005-06-01

    Full Text Available BACKGROUND: Optimal anti-Helicobacter pylori treatment has not yet been established. AIM: To evaluate H. pylori eradication using tetracycline and furazolidone versus amoxicillin and azithromycin in lansoprazole based triple therapy in northeastern of Brazil. PATIENTS AND METHODS: One hundred and four patients with H. pylori infection, as determined by rapid urease testing and histology, were randomly assigned to receive either: lansoprazole (30 mg q.d., tetracycline (500 mg q.i.d., and furazolidone (200 mg t.i.d. for 7 days (LTF; n = 52; or lansoprazole (30 mg b.i.d. and amoxicillin (1 g b.i.d. for 1 week, plus azithromycin (500 mg q.d. for the first 3 days (LAAz; n = 52. H. pylori eradication was assessed 3 months following completion of therapy by means of rapid urease testing, histology and a 14C-urea breath test. RESULTS: H. pylori eradication was achieved in 46 of 52 (88.4%, 95% CI: 77.5%-95.1% patients in LTF group and in 14 of 52 (26.9%, 95% CI: 16.2%-40,1% patients in LAAz group. On a per-protocol analysis, eradication rates were 91.8% (95% CI: 81.4%-97.3% and 28.5% (95% CI: 17.2%-42.3%, respectively in LTF and LAAz groups. CONCLUSION: The LAAz regimen yielded unacceptably low eradication rates. On the other hand, the LTF scheme represents a suitable alternative for H. pylori eradication.RACIONAL: Ainda não está estabelecida a melhor terapêutica anti-H. pylori. OBJETIVO: Avaliar a erradicação de H.pylori usando tetraciclina e furazolidona versus amoxicilina e azitromicina em terapia tríplice com lansoprazol no nordeste do Brasil. PACIENTES E MÉTODOS: Cento e quatro pacientes infectados por H. pylori, diagnosticado através do teste rápido da urease e histologia, foram selecionados aleatoriamente para receber: lansoprazol (30 mg q.d., tetraciclina (500 mg q.i.d., furazolidona (200 mg t.i.d. por 7 dias (LTF; n = 52; ou lansoprazol (30 mg b.i.d. e amoxicilina (1 g b.i.d. por 1 semana, mais azitromicina (500 mg q.d. nos primeiros 3

  13. Helicobacter pylori environmental interactions: effect of acidic conditions on H. pylori-induced gastric mucosal interleukin-8 production

    Science.gov (United States)

    Choi, Il Ju; Fujimoto, Saori; Yamauchi, Kazuyoshi; Graham, David Y.; Yamaoka, Yoshio

    2010-01-01

    Summary To explore the interactions between the host, environment and bacterium responsible for the different manifestations of Helicobacter pylori infection, we examined the effect of acidic conditions on H. pylori-induced interleukin (IL)-8 expression. AGS gastric epithelial cells were exposed to acidic pH and infected with H. pylori [wild-type strain, its isogenic cag pathogenicity island (PAI) mutant or its oipA mutant]. Exposure of AGS cells to acidic pH alone did not enhance IL-8 production. However, following exposure to acidic conditions, H. pylori infection resulted in marked enhancement of IL-8 production which was independent of the presence of the cag PAI and OipA, indicating that H. pylori and acidic conditions act synergistically to induce gastric mucosal IL-8 production. In neutral pH environments H. pylori-induced IL-8 induction involved the NF-κB pathways, the extracellular signal-regulated kinase (ERK)→ c-Fos/c-Jun→activating protein (AP-1) pathways, JNK→c-Jun→AP-1 pathways and the p38 pathways. At acidic pH H. pylori-induced augmentation of IL-8 production involved markedly upregulated the NF-κB pathways and the ERK→c-Fos→AP-1 pathways. In contrast, activation of the JNK→c-Jun→AP-1 pathways and p38 pathways were pH independent. These results might explain the clinical studies in which patients with duodenal ulcers had higher levels of IL-8 in the antral gastric mucosa than patients with simple H. pylori gastritis. PMID:17517062

  14. Synthesis and bioevaluation of novel 3,4,5-trimethoxybenzylbenzimidazole derivatives that inhibit Helicobacter pylori-induced pathogenesis in human gastric epithelial cells.

    Science.gov (United States)

    Chang, Chih-Shiang; Liu, Ju-Fang; Lin, Hwai-Jeng; Lin, Chia-Der; Tang, Chih-Hsin; Lu, Dah-Yuu; Sing, Yu-Ting; Chen, Li-Yu; Kao, Min-Chuan; Kuo, Sheng-Chu; Lai, Chih-Ho

    2012-02-01

    Helicobacter pylori infection is associated with gastritis, peptic ulcer, and even gastric malignancy. H. pylori's antibiotic resistance is the major obstacle preventing its eradication. A series of 3,4,5-trimethoxybenzylbenzimidazole derivatives were synthesized and evaluated for their anti-H. pylori activity. The compound, 2-fluorophenyl-5-methyl-1-(3,4,5-trimethoxybenzyl)benzimidazole (FMTMB), was determined as the most potent in the inhibition of H. pylori growth and pathogenesis of host cells. An in vitro H. pylori infection model revealed that FMTMB inhibited H. pylori adhesion and invasion of gastric epithelial cells. Results from this study provide evidence that FMTMB is a potent therapeutic agent that exhibits both anti-H. pylori growth properties and anti-H. pylori-induced pathogenesis of cells.

  15. Infecciones por helicobacter pylori Helicobacter pylori infections

    Directory of Open Access Journals (Sweden)

    Liliam Alvarez Gil

    1994-02-01

    Full Text Available

    Se revisan los conocimientos sobre el papel de Helicobacter pylori en varias enfermedades gastroduodenales como la gastritis crónica (GC, úlcera gástrica (UG, úlcera duodenal (UD y dispepsia no ulcerosa (DNU. La revisión abarca aspectos históricos, microbiológicos, clínicos, epidemiológicos, diagnósticos de laboratorio, terapéuticos y de patogénesis.

    The current knowledge of the role of Helicobacter Pylori in several gastroduodenal  diseases is reviewed. It includes chronic gastritis, gastric and duodenal ulcers and nonulcerous dyspepsia. The following aspects are treated in this paper: history, microbiology. Clinical presentation, epidemiology, laboratory diagnosis, therapy and pathogenesis.

  16. Exopolysaccharide production by Helicobacter pylori

    OpenAIRE

    2006-01-01

    Helicobacter pylori is a widespread Gram-negative bacterium that infects the stomach of humans leading to the onset of several gastric disorders, such as, gastritis, gastric ulcers, and cancers. Studies from developing countries with low socioeconomic status and poor management of the drinking water suggest that it may serve as an environmental reservoir of H. pylori and therefore contribute to human infection. It has been reported that H. pylori has the ability to form microbi...

  17. Copper promotes TFF1-mediated Helicobacter pylori colonization.

    Directory of Open Access Journals (Sweden)

    Sandro Montefusco

    Full Text Available The trefoil peptides (TFF1, TFF2 and TFF3 are a family of small highly conserved proteins that play an essential role in epithelial regeneration within the gastrointestinal tract, where they are mainly expressed. TFF1 expression is strongly induced after mucosal injury and it has been proposed that tff1 functions as a gastric tumor suppressor gene. Several studies confirm that tff1 expression is frequently lost in gastric cancer because of deletions, mutations or methylation of the tff1 promoter. Infection by Helicobacter pylori (H. pylori results in chronic gastritis and it can lead to the development of gastric or duodenal ulcers. Moreover, it is known that there is a strong link to the development of gastric cancer. It has been shown that H. pylori interacts with the dimeric form of TFF1 and that the rough form of lipopolysaccharide mediates this interaction. We have previously reported that the carboxy-terminus of TFF1 is able to specifically bind copper ions (Cu and that Cu binding favours the homodimerization of the peptide, thus enhancing its motogenic activity. Here, we report that the Cu-TFF1 cuprocomplex promotes adherence of H. pylori to epithelial cells. Adherence of H. pylori to gastric adenocarcinoma cells, AGS AC1 cells, induced to hyper-express TFF1 was enhanced compared to noninduced cells. Copper further promoted this interaction. A H. pylori mutant unable to bind TFF1 did not show enhanced infection of induced cells. Cu treatment induced a thickening of the mucus layer produced by the colorectal adenocarcinoma mucus secreting, goblet cells, HT29-E12 and promoted H. pylori colonisation. Finally, SPR analysis shows that the C-terminus of TFF1, involved in the binding of copper, is also able to selectively bind H. pylori RF-LPS.

  18. "Helicobacter Pylori Attachment To 7 Mamalian Cell Lines "

    Directory of Open Access Journals (Sweden)

    N. Rahimi-Fard

    2006-06-01

    Full Text Available Background and Aim: Helicobacter pylori is the etiologic agent of chronic –active gastritis, gastroduodenal ulcers in humans, and a co-factor in the occurrence of gastric cancer and mucosa-associated lymphoid tumors, Adhesion of H.pylori to the gastric mucosa is a critical and also initial step in the pathogenesis of the disease. Bacterial adhesion inhibitory agents provide a novel pharmacologic approach to the management of infectious diseases. Materials and Methods: 22 H. pylori strains, isolated from the antral biopsies of 49 patients with dyspepsia, gastritis, gastric ulcer, duodenal ulcer,…were assayed by ELISA (UPRto investigate the diversity of attachment to 7 mamalian cell lines. Results: The concentration of H.pylori and cell suspention ,the condition and temperature, can alter the attachment rate.Best bacterial concentration was equal to 1 Mc farland,and for cell suspension was 5*10 cells/ml.90 minutes in 37C incubation period result in maximum attachment. H.pylori can attach to all 7 cell lines, there are no significant differences between 22 H.pylori strains in attachment to cells. The attachment pattern of H.pylori to the cells showed significant reduction respectly from HepII, HeLa, SW742, AGS,HT29/219, HT29 to Caco-2.Maximum attachment were seen to HepII, HeLa and SW742 cells, and among these HepII was the best cells for this purpose. Conclusion: Our studies suggest that Hep II, HeLa and SW742 cells could serve as a suitable in-vitro model for the study of H.pylori adhesions, attachment, inhibition of attachment and detachment assays and among these Hep II cell is prefer recommended.

  19. Helicobacter pylori and pancreatic diseases

    Institute of Scientific and Technical Information of China (English)

    Milutin; Bulajic; Nikola; Panic; Johannes; Matthias; L?hr

    2014-01-01

    A possible role for Helicobacter pylori(H. pylori) infec-tion in pancreatic diseases remains controversial. H. pylori infection with antral predomination leading to an increase in pancreatic bicarbonate output and induc-ing ductal epithelial cell proliferation could contribute to the development of pancreatic cancer via complex interactions with the ABO genotype, dietary and smok-ing habits and N-nitrosamine exposure of the host. Although the individual study data available so far is inconsistent, several meta-analyses have reported an increased risk for pancreatic cancer among H. pylori seropositive individuals. It has been suggested that H. pylori causes autoimmune pancreatitis due to molecu-lar mimicry between H. pylori a-carbonic anhydrase(a-CA) and human CA type Ⅱ, and between H. pylori plasminogen-binding protein and human ubiquitin-protein ligase E3 component n-recognin 2, enzymes that are highly expressed in the pancreatic ductal andacinar cells, respectively. Future studies involving large numbers of cases are needed in order to examine the role of H. pylori in autoimmune pancreatitis more fully. Considering the worldwide pancreatic cancer burden, as well as the association between autoimmune pan-creatitis and other autoimmune conditions, a complete elucidation of the role played by H. pylori in the gen-esis of such conditions could have a substantial impact on healthcare.

  20. Molecular characterization of Helicobacter pylori VacA induction of IL-8 in U937 cells reveals a prominent role for p38MAPK in activating transcription factor-2, cAMP response element binding protein, and NF-kappaB activation

    DEFF Research Database (Denmark)

    Hisatsune, Junzo; Nakayama, Masaaki; Isomoto, Hajime;

    2008-01-01

    Helicobacter pylori VacA induces multiple effects on susceptible cells, including vacuolation, mitochondrial damage, inhibition of cell growth, and enhanced cyclooxygenase-2 expression. To assess the ability of H. pylori to modulate the production of inflammatory mediators, we examined the mechan......Helicobacter pylori VacA induces multiple effects on susceptible cells, including vacuolation, mitochondrial damage, inhibition of cell growth, and enhanced cyclooxygenase-2 expression. To assess the ability of H. pylori to modulate the production of inflammatory mediators, we examined...... the mechanisms by which VacA enhanced IL-8 production by promonocytic U937 cells, which demonstrated the greatest VacA-induced IL-8 release of the cells tested. Inhibitors of p38 MAPK (SB203580), ERK1/2 (PD98059), IkappaBalpha ((E)-3-(4-methylphenylsulfonyl)-2-propenenitrile), Ca(2+) entry (SKF96365......+) in mediating activation of MAPK and the canonical NF-kappaB pathway. VacA stimulated translocation of NF-kappaBp65 to the nucleus, consistent with enhancement of IL-8 expression by activation of the NF-kappaB pathway. In addition, small interfering RNA of activating transcription factor (ATF)-2 or CREB, which...

  1. Statin Decreases Helicobacter pylori Burden in Macrophages by Promoting Autophagy

    Science.gov (United States)

    Liao, Wei-Chih; Huang, Mei-Zi; Wang, Michelle Lily; Lin, Chun-Jung; Lu, Tzu-Li; Lo, Horng-Ren; Pan, Yi-Jiun; Sun, Yu-Chen; Kao, Min-Chuan; Lim, Hui-Jing; Lai, Chih-Ho

    2017-01-01

    Statins, 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors, have been found to provide protective effects against several bacterial infectious diseases. Although the use of statins has been shown to enhance antimicrobial treated Helicobacter pylori eradication and reduce H. pylori-mediated inflammation, the mechanisms underlying these effects remain unclear. In this study, in vitro and ex vivo macrophage models were established to investigate the molecular pathways involved in statin-mediated inhibition of H. pylori-induced inflammation. Our study showed that statin treatment resulted in a dose-dependent decrease in intracellular H. pylori burden in both RAW264.7 macrophage cells and murine peritoneal exudate macrophages (PEMs). Furthermore, statin yielded enhanced early endosome maturation and subsequent activation of the autophagy pathway, which promotes lysosomal fusion resulting in degradation of sequestered bacteria, and in turn attenuates interleukin (IL)-1β production. These results indicate that statin not only reduces cellular cholesterol but also decreases the H. pylori burden in macrophages by promoting autophagy, consequently alleviating H. pylori-induced inflammation. PMID:28144585

  2. Analysis of the urinary peptidome associated with Helicobacter pylori infection

    Institute of Scientific and Technical Information of China (English)

    Di Xiao; Fan-Liang Meng; Li-Hua He; Yi-Xin Gu; Jian-Zhong Zhang

    2011-01-01

    AIM: To investigate the relationship between urinary peptide changes and Helicobacter pylori (H. pylori ) infection using urinary peptidome profiling.METHODS: The study was performed in volunteers (n= 137) who gave informed consent. Urinary peptides were enriched by magnetic beads based weak cation exchange chromatography and spectrums acquired by matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry (MS). ClinProTools bioinformatics software was used for statistical analysis and the recognition of peptide patterns. The marker peptides were identified by LTQ Obitrap XL tandem MS.RESULTS: Approximately 50 proteins or peptides which loaded onto the magnetic beads were detected by MALDI-TOF MS. By optimizing the parameters of the model,the Genetic Algorithm model had good recognition capability (97%) and positive predictive value (94%).Based on the model, 2 markers with molecular masses of 6788 and 1912 Da were found that differentiated between H. pylori positive and negative volunteers.The m/z 1912 sequence was parsed as SKQFTSSTSYNRGDSTF.The peptide was identified as isoform 1 of the fibrinogen α chain precursor, whose concentration in urine was markedly higher in H. pylori infected volunteers than in H. pylori non-infected ones.CONCLUSION: The appearance of urinary fibrinogen degradation products is caused by an active H. pylori -induced process.

  3. Helicobacter pylori infection induces genetic instability of nuclear and mitochondrial DNA in gastric cells

    DEFF Research Database (Denmark)

    Machado, Ana Manuel Dantas; Figueiredo, Ceu; Touati, Eliette

    2009-01-01

    cells and chronic gastritis tissue were determined by PCR, single-stranded conformation polymorphism, and sequencing. H. pylori vacA and cagA genotyping was determined by multiplex PCR and reverse hybridization. RESULTS: Following H. pylori infection, the activity and expression of base excision repair...

  4. NikR mediates nickel-responsive transcriptional induction of urease expression in Helicobacter pylori.

    Science.gov (United States)

    van Vliet, Arnoud H M; Poppelaars, Sophie W; Davies, Beverly J; Stoof, Jeroen; Bereswill, Stefan; Kist, Manfred; Penn, Charles W; Kuipers, Ernst J; Kusters, Johannes G

    2002-06-01

    The important human pathogen Helicobacter pylori requires the abundant expression and activity of its urease enzyme for colonization of the gastric mucosa. The transcription, expression, and activity of H. pylori urease were previously demonstrated to be induced by nickel supplementation of growth media. Here it is demonstrated that the HP1338 protein, an ortholog of the Escherichia coli nickel regulatory protein NikR, mediates nickel-responsive induction of urease expression in H. pylori. Mutation of the HP1338 gene (nikR) of H. pylori strain 26695 resulted in significant growth inhibition of the nikR mutant in the presence of supplementation with NiCl(2) at > or =100 microM, whereas the wild-type strain tolerated more than 10-fold-higher levels of NiCl(2). Mutation of nikR did not affect urease subunit expression or urease enzyme activity in unsupplemented growth media. However, the nickel-induced increase in urease subunit expression and urease enzyme activity observed in wild-type H. pylori was absent in the H. pylori nikR mutant. A similar lack of nickel responsiveness was observed upon removal of a 19-bp palindromic sequence in the ureA promoter, as demonstrated by using a genomic ureA::lacZ reporter gene fusion. In conclusion, the H. pylori NikR protein and a 19-bp operator sequence in the ureA promoter are both essential for nickel-responsive induction of urease expression in H. pylori.

  5. Increased Cell Proliferation in Chronic Helicobacter pylori Positive Gastritis and Gastric Carcinoma – Correlation between Immuno-Histochemistry and Tv Image Cytometry

    Directory of Open Access Journals (Sweden)

    Erika Szaleczky

    2000-01-01

    Full Text Available Backgound: Epithelial cell proliferation activity has been reported both to be unaltered and increased in Helicobacter pylori (H. pylori associated chronic gastritis. The proliferation rate decreased following H. pylori eradication, but results are controversial whether this change is dependent on the success of eradication. We compared the cell proliferation activity of H. pylori positive and negative gastric epithelial biopsies in chronic gastritis with and without intestinal metaplasia (IM and gastric cancer by the expression of proliferation cell nuclear antigen (PCNA and Tv image cytometry, and assessed the effect of H. pylori eradication on the cell proliferation rate in the gastric epithelium.

  6. Inactivation of Helicobacter pylori by Chloramination

    Science.gov (United States)

    Three strains of Helicobacter pylori (H. pylori) were studied to determine their resistance to chloramination. H. pylori is an organism listed on the U.S. Environmental Protection Agency’s (USEPA) Contaminant Control List (CCL). H. pylori was exposed to 2ppm of pre-formed monoc...

  7. Halitosis and Helicobacter pylori infection.

    Science.gov (United States)

    Tangerman, A; Winkel, E G; de Laat, L; van Oijen, A H; de Boer, W A

    2012-03-01

    There is disagreement about a possible relationship between Helicobacter pylori (H. pylori) infection and objective halitosis, as established by volatile sulfur compounds (VSCs) in the breath. Many studies related to H. pylori used self-reported halitosis, a subjective and unreliable method to detect halitosis. In this study a possible relation between H. pylori and halitosis was evaluated, using an objective method (gas chromatography, GC) to detect the VSCs, responsible for the halitosis. The levels of the VSCs hydrogen sulfide (H(2)S), methyl mercaptan (MM) and dimethyl sulfide (DMS) were measured in mouth breath and in stomach air of 11 H. pylori positive patients and of 38 H. pylori negative patients, all with gastric pathology. Halitosis was also established by organoleptic scoring (OLS) of mouth-breath. The levels of H(2)S, MM and DMS in the mouth-breath and stomach air of the H. pylori positive patients did not differ significantly from those of the H. pylori negative patients. OLS of the mouth-breath resulted in 9 patients with halitosis, 1 out of the H. pylori positive group and 8 out of the H. pylori negative group, which is not statistically different. The concentrations of the VSCs in stomach air were in nearly all cases below the thresholds of objectionability of the various VSCs, indicating that halitosis does not originate in the stomach. The patients with gastric pathology were also compared with control patients without gastric pathology and with normal volunteers. No significant differences in VSCs in mouth breath were observed between these groups. Thus, in this study no association between halitosis and H. pylori infection was found. Halitosis, as established by GC and OLS, nearly always originates within the oral cavity and seldom or never within the stomach.

  8. Helicobacter pylori Infection in Association with Cell Proliferation,Apoptosis and Prostaglandin E2 Levels

    Institute of Scientific and Technical Information of China (English)

    PAN Kai-feng; ZHANG Yang; ZHANG Lian; MA Jun-ling; FENG Guo-shuang; ZHOU Tong; YOU Wei-cheng

    2007-01-01

    Objective: To evaluate the relationship between H. pylori infection with cell proliferation, apoptosis and PGE2 levels. Methods: A population-based study was conducted in Linqu, a high-risk area of gastric cancer in China. A total of 1523 subjects, aged 35-64, participating in a gastric cancer screening survey were investigated. H. pylori status were determined by 13C-urea breath test, expressions of Ki-67 were assessed by immunohistochemistry, apoptotic cells were detected by terminal deoxynucleotide transferase mediated dUTP nick end-labeling (TUNEL) method, and PGE2 levels were measured by enzyme immunoassay. Results: H. pylori infection was positively associated with cell proliferation activity. The mean and median percentage of Ki-67 labeling index (LI) in subjects with H. pylori positive were 14.1±10.3 and 12.0, significantly higher than those with H. pylori negative (-x±s: 8.4±7.0;median: 5.8;P<0.0001). Moreover, the prevalence rates of H. pylori infection showed a tendency to increase according to severity score of cell apoptosis (Ptrend <0.0001), from score 0 to 3, the percentage of H. pylori positivity increased from 67.5% to 96.7%. Furthermore, The mean and median of PGE2 concentration were 628.84±726.40 pg/mL and 411.33 pg/mL among subjects with H. pylori positive compared with 658.19±575.91pg/mL and 455.97 pg/mL among those with H. pylori negative (P=0.209). Conclusion: H. pylori infection was positively associated with increased cell proliferation and apoptosis activity, suggesting that H. pylori infection plays an important role in the gastric epithelial cell malignant transformation.

  9. Soluble adhesion molecules ICAM-1, VCAM-1, P-selectin in children with Helicobacter pylori infection

    Institute of Scientific and Technical Information of China (English)

    Elzbieta Maciorkowska; Maciej Kaczmarski; Anatol Panasiuk; Katarzyna Kondej-Muszynska; Andrzej Kemonai

    2005-01-01

    AIM: To assess the sICAM-1, sVCAM-1, and sP-selectin levels in children withHelicobacter pylori(H pylori)infection and to evaluate their significance for the morphological changes found in gastric mucosa.METHODS: The study included 106 children: 59children (55.7%) with chronic gastritis and positive IgG against H pylori, 29 children (27.3%) after previous H pylori infection without the bacterium colonization but with positive IgG against H pylori, and 18 children (17%) with functional disorders of the gastrointestinal system but with normal IgG against H pylori. Endoscopic and histopathological evaluation of gastric mucosa was performed based on the Sydney System classification.The evaluation of sP-selectin, sIC AM-1, sVCAM-1 levels in the sera of children was carried out using ELISA test.RESULTS: The assessment of gastritis activity degrees indicated statistically significant values in the antrum and corpus (P<0.001) of children examined. Serum sVCAM-1 levels were higher in group with gastritis due to H pylori infection than in group without infection and differed statistically (P<0.05). Serum sVCAM-1 levels proved to be the highest among other adhesive molecules in infected children and decreased after eradication of H pylori. Serum sICAM-1 levels were similar in all examined groups. Serum sP-selectin levels were similar in children with and without H pylori infection.CONCLUSION: Assessment of adhesive molecules (sPselectin, sICAM-1, sVCAM-1) in the sera of children with active H pylori infection can show the participation of sVCAM-1 in the pathogenesis of gastric mucosal inflammation, sP-selectin and sICAM-1 concentrations in the sera of children with H pylori infection after eradication cannot reveal any significant differences as compared to healthy children.

  10. Low prevalence of H. pylori Infection in HIV-Positive Patients in the Northeast of Brazil

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    Silva Cícero IS

    2011-02-01

    Full Text Available Abstract Background This study conducted in Northeastern Brazil, evaluated the prevalence of H. pylori infection and the presence of gastritis in HIV-infected patients. Methods There were included 113 HIV-positive and 141 age-matched HIV-negative patients, who underwent upper gastrointestinal endoscopy for dyspeptic symptoms. H. pylori status was evaluated by urease test and histology. Results The prevalence of H. pylori infection was significantly lower (p H. pylori status and gender, age, HIV viral load, antiretroviral therapy and the use of antibiotics. A lower prevalence of H. pylori was observed among patients with T CD4 cell count below 200/mm3; however, it was not significant. Chronic active antral gastritis was observed in 87.6% of the HIV-infected patients and in 780.4% of the control group (p = 0.11. H. pylori infection was significantly associated with chronic active gastritis in the antrum in both groups, but it was not associated with corpus chronic active gastritis in the HIV-infected patients. Conclusion We demonstrated that the prevalence of H. pylori was significantly lower in HIV-positive patients compared with HIV-negative ones. However, corpus gastritis was frequently observed in the HIV-positive patients, pointing to different mechanisms than H. pylori infection in the genesis of the lesion.

  11. Helicobacter pylori infection

    Institute of Scientific and Technical Information of China (English)

    Yvan Vandenplas

    2000-01-01

    @@ IS THERE ANYTHING NEW? Helicobacter pylori has been for many years a forgotten bacterium, since the first report on this spiral organism dated from the 19th century[1]. As early as in 1906, an association between a spiral organism and gastric carcinoma was suggested[2].Doenges reported in 1938 that on autopsy not less than 40% of human stomachs were found to be invaded by spiral organisms[3].

  12. Nitroimidazole resistance in Helicobacter pylori

    NARCIS (Netherlands)

    Van der Wouden, EJ; Thijs, JC; Van Zwet, AA; Kleibeuker, JH

    2000-01-01

    The efficacy of a nitroimidazole-containing regimen for the treatment of Helicobacter pylori infection is decreased by nitroimidazole resistance. Nitroimidazoles are metabolized by H. pylori by several nitro-reductases of which an oxygen-insensitive NADPH nitroreductase encoded by the rdxA gene is t

  13. Helicobacter pylori and Nonmalignant Diseases.

    Science.gov (United States)

    Potamitis, Georgios S; Axon, Anthony T R

    2015-09-01

    Helicobacter pylori is responsible for most peptic ulcers, plays a role in functional dyspepsia and is thought by some to influence the course of gastroesophageal reflux disease. This article addresses recent studies that have been published in connection with these diseases. H. pylori-associated peptic ulcer is declining in prevalence but the incidence of perforation and bleeding remains high especially in the elderly. All H. pylori associated peptic ulcers should be treated by eradication of the infection. Dyspepsia is a common disorder that affects up to 25% of the population. About 8% of cases that are infected with H. pylori will respond to treatment of the infection. The association between H. pylori and gastroesophageal reflux disease continues to be debated, a number of studies have shown that there is a negative association between H. pylori infection and Gastroesophageal reflux disease but treatment of H. pylori has not been shown to induce reflux or to affect the response to medication. Gastric atrophy is known to extend when acid suppression is used in infected patients implying that H. pylori treatment should be used in infected patients who are to undergo long-term Proton Pump Inhibitor therapy.

  14. Helicobacter pylori infection in pediatrics

    DEFF Research Database (Denmark)

    Wewer, Anne Vibeke; Kalach, Nicolas

    2003-01-01

    in gastric manifestations is the subject of conflicting reports. Extra-digestive manifestations are also reported in the course of this infection. The treatment of H. pylori infection is influenced by resistance of the bacteria to the antibiotics used. We suggest that eradication of H. pylori should take...

  15. Epidemiology of Helicobacter pylori infection.

    Science.gov (United States)

    Eusebi, Leonardo H; Zagari, Rocco M; Bazzoli, Franco

    2014-09-01

    Medline and PubMed databases were searched on epidemiology of Helicobacter pylori for the period of April 2013-March 2014. Several studies have shown that the prevalence of H. pylori is still high in most countries. In north European and North American populations, about one-third of adults are still infected, whereas in south and east Europe, South America, and Asia, the prevalence of H. pylori is often higher than 50%. H. pylori remains highly prevalent in immigrants coming from countries with high prevalence of H. pylori. However, the lower prevalence of infection in the younger generations suggests a further decline of H. pylori prevalence in the coming decades. Low socioeconomic conditions in childhood are confirmed to be the most important risk factors for H. pylori infection. Although the way the infection is transmitted is still unclear, interpersonal transmission appears to be the main route. Finally, H. pylori recurrence after successful eradication can still occur, but seems to be an infrequent event.

  16. Pathogenesis of Helicobacter pylori infection

    NARCIS (Netherlands)

    J.G. Kusters (Johannes); A.H.M. van Vliet (Arnoud); E.J. Kuipers (Ernst)

    2006-01-01

    textabstractHelicobacter pylori is the first formally recognized bacterial carcinogen and is one of the most successful human pathogens, as over half of the world's population is colonized with this gram-negative bacterium. Unless treated, colonization usually persists lifelong. H. pylori infection

  17. Helicobacter pylori in gastroduodenal perforation

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    Bharat B Dogra

    2014-01-01

    Full Text Available Background:peptic ulcers were earlier believed to be caused by dietary factors, gastric acid, and stress. However, in 1983, Warren and Marshall identified the correlation between Helicobacter pylori (H. pylori and peptic ulcers. It is now well established that most of the peptic ulcers occur as a result of H. pylori infection. But the co-relation between perforated peptic ulcer and H. pylori infection is not yet fully established. Aims and objectives : to study the prevalence of H. pylori infection in patients with perforated peptic ulcer. Materials and methods: this was a prospective study carried out in all cases of perforated peptic ulcer reporting in surgical wards of a medical college during 2008-2010. A total of 50 cases, presenting as acute perforation of duodenum and stomach during this period, formed the study group. After resuscitation, all the cases were subjected to emergency exploratory laparotomy. The exact site of perforation was identified, biopsy was taken from the ulcer margin from 2-3 sites and the tissue was sent for H. pylori culture and histopathological examination. Simple closure of perforation, omentoplasty, thorough peritoneal lavage and drainage was carried out. Results: out of the 50 cases of perforated peptic ulcer, 38 happened to be males, and only 12 were females. The age of the patients ranged from 20 to 70 years. All the patients underwent only emergency laparotomy. As many as 46 cases (92% turned out to be positive for H. pylori and only four cases (8% were negative for this infection. Postoperatively, patients who were found to be positive for H. pylori were put on anti-H. pylori treatment. Conclusion: there was a high prevalence of H. pylori infection in patients with perforated gastroduodenal ulcers.

  18. Helicobacter pylori-induced sonic hedgehog expression is regulated by NFκB pathway activation: The use of a novel in vitro model to study epithelial response to infection

    OpenAIRE

    Schumacher, MA; R. Feng; Aihara, E; Engevik, AC; Montrose, MH; Ottemann, KM; Zavros, Y

    2015-01-01

    © 2014 John Wiley & Sons Ltd. Helicobacter pylori (H. pylori) infection leads to acute induction of Sonic Hedgehog (Shh) in the stomach that is associated with the initiation of gastritis. The mechanism by which H. pylori induces Shh is unknown. Shh is a target gene of transcription factor Nuclear Factor-κB (NFκB). We hypothesize that NFκB mediates H. pylori-induced Shh. Materials and Methods: To visualize Shh ligand expression in response to H. pylori infection in vivo, we used a mouse model...

  19. The short-term effects of Helicobacter pylori eradication on symptoms of functional dyspepsia

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    Ayla Tezer

    2010-09-01

    Full Text Available Objectives: Helicobacter pylori (H.pylori infection is major etiologic factor of chronic active gastritis and peptic ulcer disease. Functional dyspepsia (FD is defined as “persistent or recurrent abdominal pain or discomfort centered in the upper abdomen in patient who has no definite structural or biochemical explanation of their symptoms. It is uncertain whether treatment of H.pylori infection relieves symptoms in patients with FD. We searched short term effects of H.pylori eradication for symptoms in patients with FD.Material and method: We enrolled patients with dyspeptic symptoms which were diagnosed FD and satisfied en-rollment criteria of trial. Endoscopic biopsy was taken from each patient during upper gastrointestinal endoscopy. H.pylori infected patients were assigned to seven days of treatment with 30 mgr of lansoprozole twice daily, 1000 mg of amoksisilin twice daily, and 500 mg levofloxacin once daily. Patients were assessed whether treatment was suc-cessful or not by 14C urea breathe test after 6-8 week. Also pretreatment and post treatment symptom scores were questioned.Results: There were 99 female and 68 male patients. After treatment 114 patients (68% was negative for H. pylori, 53 patients (32% remained positive. Mean of age and proportion of sex was similar in H.pylori (+ and (- groups. While 111 (97.4% of H.pylori (- patients’ symptom scores decreased, 38 (71.7% of H.pylori (+ patients’ scores de-creased. There was significant differences between two groups (p=0.001.Conclusion: Eradication of H.pylori relieves the symptoms of functional dyspepsia. New trials for long term effect of H.pylori eradication on symptoms must be conducted in future.

  20. Molecular Dynamics Study of Helicobacter pylori Urease.

    Science.gov (United States)

    Minkara, Mona S; Ucisik, Melek N; Weaver, Michael N; Merz, Kenneth M

    2014-05-13

    Helicobacter pylori have been implicated in an array of gastrointestinal disorders including, but not limited to, gastric and duodenal ulcers and adenocarcinoma. This bacterium utilizes an enzyme, urease, to produce copious amounts of ammonia through urea hydrolysis in order to survive the harsh acidic conditions of the stomach. Molecular dynamics (MD) studies on the H. pylori urease enzyme have been employed in order to study structural features of this enzyme that may shed light on the hydrolysis mechanism. A total of 400 ns of MD simulation time were collected and analyzed in this study. A wide-open flap state previously observed in MD simulations on Klebsiella aerogenes [Roberts et al. J. Am. Chem. Soc.2012, 134, 9934] urease has been identified in the H. pylori enzyme that has yet to be experimentally observed. Critical distances between residues on the flap, contact points in the closed state, and the separation between the active site Ni(2+) ions and the critical histidine α322 residue were used to characterize flap motion. An additional flap in the active site was elaborated upon that we postulate may serve as an exit conduit for hydrolysis products. Finally we discuss the internal hollow cavity and present analysis of the distribution of sodium ions over the course of the simulation.

  1. Characterization of Patients with Helicobacter pylori-Negative Peptic Ulcers

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    Roberto Hernández Conde

    2013-10-01

    Full Text Available Background: the rate of Helicobacter pylori-negative ulcers is increasing. Treatment with nonsteroidal anti-inflammatory drugs and other ulcerogenic drugs plays a significant role.Objective: to characterize patients with Helicobacter pylori-negative peptic ulcer. Methods: a case series study of patients attended by the Gastroenterology Service of the Hermanos Ameijeiras Hospital was conducted in the year 2009. Demographic, epidemiological, clinical, endoscopic and histological variables were studied. Mean and standard deviation were analyzed; logistic regression, t-Student and Chi-square tests were used. Results: A total of 269 gastric ulcers, 239 duodenal ulcers and 41 combined were diagnosed; 115 cases were Helicobacter pylori-negative and 434 were positive. Nonsteroidal anti-inflammatory drugs were associated with 33,9 % of H. pylori-negative patients and 22.8% of the positive patients. Ulcerative syndrome occurred in 47 % and 45% in both groups. All H. pylori-negative duodenal ulcers were located in the duodenal bulb as well as 96, 6 % of the positive. The antrum was the most common location for gastric ulcerations (92.3% negative; 90.5% positive. Multiple ulcers predominated in the duodenum while double ulcers prevailed in the stomach, all negative for H.pylori. Antral gastritis predominated (73. 0 % H. pilory- negative, the level of activity was higher in the positive cases (97. 0 % and intestinal metaplasia was similar for both groups. Conclusions: in patients with H. pylori-negative peptic ulcer, non-steroidal anti-inflammatory drugs should be taken into consideration as one of the main factors associated with this entity.

  2. Helicobacter pylori-negative Russell body gastritis: Case report

    Institute of Scientific and Technical Information of China (English)

    Alessandro Del Gobbo; Luca Elli; Paola Braidotti; Franca Di Nuovo; Silvano Bosari; Solange Romagnoli

    2011-01-01

    Russell body gastritis is an unusual form of chronic gas-tritis characterized by the permeation of lamina propria by numerous plasma cells with eosinophilic cytoplasmic inclusions. Very few cases have been reported in the lit-erature; the majority of which have shown Helicobacter Pylori (H. pylori) infection, thus suggesting a correlation between plasma cell presence and antigenic stimulation by H. pylori. We present a case of Russell body gastritis in a 78-year-old woman who was undergoing esophago-gastroduodenoscopy for epigastric pain. Gastric biopsy of the gastroesophageal junction showed the presence of cells with periodic acid-Schiff-positive hyaline pink bodies. Giemsa staining for H. pylori infection was nega-tive, as well as immunohistochemical detection. The cells with eosinophilic inclusions stained positive for CD138, CD79a, and κ and lambda light chains, which confirmed plasma cell origin. In particular, κ and lambda light chains showed a polyclonal origin and the patient was negative for immunological dyscrasia. The histologi-cal observations were confirmed by ultrastructural ex-amination. The cases reported in the literature associated with H. pylori infection have shown regression of plasma cells after eradication of H. pylori. Nothing is known about the progression of H. pylori-negative cases. The unusual morphological appearance of this type of chron-ic gastritis should not be misinterpreted during routine examination, and it should be distinguished from other common forms of chronic gastritis. It is mandatory to exclude neoplastic diseases such as gastric carcinoma, lymphoma and plasmocytoma by immunohistochemistry and electron microscopy, which can help with differential diagnosis. The long-term effects of plasma cells hyper-activation are still unknown, because cases of gastric tu-mor that originated in patients affected by Russell body gastritis have not been described in the literature. We are of the opinion that these patients should be

  3. Role of Probiotics in the Management of Helicobacter Pylori Infection

    Directory of Open Access Journals (Sweden)

    A Zare Javid

    2014-04-01

    Full Text Available Helicobacter pylori is a gram-negative, spiral-shaped, microaerophilic organism that colonizes the stomach of humans and causes chronic-active gastritis, peptic ulcer disease, and gastric cancers, including adenocarcinoma of the stomach and MALT (mucosal-associated lymphoid tumor lymphomas. H. pylori colonizes the stomach of over 50 % the world’s human population, primarily those who reside in developing nations. Infection is generally first acquired in children, who may be entirely asymptomatic, and then persists for life, unless specific eradication therapy is initiated. All infected individuals have mucosal inflammation in the stomach in response to the organism, but only a subset will develop disease complications, such as an ulcer in the stomach or proximal duodenum and cancer in either the body or the antrum of the stomach. It is estimated that the lifetime risk of developing peptic ulceration is roughly 15%. However, this is an exceedingly important disease, because it has serious morbidity and mortality. Eradication of H. pylori infection is not successful when using antibiotics as monotherapy or dual therapy using combinations of an acid-suppressing agent and an antibiotic or two antibiotics without acid blockage. Multiple studies show that some probiotic strains can inhibit the growth of H. pylori. To date, probiotics do not appear to have a role as sole therapy for use in the prevention or treatment of H. pylori infection. However, there is increasing evidence that a variety of probiotic agents are useful as adjunctive therapy, which can both enhance the success of eradicating the gastric pathogen while, reduce the frequency and severity of adverse effects arising from the other agents that are employed in current combination treatment regimens. Future studies should assess the role of prebiotics and synbiotics and products derived from probiotics as additional options for use in the prevention and treatment of H. pylori infection

  4. Antibacterial effect of plant extracts against Helicobacter pylori.

    Science.gov (United States)

    Nostro, A; Cellini, L; Di Bartolomeo, S; Di Campli, E; Grande, R; Cannatelli, M A; Marzio, L; Alonzo, V

    2005-03-01

    The aim of this work was to evaluate the antibacterial effect of plant extracts as alternative and[sol ]or as active agents supporting antibiotics for treating Helicobacter pylori infection. The effect of either, ethanolic or aqueous extracts from 17 plant materials were studied against one H. pylori standard strain and 11 clinical isolates using a disc diffusion test and by evaluating the minimum inhibitory concentration (MIC) on solid media. An inhibitory activity against H. pylori strains was recorded in a large percentage of tested plants. MIC values of ethanolic extracts were from two to four concentration steps lower than the aqueous ones. In particular, ethanolic extracts of Cuminum cyminum L. and Propolis expressed MIC90 values of 0.075 mg/mL. The results show a significant in vitro effect of plant extracts against H. pylori that could be considered a valuable support in the treatment of the infection and may contribute to the development of new and safe agents for inclusion in anti-H. pylori regimens.

  5. Serum Helicobacter pylori NapA antibody as a potential biomarker for gastric cancer.

    Science.gov (United States)

    Liu, Jingjing; Liu, Huimin; Zhang, Tingting; Ren, Xiyun; Nadolny, Christina; Dong, Xiaoqun; Huang, Lina; Yuan, Kexin; Tian, Wenjing; Jia, Yunhe

    2014-02-20

    Helicobacter pylori (H. pylori) infection is strongly associated with gastric cancer. However, only a minority of infected individuals ever develop gastric cancer. This risk stratification may be in part due to differences among strains. The relationship between neutrophil-activating protein (NapA) and gastric cancer is unclear. The purpose of this study is to evaluate the significance of NapA as a biomarker in gastric cancer. We used enzyme linked immunosorbent assay (ELISA) to determine the status of H. pylori infection. Indirect ELISA method was used for detection of NapA antibody titer in the serum of H. pylori infected individuals. Unconditional logistic regressions were adopted to analyze the variables and determine the association of NapA and gastric cancer. The results of study indicated serum H. pylori NapA antibody level were associated with a reduced risk for development of gastric cancer. It may be used in conjugation with other indicators for gastric cancer detection.

  6. Role of Toll-like receptors in Helicobacter pylori infection and immunity

    Institute of Scientific and Technical Information of China (English)

    Sinéad; M; Smith

    2014-01-01

    The gram-negative bacterium Helicobacter pylori(H. pylori) infects the stomachs of approximately half of the world’s population. Although infection induces an immune response that contributes to chronic gastric inflammation, the response is not sufficient to eliminate the bacterium. H. pylori infection causes peptic ulcers, gastric cancer and mucosa-associated lymphoid tissue lymphoma. Disease outcome is linked to the severity of the host inflammatory response. Gastric epithelial cells represent the first line of innate immune defence against H. pylori, and respond to infection by initiating numerous cell signalling cascades, resulting in cytokine induction and the subsequent recruitment of inflamma-tory cells to the gastric mucosa. Pathogen recognition receptors of the toll-like receptor(TLR) family mediate many of these cell signalling events. This review dis-cusses recent findings on the role of various TLRs in the recognition of H. pylori in distinct cell types, describes the TLRs responsible for the recognition of individual H. pylori components and outlines the influence of innate immune activation on the subsequent development of the adaptive immune response. The mechanistic iden-tification of host mediators of H. pylori-induced patho-genesis has the potential to reveal drug targets and opportunities for therapeutic intervention or prevention of H. pylori-associated disease by means of vaccines or immunomodulatory therapy.

  7. Helicobacter pylori in lacrimal secretions.

    Science.gov (United States)

    Batioglu-Karaaltin, Aysegul; Saatci, Ozlem; Akpinar, Meltem; Celik, Melih Ozgür; Develioglu, Omer; Yigit, Ozgur; Külekçi, Mehmet; Akarsubaşı, Alper Tunga

    2016-03-01

    The aim of this study was to investigate the presence of Helicobacter pylori in human lacrimal and nasal secretions. Eighty patients with complaints of dyspepsia who had undergone endoscopies and gastric antrum biopsies were included in the study. A total of five specimens, including 2 lacrimal secretion samples, 2 nasal mucosal swab samples, and 1 gastric antrum biopsy, were collected from each patient and investigated with polymerase chain reaction (PCR) methods consisting of the urease enzyme coding gene GlmM (UreC) and the H pylori-specific 16S rRNA coding gene. The Reflux Symptom Index and ophthalmologic complaints of the patients were recorded. The detected positivity rates of the H pylori 16S rRNA coding gene in gastric biopsies and nasal mucous and lacrimal secretions were 55, 11.2, and 20%, respectively. The patients were grouped as gastric-antrum-biopsy-negative (Group I [n = 36]) and -positive (Group II [n = 44). In Group II, H pylori positivity in the lacrimal and nasal mucous secretions was 36.3 and 18%, respectively. A comparison between the groups in terms of H pylori presence in nasal mucous and lacrimal secretions yielded statistically significant differences (p = 0.0001, p = 0.003). The simultaneous presence of H pylori in nasal mucous and lacrimal secretions was 13.6% in Group II. H pylori positivity in nasal mucous and lacrimal secretions had a positive moderate correlation (r = 0.40; p = 0.0003). The present study is the first report on the presence of H pylori in lacrimal secretions through nested PCR, which suggested the presence of a number of mechanisms for H pylori transmission to lacrimal secretions.

  8. Susceptibility of helicobacter pylori to metronidazole and its bioactive derivatives

    Directory of Open Access Journals (Sweden)

    Bannatyne Robert

    1998-01-01

    Full Text Available The hydroxy derivative of metronidazole can exhibit equal or greater activity to the parent drug against several bacteria. The susceptibility status of 22 H. pylori strains to these breakdown compounds was determined in order to determine their possible role in the therapy of H. pylori associated peptic ulcer disease. The susceptibility was determined using the agar dilution method and substantial activity (MIC90 = 0.33 .tg/ml for the hydroxy metabolite of metronidazole versus H. pylori was observed. The findings define a role for the hydroxy derivative of metronidazole in peptic ulcer disease and support the limited data on the possibility of cooperative interactions between the parent compound, its main derivatives and related companion drugs in this condition.

  9. Helicobacter pylori cytotoxin-associated gene A activates tumor necrosis factor-α and interleukin-6 in gastric epithelial cells through P300/CBP-associated factor-mediated nuclear factor-κB p65 acetylation.

    Science.gov (United States)

    Lin, Qiong; Xu, Hui; Chen, Xintao; Tang, Guorong; Gu, Lan; Wang, Yehong

    2015-10-01

    Helicobacter pylori‑initiated chronic gastritis is characterized by the cytotoxin‑associated gene (Cag) pathogenicity island‑dependent upregulation of pro‑inflammatory cytokines in gastric epithelial cells, which is largely mediated by the activation of nuclear factor (NF)‑κB as a transcription factor. However, the precise regulation of NF‑κB activation, particularly post‑translational modifications in the CagA‑induced inflammatory response, has remained elusive. The present study showed that Helicobacter pylori CagA, an important virulence factor, induced the expression of P300/CBP‑associated factor (PCAF) in gastric epithelial cells. Further study revealed that PCAF was able to physically associate with the NF‑κB p65 sub‑unit and enhance its acetylation. More importantly, PCAF‑induced p65 acetylation was shown to contribute to p65 phosphorylation and further upregulation of tumor necrosis factor (TNF)‑α and interleukin (IL)‑6 in gastric adenocarcinoma cells. In conclusion, the results of the present study indicated that Helicobacter pylori CagA enhanced TNF‑α and IL‑6 in gastric adenocarcinoma cells through PCAF‑mediated NF‑κB p65 sub‑unit acetylation.

  10. Caveolin-1 protects B6129 mice against Helicobacter pylori gastritis.

    Directory of Open Access Journals (Sweden)

    Ivana Hitkova

    Full Text Available Caveolin-1 (Cav1 is a scaffold protein and pathogen receptor in the mucosa of the gastrointestinal tract. Chronic infection of gastric epithelial cells by Helicobacter pylori (H. pylori is a major risk factor for human gastric cancer (GC where Cav1 is frequently down-regulated. However, the function of Cav1 in H. pylori infection and pathogenesis of GC remained unknown. We show here that Cav1-deficient mice, infected for 11 months with the CagA-delivery deficient H. pylori strain SS1, developed more severe gastritis and tissue damage, including loss of parietal cells and foveolar hyperplasia, and displayed lower colonisation of the gastric mucosa than wild-type B6129 littermates. Cav1-null mice showed enhanced infiltration of macrophages and B-cells and secretion of chemokines (RANTES but had reduced levels of CD25+ regulatory T-cells. Cav1-deficient human GC cells (AGS, infected with the CagA-delivery proficient H. pylori strain G27, were more sensitive to CagA-related cytoskeletal stress morphologies ("humming bird" compared to AGS cells stably transfected with Cav1 (AGS/Cav1. Infection of AGS/Cav1 cells triggered the recruitment of p120 RhoGTPase-activating protein/deleted in liver cancer-1 (p120RhoGAP/DLC1 to Cav1 and counteracted CagA-induced cytoskeletal rearrangements. In human GC cell lines (MKN45, N87 and mouse stomach tissue, H. pylori down-regulated endogenous expression of Cav1 independently of CagA. Mechanistically, H. pylori activated sterol-responsive element-binding protein-1 (SREBP1 to repress transcription of the human Cav1 gene from sterol-responsive elements (SREs in the proximal Cav1 promoter. These data suggested a protective role of Cav1 against H. pylori-induced inflammation and tissue damage. We propose that H. pylori exploits down-regulation of Cav1 to subvert the host's immune response and to promote signalling of its virulence factors in host cells.

  11. Tnterobserver variation in histopathological assessment of Helicobacter pylori gastritis

    Institute of Scientific and Technical Information of China (English)

    Ozlem Aydin; Reyhan Egilmez; Tuba Karabacak; Arzu Kanik

    2003-01-01

    Because the presence or absence of H pylori infection has important implications for therapeutic decisions based on histological assessment, the reproducibility of Sydney system is important. The study was designed to test the reproducibility of features of Helicobacter pylori gastritis,using the updated Sydney classification.METHODS: Gastric biopsies of 40 randomly selected cases of Hpylori gastritis were scored semiquantitatively by three pathologists. Variables analysed included chronic inflammation,inflammatory activity, atrophy, intestinal metaplasia, H pylori,surface epithelial damage. Κ values below 0.5 represented poor, those between 0.5 and 0.75 good and values over 0.75excellent interobserver agreement.RESULTS: The best interobserver agreement (κ=0.62) was present for intestinal metaplasia. The agreement was the poorest for evaluating atrophy (κ=0.31).CONCLUSION: Although the results of this study were in accordance with some previous studies, an excellent agreement could not be reached for any features of H pylori gastritis. This low degree of concordance is assumed to be due to the personal evaluation differences in grading the features, the lack of standardized diagnostic criteria, and the ignorance to reach a consensus about the methods to be used in grading the features of H pylori gastritis before initiating the study.

  12. Identification of Helicobacter pylori DNA in gallstones using Multiplex PCR

    Directory of Open Access Journals (Sweden)

    Shohreh Farshad

    2006-02-01

    Full Text Available Background: Recent studies showed a possible relationship between infections caused by some of Helicobacter members and gallstones formation. The aim of this study was identification of Helicobacter members in gallstones from patients with biliary diseases. Methods: Gallstones and bile samples from 33 patients were subjected to rapid urease test, culture and Multiplex-PCR using primers based on 16s rRNA and isocitrate dehydrogenase genes to identify Helicobacter genus and H. pylori species genes, respectively. This PCR was also done on bile samples from 40 autopsied gallbladders with normal pathology (as a control group. Results: In 18.1% of stones and 12.1% of bile samples, H. pylori DNA was detected using PCR. Rapid urease and cultures tests were negative for all samples. The genome of H. pylori was not detected in control group using PCR. Conclusion: H. pylori DNA was detected in gallstone, however, we are not sure of H. pylori viability in these samples. To clarify the clinical role of Helicobacter in gallbladder diseases, more investigations are needed to ascertain whether this microorganism is innocent bystander or active participant in gallstone formation.

  13. Recent Insights into Antibiotic Resistance in Helicobacter pylori Eradication

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    Wenming Wu

    2012-01-01

    Full Text Available Antibiotics have been useful in the treatment of H. pylori-related benign and malignant gastroduodenal diseases. However, emergence of antibiotic resistance often decreases the eradication rates of H. pylori infections. Many factors have been implicated as causes of treatment failure, but the main antibiotic resistance mechanisms described to date are due to point mutations on the bacterial chromosome, a consequence of a significantly phenotypic variation in H. pylori. The prevalence of antibiotic (e.g., clarithromycin, metronidazole, tetracycline, amoxicillin, and furazolidone resistance varies among different countries; it appears to be partly determined by geographical factors. Since the worldwide increase in the rate of antibiotic resistance represents a problem of relevance, some studies have been performed in order to identify highly active and well-tolerated anti-H. pylori therapies including sequential, concomitant quadruple, hybrid, and quadruple therapy. These represent a promising alternatives in the effort to overcome the problem of resistance. The aim of this paper is to review the current status of antibiotic resistance in H. pylori eradication, highlighting the evolutionary processes in detail at alternative approaches to treatment in the past decade. The underlying resistance mechanisms will be also followed.

  14. Drug therapy for Helicobacter pylori infection: problems and pitfalls.

    Science.gov (United States)

    Glupczynski, Y; Burette, A

    1990-12-01

    Antibacterial chemotherapy against Helicobacter pylori is currently being assessed by open or randomized controlled clinical studies for its efficacy in eradicating this bacterium from the stomach of patients with gastritis or gastroduodenal ulcer. Whereas there is presently no "optimal" agent and treatment scheme, the combination of some antibiotics (metronidazole, tinidazole, amoxicillin) with bismuth salts proves definitely superior in vivo to either of these agents administered alone. Several reasons have been proposed, to explain the clinical failure after treatment: insufficient concentration of active drugs in gastric mucus, instability of some agents at an acidic pH, inappropriate formulation of drug, insufficient duration of treatment, and variable compliance of patients. Recently, it has appeared from several clinical trials that H. pylori may rapidly acquire resistance to some antibiotics, and that this event might also account for clinical failure. A critical review of the literature on H. pylori treatment indicates that association of bismuth and antibiotics or of antibiotics alone both may efficiently reduce the risk of emergence of resistance and improve the therapeutic outcome. Guidelines of treatment are suggested in order to avoid the future misuse of antibiotics that would increase selection of antibiotic-resistant H. pylori and negatively affect the ecology of the gastric microflora. Likewise, an accurate definition of a subset of patients with H. pylori who really will require treatment needs to be rapidly established.

  15. Expression of 87 kD protein in the broth culture filtrate of Helicobacter pylori and its association with the vacuolating effect

    Institute of Scientific and Technical Information of China (English)

    SHI Li; YIE Gui-an; NAN Qing-zhen; SUN Yong; ZHANG Ya-li; ZHANG Zhen-shu; ZHOU Dian-yuan

    2001-01-01

    To study the vacuolating effect of Helicobacter pylori(H.pylori). Method: The vacuolating effect and its relationship with vacuolating cytotoxin antigen (an 87 kD protein) were investigated by the method of cytotoxic test, SDS-PAGE and scanning. Result: Of the 62 clinical isolates, 43 strains were H.pylori (Toxin+) with vacuolating effect, while the others were H.pylori (Toxin-) without vacuolating effect. Altogether 78.26%(36/46) patients with peptic ulcer were infected with H.pylori (Toxin+) strains, and only 42.86%(6/14) who had gastritis were infected with H.pylori (Toxin+) strains, with significant difference between them(χ2=4.83,P<0.05). A protein with relativemolecular mass of 87 kD was identified in the broth culture filter(BCF) of 30.23% H. Pylori (Toxin+) strains (13/43) but in none of that of H.pylori (Toxin-) strains, and the difference was statistically significant(P<0.05). There was a significant and concordant relationship between the OD value of the protein band and the titer of vacuolating activity of H.pylori (Toxin+) (r=0.67 and P<0.05 by linear regression analysis). Conclusion: H.pylori (Toxin+) were more often associated with peptic ulcerous diseases than with gastritis diseases. The vacuolating effect of H.pylori (Toxin+) may be caused by the 87 kD protein.

  16. Effect of Volatile Oil of Amomum on Expressions of Platelet Activating Factor and Mastocarcinoma-related Peptide in the Gastric Membrane of Chronic Gastritis Patients with Helicobacter-pylori Infection

    Institute of Scientific and Technical Information of China (English)

    HUANG Guo-dong; HUANG Yuan-hua; XIAO Mei-zhen; HUANG Dao-fu; LIU Juan; LI Jia-bang

    2008-01-01

    Objective: To observe the effect of volatile oil of amomum (VOA) on the expressions of mastocarcinoma-related peptide (PS2) and platelet activating factor (PAF) in helicobacter pylori-associated gastritis (HPG) and to analyze its potential mechanism. Methods: Eighty patients with HPG were randomly assigned to two groups, 42 patients in the treated group treated with 0.5 mL VOA, thrice per day; and the 38 patients in the control group receiving Western tertiary medicinal treatment. Gastroscopic picture and helicobacter pylori (HP) infection (by quick urease and Warthin-Starry stain) of the gastro-membrane, expressions of PS2 and PAF (by immunohistochemical assay and Western blotting) as well as the contents of aminohexose and phospholipid (by Neuhaus method) in the gastric membrane of all patients were detected before treatment and 4 weeks after treatment. The clinical efficacy in the two groups was compared. Results: The total effective rate in the treated group was 88.1%, which was significantly higher than that in the control group (78.9%, P 0.05). Conclusion: The mechanism of VOA for anti-gastritis might be related with its action in increasing the expression of PS2 and decreasing the expression of PAF, and thus regulating the hydrophobicity of the gastric membrane.

  17. [Helicobacter pylori -- 2014].

    Science.gov (United States)

    Buzás, György Miklós

    2015-02-08

    The author reviews the main achievements in Helicobacter pylori research in the past 2 years. Of the more than 1000 microRNAs described thus far, sets of over- and underexpressed samples were identified that are associated with either gastric cancer or precancerous lesions, and some of them could be either markers or therapeutic targets in the near future. Meta-analyses involved 95 new publications: the association between infection and oesophageal, colorectal, pancreatic and liver carcinomas is supported by the increased odds ratios, but the results do not reach the strength seen in gastric carcinoma. Epstein-Barr virus is an emerging pathogen: 10% of gastric cancers are virus-associated; the prevalence of the virus in normal mucosa, chronic gastritis and peptic ulcer are currently being studied. Current Helicobacter pylori eradication regimens frequently achieve suboptimal results: a few optimisation methods are presented, although not all are supported by the meta-analyses. In 2013, the European Helicobacter Study Group proposed the development of a pan-European registry; data from 5792 patients registered so far indicated that many therapeutic regimens resulted in a low eradication rate. In 2013, the Healthy Stomach Initiative was started with the aim of supporting and disseminating research performed in the field of healthy and diseased stomachs.

  18. Helicobacter pylori infection in pediatrics

    DEFF Research Database (Denmark)

    Wewer, Anne Vibeke; Kalach, Nicolas

    2003-01-01

    A high prevalence and early colonization of Helicobacter pylori infection in childhood was described again this year in developing countries in contrast to developed ones. Upper gastrointestinal endoscopy including gastric biopsies remains the diagnostic gold standard method for this infection...

  19. Management of Helicobacter pylori infections

    NARCIS (Netherlands)

    Abadi, Amin Talebi Bezmin; Kusters, Johannes G

    2016-01-01

    BACKGROUND: Infection with Helicobacter pylori is associated with severe digestive diseases including chronic gastritis, peptic ulcer disease, and gastric cancer. Successful eradication of this common gastric pathogen in individual patients is known to prevent the occurrence of peptic ulcer disease

  20. The role of acid inhibition in Helicobacter pylori eradication [version 1; referees: 3 approved

    Directory of Open Access Journals (Sweden)

    David R. Scott

    2016-07-01

    Full Text Available Infection of the stomach by the gastric pathogen Helicobacter pylori results in chronic active gastritis and leads to the development of gastric and duodenal ulcer disease and gastric adenocarcinoma. Eradication of H. pylori infection improves or resolves the associated pathology. Current treatments of H. pylori infection rely on acid suppression in combination with at least two antibiotics. The role of acid suppression in eradication therapy has been variously attributed to antibacterial activity of proton pump inhibitors directly or through inhibition of urease activity or increased stability and activity of antibiotics. Here we discuss the effect of acid suppression on enhanced replicative capacity of H. pylori to permit the bactericidal activity of growth-dependent antibiotics. The future of eradication therapy will rely on improvement of acid inhibition along with current antibiotics or the development of novel compounds targeting the organism’s ability to survive in acid.

  1. Anti-bacterial effects of enzymatically-isolated sialic acid from glycomacropeptide in a Helicobacter pylori-infected murine model

    Science.gov (United States)

    Noh, Hye-Ji; Koh, Hong Bum; Kim, Hee-Kyoung; Cho, Hyang Hyun

    2017-01-01

    BACKGROUND/OBJECTIVES Helicobacter pylori (H. pylori) colonization of the stomach mucosa and duodenum is the major cause of acute and chronic gastroduodenal pathology in humans. Efforts to find effective anti-bacterial strategies against H. pylori for the non-antibiotic control of H. pylori infection are urgently required. In this study, we used whey to prepare glycomacropeptide (GMP), from which sialic acid (G-SA) was enzymatically isolated. We investigated the anti-bacterial effects of G-SA against H. pylori in vitro and in an H. pylori-infected murine model. MATERIALS/METHODS The anti-bacterial activity of G-SA was measured in vitro using the macrodilution method, and interleukin-8 (IL-8) production was measured in H. pylori and AGS cell co-cultures by ELISA. For in vivo study, G-SA 5 g/kg body weight (bw)/day and H. pylori were administered to mice three times over one week. After one week, G-SA 5 g/kg bw/day alone was administered every day for one week. Tumor necrosis factor-α (TNF-α), IL-1β, IL-6, and IL-10 levels were measured by ELISA to determine the anti-inflammatory effects of G-SA. In addition, real-time PCR was performed to measure the genetic expression of cytotoxin-associated gene A (cagA). RESULTS G-SA inhibited the growth of H. pylori and suppressed IL-8 production in H. pylori and in AGS cell co-cultures in vitro. In the in vivo assay, administration of G-SA reduced levels of IL-1β and IL-6 pro-inflammatory cytokines whereas IL-10 level increased. Also, G-SA suppressed the expression of cagA in the stomach of H. pylori-infected mice. CONCLUSION G-SA possesses anti-H. pylori activity as well as an anti-H. pylori-induced gastric inflammatory effect in an experimental H. pylori-infected murine model. G-SA has potential as an alternative to antibiotics for the prevention of H. pylori infection and H. pylori-induced gastric disease prevention. PMID:28194260

  2. Helicobacter pylori VacA enhances prostaglandin E2 production through induction of cyclooxygenase 2 expression via a p38 mitogen-activated protein kinase/activating transcription factor 2 cascade in AZ-521 cells

    DEFF Research Database (Denmark)

    Hisatsune, Junzo; Yamasaki, Eiki; Nakayama, Masaaki;

    2007-01-01

    Treatment of AZ-521 cells with Helicobacter pylori VacA increased cyclooxygenase 2 (COX-2) mRNA in a time- and dose-dependent manner. A p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, blocked elevation of COX-2 mRNA levels, whereas PD98059, which blocks the Erk1/2 cascade......A-induced COX-2 expression. In parallel with COX-2 expression, VacA increased prostaglandin E(2) (PGE(2)) production, which was inhibited by SB203580 and NS-398, a COX-2 inhibitor. VacA-induced PGE(2) production was markedly attenuated in AZ-521 cells stably expressing DN-p38. VacA increased transcription...... promoter activation. The reduction of ATF-2 expression in AZ-521 cells transformed with ATF-2-small interfering RNA duplexes resulted in suppression of COX-2 expression. Thus, VacA enhances PGE(2) production by AZ-521 cells through induction of COX-2 expression via the p38 MAPK/ATF-2 cascade, leading...

  3. Helicobacter pylori in gastric carcinogenesis

    Institute of Scientific and Technical Information of China (English)

    Hyo; Jun; Ahn; Dong; Soo; Lee

    2015-01-01

    Gastric cancer still is a major concern as the third most common cancer worldwide, despite declining rates of incidence in many Western countries. Helicobacter pylori(H. pylori) is the major cause of gastric carcinogenesis, and its infection insults gastric mucosa leading to theoccurrence of atrophic gastritis which progress to intestinal metaplasia, dysplasia, early gastric cancer, and advanced gastric cancer consequently. This review focuses on multiple factors including microbial virulence factors, host genetic factors, and environmental factors, which can heighten the chance of occurrence of gastric adenocarcinoma due to H. pylori infection. Bacterial virulence factors are key components in controlling the immune response associated with the induction of carcinogenesis, and cag A and vac A are the most well-known pathogenic factors. Host genetic polymorphisms contribute to regulating the inflammatory response to H. pylori and will become increasingly important with advancing techniques. Environmental factors such as high salt and smoking may also play a role in gastric carcinogenesis. It is important to understand the virulence factors, host genetic factors, and environmental factors interacting in the multistep process of gastric carcinogenesis. To conclude, prevention via H. pylori eradication and controlling environmental factors such as diet, smoking, and alcohol is an important strategy to avoid H. pylori-associated gastric carcinogenesis.

  4. Helicobacter pylori infection in Chile.

    Science.gov (United States)

    Figueroa, G; Acuña, R; Troncoso, M; Portell, D P; Toledo, M S; Valenzuela, J

    1997-11-01

    This article summarizes studies designed to evaluate the role of Helicobacter pylori infection in Chile, described in 21 reports from nine centers in various Chilean regions published between 1985 and 1995. According to their data, H. pylori infection is quite frequent among patients with a variety of gastric conditions, including adults (43%-92%) and children (6%-100%). Levels of specific IgG antibodies to H. pylori are also elevated among patients with duodenal ulcers (100%) and gastritis (86%) as well as asymptomatic adults (75%). Combination therapy with three (but not two) drugs has been proved effective, with clinical improvement, ulcer cure, and H. pylori eradication occurring in well-controlled studies. Available evidence suggests that antibiotic resistance is not a major problem in treatment. The H. pylori reinfection rate is low (4.2% per year), suggesting that combination therapy with three drugs constitutes a cost-effective alternative for treating colonized symptomatic patients. Concurrent preliminary studies revealed that antibodies to VacA but not CagA proteins correlate with disease severity in Chilean patients. It can be concluded that local research assists local administrators of health resources to implement adequate policies to prevent, control, and treat H. pylori-related pathologies.

  5. Comparative genomics of Helicobacter pylori

    Institute of Scientific and Technical Information of China (English)

    Quan-Jiang Dong; Qing Wang; Ying-Nin Xin; Ni Li; Shi-Ying Xuan

    2009-01-01

    Genomic sequences have been determined for a number of strains of Helicobacter pylori (H pylori) and related bacteria.With the development of microarray analysis and the wide use of subtractive hybridization techniques,comparative studies have been carried out with respect to the interstrain differences between H pylori and inter-species differences in the genome of related bacteria.It was found that the core genome of H pylori constitutes 1111 genes that are determinants of the species properties.A great pool of auxillary genes are mainly from the categories of cag pathogenicity islands,outer membrane proteins,restriction-modification system and hypothetical proteins of unknown function.Persistence of H pylori in the human stomach leads to the diversification of the genome.Comparative genomics suggest that a host jump has occurs from humans to felines.Candidate genes specific for the development of the gastric diseases were identified.With the aid of proteomics,population genetics and other molecular methods,future comparative genomic studies would dramatically promote our understanding of the evolution,pathogenesis and microbiology of H pylori.

  6. Efficacy of the eradication of Helicobacter pylori infection in patients with chronic urticaria. A placebo-controlled double blind study.

    Science.gov (United States)

    Gaig, P; García-Ortega, P; Enrique, E; Papo, M; Quer, J C; Richard, C

    2002-01-01

    Helicobacter pylori has been involved in the pathogenesis of chronic idiopathic urticaria (CIU) in patients suffering both CIU and H. pylori infection. We selected 49 patients with 13C urea breath test positive, long-lasting CIU and H. pylori infection; 20 remained symptomatic, had positive urease test or H. pylori histologic identification in gastric biopsy material and accepted to participate in a pacebo-controlled treatment trial. They were randomized for a 7-day, double-blind, placebo-controlled H. pylori eradication treatment with amoxicillin, clarithromycin and omeprazol or placebo. H. pylori eradication was assessed by a second 13C urea breath test six weeks after the end of treatment. We observed a significant improvement of more than 70 % of CIU; baseline clinical score was seen in 4 of the 9 (44 %) patients who eradicated H. pylori after active treatment and in 1 of the 7 (12,3 %) of those who did not (p = 0.19). No clinical differences in CIU characteristics were found between patients with and without improvement. No serious adverse effects were observed in either treatment group. We conclude that the eradication of H. pylori may be useful for patients suffering long-lasting CIU and H. pylori infection, although theses results did not reach statistical significance probably owing to the strict conditions of the recruitment.

  7. Comparative Analysis of the Interaction of Helicobacter pylori with Human Dendritic Cells, Macrophages, and Monocytes

    Science.gov (United States)

    Fehlings, Michael; Drobbe, Lea; Moos, Verena; Renner Viveros, Pablo; Hagen, Jana; Beigier-Bompadre, Macarena; Pang, Ervinna; Belogolova, Elena; Churin, Yuri; Schneider, Thomas; Meyer, Thomas F.; Aebischer, Toni

    2012-01-01

    Helicobacter pylori may cause chronic gastritis, gastric cancer, or lymphoma. Myeloid antigen-presenting cells (APCs) are most likely involved in the induction and expression of the underlying inflammatory responses. To study the interaction of human APC subsets with H. pylori, we infected monocytes, monocyte-derived dendritic cells (DCs), and monocyte-derived (classically activated; M1) macrophages with H. pylori and analyzed phenotypic alterations, cytokine secretion, phagocytosis, and immunostimulation. Since we detected CD163+ (alternatively activated; M2) macrophages in gastric biopsy specimens from H. pylori-positive patients, we also included monocyte-derived M2 macrophages in the study. Upon H. pylori infection, monocytes secreted interleukin-1β (IL-1β), IL-6, IL-10, and IL-12p40 (partially secreted as IL-23) but not IL-12p70. Infected DCs became activated, as shown by the enhanced expression of CD25, CD80, CD83, PDL-1, and CCR7, and secreted IL-1β, IL-6, IL-10, IL-12p40, IL-12p70, and IL-23. However, infection led to significantly downregulated CD209 and suppressed the constitutive secretion of macrophage migration inhibitory factor (MIF). H. pylori-infected M1 macrophages upregulated CD14 and CD32, downregulated CD11b and HLA-DR, and secreted mainly IL-1β, IL-6, IL-10, IL-12p40, and IL-23. Activation of DCs and M1 macrophages correlated with increased capacity to induce T-cell proliferation and decreased phagocytosis of dextran. M2 macrophages upregulated CD14 and CD206 and secreted IL-10 but produced less of the proinflammatory cytokines than M1 macrophages. Thus, H. pylori affects the functions of human APC subsets differently, which may influence the course and the outcome of H. pylori infection. The suppression of MIF in DCs constitutes a novel immune evasion mechanism exploited by H. pylori. PMID:22615251

  8. Does Helicobacter pylori affect portal hypertensive gastropathy?

    Directory of Open Access Journals (Sweden)

    Al Mofleh Ibrahim

    2007-01-01

    Full Text Available Helicobacter pylori (H. pylori is a major etiological factor of peptic ulcer disease (PUD. It is supposed to be a risk factor for the more frequently encountered PUD in patients with liver cirrhosis. Several investigators have evaluated the effect of H. pylori on liver cirrhosis, portal hypertensive gastropathy (PHG and encephalopathy with controversial results. Some reports have shown a higher seroprevalence and suggested a synergistic effect of H. pylori on liver cirrhosis and PHG. However, this increased prevalence is associated with a negative histology and is not influenced by the cause of cirrhosis, PHG, Child class or gender. Most studies have not found any correlation between H. pylori and PHG. In contrast, other studies have reported a markedly lower prevalence of H. pylori in cirrhotics with duodenal ulcer compared to controls. The aim of this article is to review the relationship between H. pylori infection and portal hypertensive gastropathy and the role of H. pylori eradication in cirrhotic patients.

  9. What Do We Do about Helicobacter pylori?

    Directory of Open Access Journals (Sweden)

    CJ Hawkey

    1999-01-01

    Full Text Available Heliobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs cause ulcers by different mechanisms. Under some circumstances, patients infected with H pylori may be less prone to NSAID-associated ulcers than those who are H pylori-negative. Eradication trials have yielded differing results. However, those who have studied patients who have a past history of ulcer disease and are already established on NSAIDs have shown no benefit from H pylori eradication.

  10. A Dynamic Zn Site in Helicobacter pylori HypA: A Potential Mechanism for Metal-Specific Protein Activity

    Energy Technology Data Exchange (ETDEWEB)

    Kennedy,D.; Herbst, R.; Iwig, J.; Chivers, P.; Maroney, M.

    2007-01-01

    HypA is an accessory protein and putative metallochaperone that is critical for supplying nickel to the active site of NiFe hydrogenases. In addition to binding Ni(II), HypA is known to contain a Zn site that has been suggested to play a structural role. X-ray absorption spectroscopy has been used to show that the Zn site changes structure upon binding nickel, from a S{sub 3}(O/N)-donor ligand environment to an S{sub 4}-donor ligand environment. This provides a potential mechanism for discriminating Ni(II) from other divalent metal ions. The Ni(II) site is shown to be a six-coordinate complex composed of O/N-donors including two histidines. As such, it resembles the nickel site in UreE, a nickel metallochaperone involved in nickel incorporation into urease.

  11. Helicobacter pylori Seropositivity in Children With Asthma

    OpenAIRE

    Yousefichaijan; Mosayebi; Sharafkhah; Kahbazi; Heydarbagi; Rafiei

    2016-01-01

    Background Some studies have reported an association between Helicobacter pylori (H. pylori) colonization and the occurrence of asthma or other allergies. However, data are inconsistent, and few studies have been performed in children. Objectives The current study aimed to investigate H. pylori seropositivity in children with and without asthma. Patients and Methods This cross-sect...

  12. EXAMINATION OF THE PROTEIN PROFILE OF HELICOBACTER PYLORI UNDER DIFFERENT GROWTH CONDITIONS USING MATRIX-ASSISTED LASER DESORPTION MASS SPECTROMETRY

    Science.gov (United States)

    US EPA currently has H. pylori on its Contaminant Candidate List 2 (CCL 2), methods are needed to detect the occurrence of viable H. pylori in drinking water. H. pyloi is an interesting microorganism because it can change from a cultural and metabolically active state with a heli...

  13. Induction of CD69 expression by cagPAI-positive Helicobacter pylori infection

    Institute of Scientific and Technical Information of China (English)

    Naoki Mori; Chie Ishikawa; Masachika Senba

    2011-01-01

    AIM: To investigate and elucidate the molecular mech-anism that regulates inducible expression of CD69 by Helicobacter pylori (H. pylori ) infection.METHODS: The expression levels of CD69 in a T-cell line, Jurkat, primary human peripheral blood mononu-clear cells (PBMCs), and CD4+T cells, were assessed by immunohistochemistry, reverse transcription polymerase chain reaction, and flow cytometry. Activation of CD69 promoter was detected by reporter gene. Nuclear factor (NF)-κB activation in Jurkat cells infected with H. pylori was evaluated by electrophoretic mobility shift assay. The role of NF-κB signaling in H. pylori -induced CD69 expression was analyzed using inhibitors of NF-κB and dominant-negative mutants. The isogenic mutants with disrupted cag pathogenicity island ( cagPAI) and virD4 were used to elucidate the role of cagPAI-encoding type Ⅳ secretion system and CagA in CD69 expression.RESULTS: CD69 staining was detected in mucosal lymphocytes and macrophages in specimens of pa-tients with H. pylori -positive gastritis. Although cagPAI-positive H. pylori and an isogenic mutant of virD4 induced CD69 expression, an isogenic mutant of cag-PAI failed to induce this in Jurkat cells. H. pylori also induced CD69 expression in PBMCs and CD4+T cells. The activation of the CD69 promoter by H. pylori was mediated through NF-κB. Transfection of dominant-negative mutants of IκBs, IκB kinases, and NF-κB-inducing kinase inhibited H. pylori -induced CD69 activation. Inhibitors of NF-κB suppressed H. pylori -induced CD69 mRNA expression.CONCLUSION: The results suggest that H. pylori in-duces CD69 expression through the activation of NF-κB. cagPAI might be relevant in the induction of CD69 expression in T cells. CD69 in T cells may play a role in H. pylori -induced gastritis.

  14. Characterization of the respiratory chain of Helicobacter pylori

    DEFF Research Database (Denmark)

    Chen, M; Andersen, L P; Zhai, L

    1999-01-01

    The respiratory chain of Helicobacter pylori has been investigated. The total insensitivity of activities of NADH dehydrogenase to rotenone and of NADH-cytochrome c reductase to antimycin is indicative of the absence of the classical complex I of the electron transfer chain in this bacterium. NADPH...

  15. Metabolic consequences of Helicobacter pylori infection and eradication.

    Science.gov (United States)

    Buzás, György Miklós

    2014-05-14

    Helicobacter pylori (H. pylori) is still the most prevalent infection of the world. Colonization of the stomach by this agent will invariably induce chronic gastritis which is a low-grade inflammatory state leading to local complications (peptic ulcer, gastric cancer, lymphoma) and remote manifestations. While H. pylori does not enter circulation, these extragastric manifestations are probably mediated by the cytokines and acute phase proteins produced by the inflammed mucosa. The epidemiologic link between the H. pylori infection and metabolic changes is inconstant and controversial. Growth delay was described mainly in low-income regions with high prevalence of the infection, where probably other nutritional and social factors contribute to it. The timely eradication of the infection will lead to a more healthy development of the young population, along with preventing peptic ulcers and gastric cancer An increase of total, low density lipoprotein and high density liporotein cholesterol levels in some infected people creates an atherogenic lipid profile which could promote atherosclerosis with its complications, myocardial infarction, stroke and peripheral vascular disease. Well designed and adequately powered long-term studies are required to see whether eradication of the infection will prevent these conditions. In case of glucose metabolism, the most consistent association was found between H. pylori and insulin resistance: again, proof that eradication prevents this common metabolic disturbance is expected. The results of eradication with standard regimens in diabetics are significantly worse than in non-diabetic patients, thus, more active regimens must be found to obtain better results. Successful eradication itself led to an increase of body mass index and cholesterol levels in some populations, while in others no such changes were encountered. Uncertainities of the metabolic consequences of H. pylori infection must be clarified in the future.

  16. Helicobacter pylori infection: approach of primary care physicians in a developing country

    Directory of Open Access Journals (Sweden)

    Ali Shah Hasnain

    2009-04-01

    Full Text Available Abstract Background The aim of the study was to assess the knowledge and practices of primary care physicians in diagnosis and management of Helicobacter pylori (H. pylori infection in developing country. Methods This convenient sample based, cross sectional study was conducted in primary care physicians of Karachi, Pakistan from March 2008 to August 2008 through a pretested self-designed questionnaire, which contained 11 items pertaining to H. pylori route of transmission, diagnosis, indication for testing, treatment options, follow up and source of information. Results Out of 509 primary care physicians, 451 consented to participate with the response rate of 88.6%. Responses of 426 primary care physicians were analyzed after excluding 19 physicians. 78% of the physicians thought that contaminated water was the source of spread of infection, dyspepsia was the most frequent indication for investigating H. pylori infection (67% of the physicians, while 43% physicians were of the view that serology was the most appropriate test to diagnose active H. pylori infection. 77% of physicians thought that gastric ulcer was the most compelling indication for treatment, 61% physicians preferred Clarithromycin based triple therapy for 7–14 days. 57% of the physicians would confirm H. pylori eradication after treatment in selected patients and 47% physicians preferred serological testing for follow-up. In case of treatment failure, only 36% of the physicians were in favor of gastroenterologist referral. Conclusion The primary care physicians in this study lacked in knowledge regarding management of H. pylori infection. Internationally published guidelines and World gastroenterology organization (WGO practice guideline on H. pylori for developing countries have little impact on current practices of primary care physicians. We recommend more teaching programs, continuous medical education activities regarding H. pylori infection.

  17. Application of Stool-PCR test for diagnosis of Helicobacter pylori infection in children

    Institute of Scientific and Technical Information of China (English)

    Tahereh Falsafi; Raha Favaedi; Fatemeh Mahjoub; Mehri Najafi

    2009-01-01

    AIM: To evaluate the usefulness of stool-PCR test for diagnosis of Helicobacter pylori ( H pylori) infection in pediatric populations.METHODS: Based on endoscopic features (including nodular gastritis, erosive duodenitis and ulcer) and/or a positive rapid urease test (RUT) obtained during endoscopy, 28 children from a group of children admitted to the Children's Medical Center of Tehran for persistent upper gastrointestinal problems were selected to compare biopsy-based tests with stool-PCR. Their gastric activity and bacterial density were graded by the updated Sydney system, and their first stool after endoscopy was stored at -70℃. Biopsies were cultured on modified campy-blood agar plates and identified by gram-staining, biochemical tests, and PCR. Two methods of phenol-chloroform and boiling were used for DNA extraction from H pylori isolates.Isolation of DNA from stool was performed using a stool DNA extraction kit (Bioneer Inc, Korea). PCR was performed using primers for detection of vacA, cagA,and 16srRNA genes in both isolates and stool.RESULTS: Sixteen out of 28 child patients (57%) were classified as H pylori positive by biopsy-based tests, of which 11 (39%) were also positive by stool-PCR. Sensitivity and specificity of stool-PCR was 62.5% and 92.3% respectively. H pylori was observed in histological sections for 10 out of 11 stool-positive patients. Association was observed between higher score of H pylori in histology and positivity of stool-PCR. Also association was observed between the more severe form of gastritis and a positive stool-PCR.CONCLUSION: Association between higher score of H pylori in histology and a positive stool-PCR make it a very useful test for detection of H pylori active infection in children. We also suggest that a simple stool-PCR method can be a useful test for detection of H pylori virulence genes in stool.

  18. Helicobacter pylori infection and gastroduodenal diseases in Vietnam: a cross-sectional, hospital-based study

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    Okimoto Tadayoshi

    2010-09-01

    Full Text Available Abstract Background The rate of H. pylori infection in Vietnam is reportedly high, but the spectrum of H. pylori-associated gastroduodenal diseases has not been systematically investigated. Moreover, despite the similarities of ethnicity and diet, the age-standardized incidence rate of gastric cancer in the northern city of Hanoi is higher than that in the southern city of Ho Chi Minh, but the reason for this phenomenon is unknown. The virulence of Vietnamese H. pylori has also not been investigated in detail. Methods Individuals undergoing esophagogastroduodenoscopy were randomly recruited. H. pylori infection status was determined based on the combined results of culture, histology, immunohistochemistry, rapid urine test and serum ELISA. Peptic ulcer (PU and gastroesophageal reflux disease was diagnosed by endoscopy, and chronic gastritis was determined histologically. H. pylori virulence factors were investigated by PCR and sequencing. Results Among the examined patients, 65.6% were infected with H. pylori. The prevalence of infection was significantly higher in those over 40 years of age than in those aged ≤40. Chronic gastritis was present in all H. pylori-infected individuals, 83.1% of whom had active gastritis, and 85.3% and 14.7% had atrophy and intestinal metaplasia, respectively. PU was present in 21% of infected patients, whereas its incidence was very low in non-infected individuals. The prevalence of PU was significantly higher in Hanoi than in Ho Chi Minh. The prevalence of vacA m1, which has been identified as an independent risk factor for PU in Vietnam, was significantly higher among H. pylori isolates from Hanoi than among those from Ho Chi Minh. Conclusions H. pylori infection is common in Vietnam and is strongly associated with PU, active gastritis, atrophy and intestinal metaplasia. vacA m1 is associated with an increased risk for PU and might contribute to the difference in the prevalence of PU and gastric cancer between

  19. Synthesis, molecular docking and biological evaluation of metronidazole derivatives as potent Helicobacter pylori urease inhibitors.

    Science.gov (United States)

    Mao, Wen-Jun; Lv, Peng-Cheng; Shi, Lei; Li, Huan-Qiu; Zhu, Hai-Liang

    2009-11-01

    Fourteen metronidazole derivatives (compounds 3a-f and 4b-h) have been synthesized by coupling of metronidazole and salicylic acid derivatives. All of them are reported for the first time. Their chemical structures are characterized by (1)H NMR, MS, and elemental analysis. The inhibitory activities against Helicobacter pylori urease have been investigated in vitro and many compounds have showed promising potential inhibitory activities of H. pylori urease. The effect of compounds 4b (IC(50)=26 microM) and 4 g (IC(50)=12 microM) was comparable with that of acetohydroxamic acid, a well known H. pylori urease inhibitor used as a positive control. The experimental values of IC(50) showed that inhibitor was potent urease inhibitor. A docking analysis using the autodock 4.0 program could explain the inhibitory activities of compound 4 g against H. pylori urease.

  20. The Prevalence of Helicobacter pylori Infection Decreases with Older Age in Atrophic Gastritis

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    Shaohua Chen

    2013-01-01

    Full Text Available The clinical pathological characteristics of 3969 adult patients with chronic atrophic gastritis were retrospectively studied. The positivity of intestinal metaplasia and dysplasia in atrophic gastric specimens increased with age; however, H. pylori positivity and inflammatory activity decreased significantly with increased age. H. pylori infection was present in 21.01% of chronic atrophic gastritis patients, and 92.33% of the subjects with H. pylori infection were found to have simultaneous inflammatory activity. The intestinal metaplasia and dysplasia positivity markedly increased as the degree of gastric atrophy increased. In conclusion, the incidence of H. pylori infection decreased with age and correlated significantly with inflammatory activity in atrophic gastritis patients. The intestinal metaplasia and dysplasia positivity notably increased as the degree of gastric atrophy increased. Large population-based prospective studies are needed to better understand the progression of CAG.

  1. Gastric Carcinogenesis and Underlying Molecular Mechanisms: Helicobacter pylori and Novel Targeted Therapy

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    Toshihiro Nishizawa

    2015-01-01

    Full Text Available The oxygen-derived free radicals that are released from activated neutrophils are one of the cytotoxic factors of Helicobacter pylori-induced gastric mucosal injury. Increased cytidine deaminase activity in H. pylori-infected gastric tissues promotes the accumulation of various mutations and might promote gastric carcinogenesis. Cytotoxin-associated gene A (CagA is delivered into gastric epithelial cells via bacterial type IV secretion system, and it causes inflammation and activation of oncogenic pathways. H. pylori infection induces epigenetic transformations, such as aberrant promoter methylation in tumor-suppressor genes. Aberrant expression of microRNAs is also reportedly linked to gastric tumorogenesis. Moreover, recent advances in molecular targeting therapies provided a new interesting weapon to treat advanced gastric cancer through anti-human epidermal growth factor receptor 2 (HER-2 therapies. This updated review article highlights possible mechanisms of gastric carcinogenesis including H. pylori-associated factors.

  2. Genetic microheterogeneity and phenotypic variation of Helicobacter pylori arginase in clinical isolates

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    Spadafora Domenico

    2007-04-01

    Full Text Available Abstract Background Clinical isolates of the gastric pathogen Helicobacter pylori display a high level of genetic macro- and microheterogeneity, featuring a panmictic, rather than clonal structure. The ability of H. pylori to survive the stomach acid is due, in part, to the arginase-urease enzyme system. Arginase (RocF hydrolyzes L-arginine to L-ornithine and urea, and urease hydrolyzes urea to carbon dioxide and ammonium, which can neutralize acid. Results The degree of variation in arginase was explored at the DNA sequence, enzyme activity and protein expression levels. To this end, arginase activity was measured from 73 minimally-passaged clinical isolates and six laboratory-adapted strains of H. pylori. The rocF gene from 21 of the strains was cloned into genetically stable E. coli and the enzyme activities measured. Arginase activity was found to substantially vary (>100-fold in both different H. pylori strains and in the E. coli model. Western blot analysis revealed a positive correlation between activity and amount of protein expressed in most H. pylori strains. Several H. pylori strains featured altered arginase activity upon in vitro passage. Pairwise alignments of the 21 rocF genes plus strain J99 revealed extensive microheterogeneity in the promoter region and 3' end of the rocF coding region. Amino acid S232, which was I232 in the arginase-negative clinical strain A2, was critical for arginase activity. Conclusion These studies demonstrated that H. pylori arginase exhibits extensive genotypic and phenotypic variation which may be used to understand mechanisms of microheterogeneity in H. pylori.

  3. Protective effect of Korean Red Ginseng extract against Helicobacter pylori-induced gastric inflammation in Mongolian gerbils

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    Minkyung Bae

    2014-01-01

    Full Text Available Helicobacter pylori-induced gastric inflammation includes induction of inflammatory mediators interleukin (IL-8 and inducible nitric oxide synthase (iNOS, which are mediated by oxidant-sensitive transcription factor NF-κB. High levels of lipid peroxide (LPO and increased activity of myeloperoxidase (MPO, a biomarker of neutrophil infiltration, are observed in H. pylori-infected gastric mucosa. Panax ginseng Meyer, a Korean herb medicine, is widely used in Asian countries for its biological activities including anti-inflammatory efficacy. The present study aims to investigate whether Korean Red Ginseng extract (RGE inhibits H. pylori-induced gastric inflammation in Mongolian gerbils. One wk after intragastric inoculation with H. pylori, Mongolian gerbils were fed with either the control diet or the diet containing RGE (200 mg RGE/gerbil for 6 wk. The following were determined in gastric mucosa: the number of viable H. pylori in stomach; MPO activity; LPO level; mRNA and protein levels of keratinocyte chemoattractant factor (KC, a rodent IL-8 homolog, IL-1β, and iNOS; protein level of phospho-IκBα (which reflects the activation of NF-κB; and histology. As a result, RGE suppressed H. pylori-induced mRNA and protein levels of KC, IL-1β, and iNOS in gastric mucosa. RGE also inhibited H. pylori-induced phosphorylation of IκBα and increases in LPO level and MPO activity of gastric mucosa. RGE did not affect viable H. pylori colonization in the stomach, but improved the histological grade of infiltration of polymorphonuclear neutrophils, intestinal metaplasia, and hyperplasia. In conclusion, RGE inhibits H. pylori-induced gastric inflammation by suppressing induction of inflammatory mediators (KC, IL-1β, iNOS, MPO activity, and LPO level in H. pylori-infected gastric mucosa.

  4. Effect of Di(2-ethylhexylphthalate on Helicobacter pylori-Induced Apoptosis in AGS Cells

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    Chuang-Hao Lin

    2013-01-01

    Full Text Available Plastic products are wildly used in human life. Di(2-ethylhexylphthalate (DEHP is an essential additive in plastic manufacturing and is used as plasticizer for many products including plastic food packaging. DEHP is a teratogenic compound and can cause potent reproductive toxicity. DEHP can also cause liver damage, peroxisome proliferation, and carcinogenesis. DEHP is also strongly associated with peptic ulcers and gastric cancer; however, the underlying effect and mechanism of DEHP on the gastrointestinal tract are not entirely clear. The oral infection route of H. pylori parallels the major ingestion route of DEHP into the human body. Therefore, we wanted to study the effect of DEHP and H. pylori exposure on the human gastric epithelial cell line, AGS (gastric adenocarcinoma. The viability of the AGS cell line was significantly lower in 80 μM-DEHP and H. pylori (MOI = 100 : 1 coexposure than DEHP or H. pylori alone. DEHP and H. pylori coexposure also induced caspase-3 activation, and increased Bax/Bcl-2 ratio and DNA fragmentation in AGS cells. These results indicate that DEHP can enhance H. pylori cytotoxicity and induce gastric epithelial cell apoptosis. Therefore, it is possible that DEHP and H. pylori coexposure might enhance the disruption of the gastric mucosa integrity and potentially promote the pathogenesis of gastric carcinogenesis.

  5. Helicobacter pylori Genotypes Associated with Gastric Histo-Pathological Damages in a Moroccan Population

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    Alaoui Boukhris, Samia; Amarti, Afaf; El Rhazi, Karima; El Khadir, Mounia; Benajah, Dafr-Allah; Ibrahimi, Sidi Adil; Nejjari, Chakib; Mahmoud, Mustapha; Souleimani, Abdellah; Bennani, Bahia

    2013-01-01

    H. pylori persistent infection induces chronic gastritis and is associated with peptic ulcer disease and gastric carcinoma development. The severity of these diseases is related to human’s genetic diversity, H. pylori genetic variability and environmental factors. To identify the prevalence of histo-pathological damages caused by H. pylori infection in Moroccan population, and to determine their association to H. pylori genotypes, a prospective study has been conducted during 3 years on patients attending the gastroenterology department of Hassan II University Hospital (CHU) of Fez, Morocco. A total of 801 Moroccan adults’ patients were recruited; H. pylori was diagnosed and genotyped by PCR in biopsy specimens and histological exam was performed. We found a high rate of glandular atrophy. Chronic inflammation, neutrophil activity and glandular atrophy showed statistically significant association with H. pylori infection. However, intestinal metaplasia was inversely associated to this infection and no association was observed with gastric cancer cases. A statistically significant association was found between intestinal metaplasia and vacAs1 and vac Am1 genotypes in patients aged 50 years and more but not in younger. This last genotype is also associated to gastric cancer. In this study, gastric cancer showed no significant association with H. pylori. Further studies are warranted to determine the role of other etiological agents such as Epstein-Barr virus, human papillomavirus and possibly environmental and dietetic factors in the occurrence of this pathology. PMID:24349327

  6. Helicobacter pylori and gastroduodenal pathology: New threats of the old friend

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    Sechi Leonardo A

    2005-01-01

    Full Text Available Abstract The human gastric pathogen Helicobacter pylori causes chronic gastritis, peptic ulcer disease, gastric carcinoma, and mucosa-associated lymphoid tissue (MALT lymphoma. It infects over 50% of the worlds' population, however, only a small subset of infected people experience H. pylori-associated illnesses. Associations with disease-specific factors remain enigmatic years after the genome sequences were deciphered. Infection with strains of Helicobacter pylori that carry the cytotoxin-associated antigen A (cagA gene is associated with gastric carcinoma. Recent studies revealed mechanisms through which the cagA protein triggers oncopathogenic activities. Other candidate genes such as some members of the so-called plasticity region cluster are also implicated to be associated with carcinoma of stomach. Study of the evolution of polymorphisms and sequence variation in H. pylori populations on a global basis has provided a window into the history of human population migration and co-evolution of this pathogen with its host. Possible symbiotic relationships were debated since the discovery of this pathogen. The debate has been further intensified as some studies have posed the possibility that H. pylori infection may be beneficial in some humans. This assumption is based on increased incidence of gastro-oesophageal reflux disease (GERD, Barrett's oesophagus and adenocarcinoma of the oesophagus following H. pylori eradication in some countries. The contribution of comparative genomics to our understanding of the genome organisation and diversity of H. pylori and its pathophysiological importance to human healthcare is exemplified in this review.

  7. Identification of Helicobacter pylori infection in symptomatic patients in Surabaya, Indonesia, using five diagnostic tests.

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    Miftahussurur, M; Shiota, S; Suzuki, R; Matsuda, M; Uchida, T; Kido, Y; Kawamoto, F; Maimunah, U; Adi, P; Rezkitha, Y; Nasronudin; Nusi, I; Yamaoka, Y

    2015-04-01

    SUMMARY The prevalence of Helicobacter pylori infection in Indonesia is controversial. We examined the H. pylori infection rate in 78 patients in a hospital in Surabaya using five different tests, including culture, histology, immunohistochemistry, rapid urease test, and urine antibody test. Furthermore, we analysed virulence factors in H. pylori strains from Indonesia. The H. pylori infection rate was only 11.5% in all patients studied, and 2.3% of Javanese patients and 18.0% of Chinese patients were infected (P = 0.01). Although severe gastritis was not observed, activity and inflammation were significantly higher in patients positive for H. pylori than in patients negative for H. pylori. Among genotypes identified from five isolated strains, cagA was found in four; two were vacA s1m1. All cagA-positive strains were oipA 'on' and iceA1 positive. We confirmed both a low H. pylori infection rate and a low prevalence of precancerous lesions in dyspeptic patients in a Surabaya hospital, which may contribute to the low incidence of gastric cancer in Indonesia.

  8. Role of Regulatory T-cells in Different Clinical Expressions of Helicobacter pylori Infection.

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    Bagheri, Nader; Azadegan-Dehkordi, Fatemeh; Rahimian, Ghorbanali; Rafieian-Kopaei, Mahmoud; Shirzad, Hedayatollah

    2016-05-01

    Helicobacter pylori (H. pylori) colonization induces vigorous innate and specific immune responses; however, the infection does not disappear and a chronic active gastritis continues if left untreated. It has been shown that the topographical pattern and immune response of gastritis are the main reasons for the bacteria persistence and the clinical outcome. Gastritis due to H. pylori is caused by a complicated interaction among a variety of T cell subsets. Regulatory T (Treg) cells suppressing the immune response of antigen-specific T-cells have recently been demonstrated to play a key role in chronic inflammation by immunologic tolerance. Treg cells have been identified as the major regulatory component of the adaptive immune response and being involved in H. pylori-related inflammation and bacterial persistence. There have been many controversies over the role of Treg cells in H. pylori infection. Many studies have shown that the local Treg response protects the gastric mucosa from intensified inflammation and tissue damage, and the risk of H. pylori-associated diseases has an inverse correlation with Treg accumulation, even if the decrease in the inflammatory response is recognized by Treg it causes increase in bacterial density. This paper reviews the role of Treg in different clinical expressions of H. pylori infection.

  9. The Role of Helicobacter pylori Seropositivity in Insulin Sensitivity, Beta Cell Function, and Abnormal Glucose Tolerance

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    Lou Rose Malamug

    2014-01-01

    Full Text Available Infection, for example, Helicobacter pylori (H. pylori, has been thought to play a role in the pathogenesis of type 2 diabetes mellitus (T2DM. Our aim was to determine the role of H. pylori infection in glucose metabolism in an American cohort. We examined data from 4,136 non-Hispanic white (NHW, non-Hispanic black (NHB, and Mexican Americans (MA aged 18 and over from the NHANES 1999-2000 cohort. We calculated the odds ratios for states of glucose tolerance based on the H. pylori status. We calculated and compared homeostatic model assessment insulin resistance (HOMA-IR and beta cell function (HOMA-B in subjects without diabetes based on the H. pylori status. The results were adjusted for age, body mass index (BMI, poverty index, education, alcohol consumption, tobacco use, and physical activity. The H. pylori status was not a risk factor for abnormal glucose tolerance. After adjustment for age and BMI and also adjustment for all covariates, no difference was found in either HOMA-IR or HOMA-B in all ethnic and gender groups except for a marginally significant difference in HOMA-IR in NHB females. H. pylori infection was not a risk factor for abnormal glucose tolerance, nor plays a major role in insulin resistance or beta cell dysfunction.

  10. EGFR tyrosine kinase inhibitory peptide attenuates Helicobacter pylori-mediated hyper-proliferation in AGS enteric epithelial cells

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    Himaya, S.W.A. [Marine Bio-Process Research Center, Pukyong National University, Nam-Gu, Busan, 608-737 (Korea, Republic of); Dewapriya, Pradeep [Department of Chemistry, Pukyong National University, Nam-Gu, Busan, 608-737 (Korea, Republic of); Kim, Se-Kwon, E-mail: sknkim@pknu.ac.kr [Marine Bio-Process Research Center, Pukyong National University, Nam-Gu, Busan, 608-737 (Korea, Republic of); Department of Chemistry, Pukyong National University, Nam-Gu, Busan, 608-737 (Korea, Republic of)

    2013-06-15

    Helicobacter pylori infection is one of the most critical causes of stomach cancer. The current study was conducted to explore the protective effects of an isolated active peptide H-P-6 (Pro-Gln-Pro-Lys-Val-Leu-Asp-Ser) from microbial hydrolysates of Chlamydomonas sp. against H. pylori-induced carcinogenesis. The peptide H-P-6 has effectively suppressed H. pylori-induced hyper-proliferation and migration of gastric epithelial cells (AGS). However, the peptide did not inhibit the viability of the bacteria or invasion into AGS cells. Therefore, the effect of the peptide on regulating H. pylori-induced molecular signaling was investigated. The results indicated that H. pylori activates the EGFR tyrosine kinase signaling and nuclear translocation of the β-catenin. The EGFR activation has led to the up-regulation of PI3K/Akt signaling pathway. Moreover, the nuclear translocation levels of β-catenin were significantly increased as a result of Akt mediated down-regulation of GSK3/β protein levels in the cytoplasm. Both of these consequences have resulted in increased expression of cell survival and migration related genes such as c-Myc, cyclin-D, MMP-2 and matrilysin. Interestingly, the isolated peptide potently inhibited H. pylori-mediated EGFR activation and thereby down-regulated the subsequent P13K/Akt signaling leading to β-catenin nuclear translocation. The effect of the peptide was confirmed with the use of EGFR tyrosine kinase inhibitor AG1487 and molecular docking studies. Collectively this study identifies a potent peptide which regulates the H. pylori-induced hyper-proliferation and migration of AGS cells at molecular level. - Highlights: • Chlamydomonas sp. derived peptide H-P-6 inhibits H. pylori-induced pathogenesis. • H-P-6 suppresses H. pylori-induced hyper-proliferation and migration of AGS cells. • The peptide inhibits H. pylori-induced EGFR activation.

  11. Epidemiology of Helicobacter pylori infection.

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    Leja, Mārcis; Axon, Anthony; Brenner, Hermann

    2016-09-01

    This review of recent publications related to the epidemiology of Helicobacter pylori highlights the origin of the infection, its changing prevalence, transmission, and outcome. A number of studies have addressed the ancestor roots of the bacteria, and the first genomewide analysis of bacterial strains suggests that its coexistence with humans is more ancient than previously thought. As opposed to the generally declining prevalence of H. pylori (including China and Japan), in Sweden, the prevalence of atrophic gastritis in the young population has risen. The prevalence of the infection remains high in the indigenous populations of the Arctic regions, and reinfection rates are high. A high prevalence is permanently found in the Siberian regions of Russia as well. Several studies, some of which used multiplex serology, addressed prevalence of and risks associated with various H. pylori serotypes, thereby enabling more precise risk assessment. Transmission of H. pylori was discussed, specifically fecal-oral transmission and the use of well-water and other unpurified water. Finally, the long-term course of H. pylori infection was considered, with an estimated 89% of noncardia gastric cancer cases being attributable to the infection.

  12. Correlation of Helicobacter pylori and gastric carcinoma.

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    Khanna A

    2002-01-01

    Full Text Available BACKGROUND: Difference of opinion about the prevalence of H. pylori association with gastric cancer exists in the literature. AIMS: To study the correlation of Helicobacter pylori (H. pylori to gastric carcinoma. METHODS: 50 proved cases of gastric cancer were studied by rapid urease test, culture, histopathology and ELISA test for H. pylori IgG. RESULTS: 68% of cases of gastric cancer were found to be positive for H. pylori infection as compared to 74% of healthy controls. CONCLUSIONS: The prevalence rate of H. pylori infection in our patients of gastric cancer was lower than in the control population though statistically not significant, suggesting that H. pylori may not be responsible for gastric carcinogenesis in this population.

  13. Effect of the Vacuolation of Helicobacter Pylori

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    Cytotoxic test in vitro combined with cytochemical stain, fluorescent stain, transmission electronmicrograph was used to study the vacuolated effect by helicobacter pylori (H.pylori) (Toxin+) and its pathological mechanism. 78.26 % patients with peptic ulcer associated with H.pylori was infected with H.pylori (Toxin+), while 42.86 % patients with gastritis was infected with H.pylori (Toxin+). It was positive in vacuole with acridine orange and acid phosphatase stain. Transmission electronmicrograph of vacuole revealed the presence of abounding membrane. There was a closed relationship between infection with H.pylori (Toxin+) and peptic ulcer disease. The vacuole induced by H.pylori (Toxin+) was autophagosome, which was pathological phenomenon induced by toxin.

  14. Helicobacter pylori infection and skin disorders.

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    Kutlubay, Zekayi; Zara, Tuba; Engin, Burhan; Serdaroğlu, Server; Tüzün, Yalçin; Yilmaz, Erkan; Eren, Bülent

    2014-08-01

    Helicobacter pylori is a Gram-negative bacterium that has been linked to peptic ulcer disease, gastric lymphoma, and gastric carcinoma. Apart from its well-demonstrated role in gastroduodenal diseases, some authors have suggested a potential role of Helicobacter pylori infection in several extra-intestinal pathologies including haematological, cardiovascular, neurological, metabolic, autoimmune, and dermatological diseases. Some studies suggest an association between Helicobacter pylori infection and skin diseases such as chronic idiopathic urticaria and rosacea. There have also been few case reports documenting association between Helicobacter pylori and psoriasis vulgaris, Behçet's disease, alopecia areata, Henoch-Schönlein purpura, and Sweet's syndrome. However, more systematic studies are required to clarify the proposed association between Helicobacter pylori and skin diseases; most of the studies do not show relevant relationships of these diseases with Helicobacter pylori infections. This review discusses skin diseases that are believed to be associated with Helicobacter pylori.

  15. Early or late antibiotic intervention prevents Helicobacter pylori-induced gastric cancer in a mouse model.

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    Zhang, Songhua; Lee, Dong Soo; Morrissey, Rhiannon; Aponte-Pieras, Jose R; Rogers, Arlin B; Moss, Steven F

    2014-12-01

    H. pylori infection causes gastritis, peptic ulcers and gastric cancer. Eradicating H. pylori prevents ulcers, but to what extent this prevents cancer remains unknown, especially if given after intestinal metaplasia has developed. H. pylori infected wild-type (WT) mice do not develop cancer, but mice lacking the tumor suppressor p27 do so, thus providing an experimental model of H. pylori-induced cancer. We infected p27-deficient mice with H. pylori strain SS1 at 6-8 weeks of age. Persistently H. pylori-infected WT C57BL/6 mice served as controls. Mice in the eradication arms received antimicrobial therapy (omeprazole, metronidazole and clarithromycin) either "early" (at 15 weeks post infection, WPI) or "late" at 45 WPI. At 70 WPI, mice were euthanized for H. pylori determination, histopathology and cytokine/chemokine expression. Persistently infected mice developed premalignant lesions including high-grade dysplasia, whereas those given antibiotics did not. Histologic activity scores in the eradication groups were similar to each other, and were significantly decreased compared with controls for inflammation, epithelial defects, hyperplasia, metaplasia, atrophy and dysplasia. IP-10 and MIG levels in groups that received antibiotics were significantly lower than controls. There were no significant differences in expression of IFN-γ, TNF-α, IL-1β, RANTES, MCP-1, MIP-1α or MIP-1β among the three groups. Thus, H. pylori eradication given either early or late after infection significantly attenuated gastric inflammation, gastric atrophy, hyperplasia, and dysplasia in the p27-deficient mice model of H. pylori-induced gastric cancer, irrespective of the timing of antibiotic administration. This was associated with reduced expression of IP-10 and MIG.

  16. High efficacy of gemifloxacin-containing therapy in Helicobacter Pylori eradication

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    Mahmoudi, Laleh; Farshad, Shohreh; Seddigh, Mehrdad; Mahmoudi, Paria; Ejtehadi, Fardad; Niknam, Ramin

    2016-01-01

    Abstract Background: Helicobacter pylori (H pylori) is a common gastric pathogen which is associated with chronic gastritis, peptic ulcer, and gastric cancer. It has worldwide distribution with higher incidence in developing countries. Gemifloxacin is a fluoroquinolone antibiotic with documented in vitro activity against H pylori. Considering that there is no clinical data to verify gemifloxacin efficacy in H pylori eradication, this pilot clinical trial was designed. Methods: This prospective pilot study was performed during February 2014 to February 2015. A regimen of gemifloxacin (320 mg single dose) plus twice daily doses of amoxicillin1g, bismuth 240 mg, and omeprazole 20 mg for 14 days were prescribed for H pylori infected patients in whom a first-line standard quadruple therapy (clarithromycin–amoxicillin–bismuth–omeprazole) had failed. To confirm H pylori eradication a 13C-urea breath test was performed 4 weeks after treatment. Compliance and incidence of adverse effects were evaluated by questionnaires. Results: A total of 120 patients were enrolled consecutively; out of which 106 patients achieved H pylori eradication; per-protocol and intention-to-treat eradication rates were 91.4% (95% CI: 85.5–97.6) and 88.3% (95% CI: 75.4–92.4) respectively. Three patients (2.5%) failed to take at least 80% of the drugs and excluded from the final analysis. Adverse effects were reported in 42% of patients, most commonly including nausea (15%) and diarrhea (13.3%), which was intense in 1 patient and led to the discontinuation of treatment. In total, 96.7% (116/120) of the patients took the medications correctly. Conclusion: This study revealed that gemifloxacin-containing quadruple therapy provides high H pylori eradication rate (≥90% PP cure rate), and this agent can be included in the list of second-line H pylori therapeutic regimens. PMID:27759625

  17. Pre-endoscopic screening for Helicobacter pylori and celiac disease in young anemic women

    Institute of Scientific and Technical Information of China (English)

    Lucy Vannella; Debora Gianni; Edith Lahner; Antonio Amato; Enzo Grossi; Gianfranco Delle Fave; Bruno Annibale

    2009-01-01

    AIM:To evaluate the usefulness of pre-endoscopic serological screening for Helicobacter pylori (H pylori) infection and celiac disease in women aged<50 years affected by iron-deficiency anemia (IDA).METHODS:One hundred and fifteen women aged<50 years with IDA were tested by human recombinant tissue transglutaminase IgA antibodies (tTG) and anti- H pylori IgG antibodies.tTG and H pylori IgG antibody were assessed using an enzyme-linked immunosorbent assay (ELISA).All women were invited to undergo upper GI endoscopy.During gastroscopy,biopsies were collected from antrum (n=3),gastric body (n=3) and duodenum (n=4) in all patients,irrespective of test results.The assessment of gastritis was performed according to the Sydney system and celiac disease was classified by Marsh's System.RESULTS:45.2% women were test-positive:41 patients positive for H pylori antibodies,9 patients for tTG and 2 patients for both.The gastroscopy compl iance rate of test-posi t ive women was significantly increased with respect to those testnegative (65.4% vs 42.8%;Fisher test P=0.0239).The serological results were confirmed by gastroscopy in 100% of those with positive H pylori antibodies,in 50% of those with positive tTG and in 81.5% of testnegative patient.Sensitivity and specificity were 84.8% and 100%,respectively for H pylori infection and,80% and 92.8% for tTG.Twenty-eight patients had positive H pylori antibodies and in all the patients,an active H pylori infection was found.In particular,in 23 out of 28 (82%) patients with positive H pylori antibodies,a likely cause of IDA was found because of the active inflammation involving the gastric body.CONCLUSION:Anti- H pylori IgG antibody and tTG IgA antibody testing is able to select women with IDA to submit for gastroscopy to identify H pylori pangastritis and/or celiac disease,likely causes of IDA.2009 The WJG Press and Baishideng.All rights reserved.

  18. A low prevalence of H pylori and endoscopic findings in HTV-positive Chinese patients with gastrointestinal symptoms

    Institute of Scientific and Technical Information of China (English)

    2007-01-01

    AIM: To compare the prevalence of H pylori infection,peptic ulcer, cytomegalovirus (CMV) infection and Candida esophagitis in human immunodeficiency virus (HIV)-positive and HIV-negative patients, and evaluate the impact of CD4 lymphocyte on H pylori and opportunistic infections.METHODS: A total of 151 patients (122 HIV-positive and 29 HIV-negative) with gastrointestinal symptoms were examined by upper endoscopy and biopsy. Samples were assessed to determine the prevalence of H pylori infection,CMV, candida esophagitis and histologic chronic gastritis.RESULTS: The prevalence of H pylori was less common in HIV-positive patients (22.1%) than in HIV-negative controls (44.8%; P < 0.05), and the prevalence of H pylori displayed a direct correlation with CD4 count stratification in HIV-positive patients. In comparison with HIV-negative group, HIV-positive patients had a lower incidence of peptic ulcer (20.7% vs 4.1%; P < 0.01), but a higher prevalence of chronic atrophy gastritis (6.9% vs 24.6%; P < 0.05), Candida esophagitis and CMV infection. Unlike HIV-negative group, H pylori infection had a close relationship to chronic active gastritis (P<0.05). In HIV-positive patients, chronic active gastritis was not significantly different between those with H pylori infection and those without.CONCLUSION: The lower prevalence of H pylori infection and peptic ulcer in HTV-positive patients with gastrointestinal symptoms suggests a different mechanism of peptic ulcerogenesis and a different role of H pylori infection in chronic active gastritis and peptic ulcer.The pathogen of chronic active gastritis in HIV-positive patients may be different from the general population that is closely related to H pylori infection.

  19. Diagnosis of Helicobacter pylori Infection.

    Science.gov (United States)

    Tongtawee, Taweesak; Kaewpitoon, Soraya; Kaewpitoon, Natthawut; Dechsukhum, Chavaboon; Leeanansaksiri, Wilairat; Loyd, Ryan A; Matrakool, Likit; Panpimanmas, Sukij

    2016-01-01

    Helicobacter pylori infection plays an important role in the pathogenesis of chronic gastritis, peptic ulcer disease and gastric malignancy. A diagnosis of infection is thus an important part of a treatment strategy of many gastrointestinal tract diseases. Many diagnostic tests are available but all have some limitations in different clinical situations and laboratory settings. A single gold standard cannot available, but be used for diagnosis of Helicobacter pylori infection in daily clinical practice in all areas, so several techniques have been developed to give reliable results, especially focusing on real time endoscopic features. The narrow band imaging system (NBI) and high resolution endoscopy are imaging techniques for enhanced visualization of infected mucosa and premalignant gastric lesions. The aim of this article is to review the current diagnostic options and possible future developments detection of Helicobacter pylori infection.

  20. Serum Helicobacter pylori NapA antibody as a potential biomarker for gastric cancer

    OpenAIRE

    Jingjing Liu; Huimin Liu; Tingting Zhang; Xiyun Ren; Christina Nadolny; Xiaoqun Dong; Lina Huang; Kexin Yuan; Wenjing Tian; Yunhe Jia

    2014-01-01

    Helicobacter pylori (H. pylori) infection is strongly associated with gastric cancer. However, only a minority of infected individuals ever develop gastric cancer. This risk stratification may be in part due to differences among strains. The relationship between neutrophil-activating protein (NapA) and gastric cancer is unclear. The purpose of this study is to evaluate the significance of NapA as a biomarker in gastric cancer. We used enzyme linked immunosorbent assay (ELISA) to determine the...

  1. Polysorbate 80 and Helicobacter pylori: a microbiological and ultrastructural study

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    Figura Natale

    2012-09-01

    Full Text Available Abstract Background The frequent occurrence of chemoresistant strains reduces the chances of eradication of H. pylori infection and prompted the investigation of non-antibiotic substances active against this organism. Some surfactants enhance the effectiveness of antibiotics for their permeabilizing properties towards bacteria. We examined the antimicrobial activity to H. pylori of the surfactant polysorbate 80, used alone and in association with amoxicillin, clarithromycin, metronidazole, levofloxacin and tetracycline. We also aimed to study the ultrastructural alterations caused upon H. pylori by polysorbate 80, alone and in combination with antibiotics. Twenty-two H. pylori strains were tested using the broth dilution method. After incubation, broth from each dilution was subcultured onto agar enriched with foetal bovine serum to determine the minimum bactericidal concentration (MBC. Synergistic effect of polysorbate 80 with antibiotics was investigated by the broth dilution and disc diffusion techniques. Ultrastructural alterations of organisms treated with polysorbate 80, alone and in association with antibiotics were analyzed by transmission electron microscopy. Results MBCs of polysorbate 80 ranged from 2.6 (1.1 μg/ml to 32 (0 μg/ml. Polysorbate 80 exerted a synergistic effect when associated with metronidazole and clarithromycin: polysorbate 80 and metronidazole MBCs decreased by ≥ 4 fold; clarithromycin MBCs for two resistant strains decreased by 20 and 1000 times. The principal alteration caused by polysorbate 80 consisted in the detachment of the outer membrane of bacteria. Conclusions The bactericidal activity of polysorbate 80 and the synergistic effect of the association with metronidazole and clarithromycin could be useful in the treatment of H. pylori infection.

  2. Lactobacillus acidophilus ameliorates H. pylori-induced gastric inflammation by inactivating the Smad7 and NFκB pathways

    Directory of Open Access Journals (Sweden)

    Yang Yao-Jong

    2012-03-01

    Full Text Available Abstract Background H. pylori infection may trigger Smad7 and NFκB expression in the stomach, whereas probiotics promote gastrointestinal health and improve intestinal inflammation caused by pathogens. This study examines if probiotics can improve H. pylori-induced gastric inflammation by inactivating the Smad7 and NFκB pathways. Results Challenge with H. pylori increased IL-8 and TNF-α expressions but not TGF-β1 in MKN45 cells. The RNA levels of Smad7 in AGS cells increased after H. pylori infection in a dose-dependent manner. A higher dose (MOI 100 of L. acidophilus pre-treatment attenuated the H. pylori-induced IL-8 expressions, but not TGF-β1. Such anti-inflammatory effect was mediated via increased cytoplasmic IκBα and depletion of nuclear NFκB. L. acidophilus also inhibited H. pylori-induced Smad7 transcription by inactivating the Jak1 and Stat1 pathways, which might activate the TGF-β1/Smad pathway. L. acidophilus pre-treatment ameliorated IFN-γ-induced Smad7 translation level and subsequently reduced nuclear NF-κB production, as detected by western blotting. Conclusions H. pylori infection induces Smad7, NFκB, IL-8, and TNF-α production in vitro. Higher doses of L. acidophilus pre-treatment reduce H. pylori-induced inflammation through the inactivation of the Smad7 and NFκB pathways.

  3. 三种抗幽门螺杆菌法治疗复发性口腔溃疡的疗效观察%Effects of three anti-Helicobacter pyloritreatments to recurrent oral ulcer

    Institute of Scientific and Technical Information of China (English)

    唐金菊; 杨永进; 李广

    2014-01-01

    目的:探讨三种抗幽门螺杆菌法治疗复发性口腔溃疡(ROU)的疗效。方法选择幽门螺杆菌唾液测试板(HPS)检测阳性的ROU患者159例,分为A、B、C三组,各组处理措施为:A组:复方氯己定含漱液含漱;B组:A组处理方法+牙周洁治;C组:B组处理方法+三联药物(枸橼酸泌钾颗粒、克拉霉素片、替硝唑片);观察三组患者的治疗期疗效和治疗后3个月疗效。结果三组患者平均溃疡期、疼痛指数和间歇期均有统计学差异(P<0.05),其中C组改善最明显;总溃疡数组间无统计学差异(P>0.05)。结论联合使用含漱液、牙周洁治和三联药物治疗HPS阳性ROU有明显疗效,提示ROU和幽门螺杆菌可能有关。%ObjectiveTo investigate the effects of three anti-H.pylori treatments to recurrent oral ulcer(ROU).Methods159 ROU patients tested positive using H.pylori Saliva Test Cassette (HPS) were collected and divided into group A, B, C. Treatment measures were as follows: group A: compound chlorhexidine gargle; group B: A+periodontal scaling; group C: B+triple-drug (potassium citrate secretion granules, clarithromycin tablets, tinidazole tablets).Results The duration, pain and interval of ulcers of three groups' patients were different (P0.05).Conclusion The combined treatment effect of gargle, periodontal scaling and triple drug therapy for HPS positive ROU patients is significant effect, suggesting ROU and H. pylori may have a relationship.

  4. Dispepsia ed Helicobacter pylori

    Directory of Open Access Journals (Sweden)

    Giovanni Fornaciari

    2003-09-01

    Full Text Available The effect of Helicobacter pylori (HP eradication on functional dyspepsia has been analysed in several clinical trials, including large, controlled and well-designed studies as well as small, flowed studies. The results of these studies indicate that HP infection does not play a major role in the aetiology of this disease and that HP eradication improves dyspeptic symptoms in no more than 15% of patients as compared to placebo. From a practical point of view 15 patients need to be treated for one to benefit while, in duodenal ulcer, 1.4 patient need to be treated for one to benefit. It remains to be elucidated if HP eradication in functional dyspepsia is useful to reduce the risk of developing organic dyspepsia (namely peptic ulcer in functional dyspepsia. In uninvestigated dyspepsia the management of HP infection in primary care has been fully debated.Two therapeutics strategies have been proposed: test and scope and test and treat. The value of test and treat strategy over alternative strategies has been demonstrated in several decision analyses. HP test and scope increases costs in primary care without improving symptoms and saves only 15% of endoscopies.

  5. Possible involvement of put A gene in Helicobacter pylori colonization in the stomach and motility.

    Science.gov (United States)

    Nakajima, Kazuhiko; Inatsu, Sakiko; Mizote, Tomoko; Nagata, Yoko; Aoyama, Kazue; Fukuda, Yoshihiro; Nagata, Kumiko

    2008-02-01

    H. pylori is a gram-negative bacterium associated with gastric inflammation and peptic ulcer and considered a risk factor for gastric cancer in its natural habitat. However, the energy metabolism of H. pylori in the stomach remains to be clarified. H. pylori shows rather high respiratory activity with L-proline and significantly large amounts of L-proline are present in the gastric juice from H. pylori infected patients. We constructed a disrupted mutant of the put A gene, which encodes the proline utilization A (Put A) flavin-linked enzyme, in order to examine the role of put A in the gastric colonization of H. pylori. The put A disrupted mutant, DeltaputA, was constructed by inserting a chloramphenicol resistant gene into put A. DeltaputA did not show respiratory activity using L-proline and could not incorporate L-proline into cells. DeltaputA also did not show motility in response to amino acids and did not display the swarming activity observed with the wild-type. DeltaputA had lost its ability to colonize the stomach of nude mice, an ability possessed by the wild-type. These findings indicate that put A may play an important role in H. pylori colonization on the gastric mucus layer.

  6. Alternative therapies for Helicobacter pylori: probiotics and phytomedicine.

    Science.gov (United States)

    Vítor, Jorge M B; Vale, Filipa F

    2011-11-01

    Helicobacter pylori is a common human pathogen infecting about 30% of children and 60% of adults worldwide and is responsible for diseases such as gastritis, peptic ulcer and gastric cancer. Treatment against H. pylori is based on the use of antibiotics, but therapy failure can be higher than 20% and is essentially due to an increase in the prevalence of antibiotic-resistant bacteria, which has led to the search for alternative therapies. In this review, we discuss alternative therapies for H. pylori, mainly phytotherapy and probiotics. Probiotics are live organisms or produced substances that are orally administrated, usually in addition to conventional antibiotic therapy. They may modulate the human microbiota and promote health, prevent antibiotic side effects, stimulate the immune response and directly compete with pathogenic bacteria. Phytomedicine consists of the use of plant extracts as medicines or health-promoting agents, but in most cases the molecular mode of action of the active ingredients of these herbal extracts is unknown. Possible mechanisms include inhibition of H. pylori urease enzyme, disruption of bacterial cell membrane, and modulation of the host immune system. Other alternative therapies are also reviewed.

  7. Structural Insights into Polymorphic ABO Glycan Binding by Helicobacter pylori.

    Science.gov (United States)

    Moonens, Kristof; Gideonsson, Pär; Subedi, Suresh; Bugaytsova, Jeanna; Romaõ, Ema; Mendez, Melissa; Nordén, Jenny; Fallah, Mahsa; Rakhimova, Lena; Shevtsova, Anna; Lahmann, Martina; Castaldo, Gaetano; Brännström, Kristoffer; Coppens, Fanny; Lo, Alvin W; Ny, Tor; Solnick, Jay V; Vandenbussche, Guy; Oscarson, Stefan; Hammarström, Lennart; Arnqvist, Anna; Berg, Douglas E; Muyldermans, Serge; Borén, Thomas; Remaut, Han

    2016-01-13

    The Helicobacter pylori adhesin BabA binds mucosal ABO/Le(b) blood group (bg) carbohydrates. BabA facilitates bacterial attachment to gastric surfaces, increasing strain virulence and forming a recognized risk factor for peptic ulcers and gastric cancer. High sequence variation causes BabA functional diversity, but the underlying structural-molecular determinants are unknown. We generated X-ray structures of representative BabA isoforms that reveal a polymorphic, three-pronged Le(b) binding site. Two diversity loops, DL1 and DL2, provide adaptive control to binding affinity, notably ABO versus O bg preference. H. pylori strains can switch bg preference with single DL1 amino acid substitutions, and can coexpress functionally divergent BabA isoforms. The anchor point for receptor binding is the embrace of an ABO fucose residue by a disulfide-clasped loop, which is inactivated by reduction. Treatment with the redox-active pharmaceutic N-acetylcysteine lowers gastric mucosal neutrophil infiltration in H. pylori-infected Le(b)-expressing mice, providing perspectives on possible H. pylori eradication therapies.

  8. Helicobacter pylori neutrophil-activating protein induces release of histamine and interleukin-6 through G protein-mediated MAPKs and PI3K/Akt pathways in HMC-1 cells.

    Science.gov (United States)

    Tsai, Chung-Che; Kuo, Ting-Yu; Hong, Zhi-Wei; Yeh, Ying-Chieh; Shih, Kuo-Shun; Du, Shin-Yi; Fu, Hua-Wen

    2015-01-01

    Helicobacter pylori neutrophil-activating protein (HP-NAP) activates several innate leukocytes including neutrophils, monocytes, and mast cells. It has been reported that HP-NAP induces degranulation and interleukin-6 (IL-6) secretion of rat peritoneal mast cells. However, the molecular mechanism is not very clear. Here, we show that HP-NAP activates human mast cell line-1 (HMC-1) cells to secrete histamine and IL-6. The secretion depends on pertussis toxin (PTX)-sensitive heterotrimeric G proteins but not on Toll-like receptor 2. Moreover, HP-NAP induces PTX-sensitive G protein-mediated activation of extracellular signal-regulated kinase 1/2 (ERK1/2), p38-mitogen-activated protein kinase (p38 MAPK), and Akt in HMC-1 cells. Inhibition of ERK1/2, p38 MAPK, or phosphatidylinositol 3-kinase (PI3K) suppresses HP-NAP-induced release of histamine and IL-6 from HMC-1 cells. Thus, the activation of HMC-1 cells by HP-NAP is through Gi-linked G protein-coupled receptor-mediated MAPKs and PI3K/Akt pathways.

  9. Protein interaction network related to Helicobacter pylori infection response

    Institute of Scientific and Technical Information of China (English)

    Kyu Kwang Kim; Han Bok Kim

    2009-01-01

    AIM: To understand the complex reaction of gastric inflammation induced by Helicobacter pylori (H pylori ) in a systematic manner using a protein interaction network. METHODS: The expression of genes significantly changed on microarray during H pylori infection was scanned from the web literary database and translated into proteins. A network of protein interactions was constructed by searching the primary interactions of selected proteins. The constructed network was mathematically analyzed and its biological function was examined. In addition, the nodes on the network were checked to determine if they had any further functional importance or relation to other proteins by extending them.RESULTS: The scale-free network showing the relationship between inflammation and carcinogenesis was constructed. Mathematical analysis showed hub and bottleneck proteins, and these proteins were mostly related to immune response. The network contained pathways and proteins related to H pylori infection, such as the JAK-STAT pathway triggered by interleukins. Activation of nuclear factor (NF)-kB, TLR4, and other proteins known to function as core proteins of immune response were also found.These immune-related proteins interacted on the network with pathways and proteins related to the cell cycle, cell maintenance and proliferation, and transcription regulators such as BRCA1, FOS, REL, and zinc finger proteins. The extension of nodes showed interactions of the immune proteins with cancerrelated proteins. One extended network, the core network, a summarized form of the extended network, and cell pathway model were constructed. CONCLUSION: Immune-related proteins activated by H pylori infection interact with proto-oncogene proteins. The hub and bottleneck proteins are potential drug targets for gastric inflammation and cancer.

  10. Molecular cross-talk between Helicobacter pylori and human gastric mucosa

    Institute of Scientific and Technical Information of China (English)

    Vittorio Ricci; Marco Romano; Patrice Boquet

    2011-01-01

    Helicobacter pylori (H. pylori ) has co-evolved with humans to be transmitted from person to person and to colonize the stomach persistently. A well-choreographed equilibrium between the bacterial effectors and host responses permits microbial persistence and health of the host, but confers a risk for serious diseases including gastric cancer. During its long coexistence with humans, H. pylori has developed complex strategies to limit the degree and extent of gastric mucosal damage and inflammation, as well as immune effector activity. The present editorial thus aims to introduce and comment on major advances in the rapidly developing area of H. pylori /human gastric mucosa interaction (and its pathological sequelae), which is the result of millennia of co-evolution of, and thus of reciprocal knowledge between, the pathogen and its human host.

  11. Cytokines, cytokine gene polymorphisms and Helicobacter pylori infection: friend or foe?

    Science.gov (United States)

    Figueiredo, Camila A; Marques, Cintia Rodrigues; Costa, Ryan dos Santos; da Silva, Hugo Bernardino F; Alcantara-Neves, Neuza M

    2014-05-14

    Helicobacter pylori (H. pylori) is a flagellated, spiral-shaped, microaerophilic Gram-negative bacillus that colonises the gastric mucosa of more than 50% of the human population. Infection is a risk factor for gastritis, ulcer disease and stomach cancer. Immunity against H. pylori is mainly related to Th1/Th17 skewing, and the activation of regulatory T cells is the main strategy used to limit inflammatory responses, which can result in the pathogen persistence and can lead to chronic gastrointestinal diseases, including cancer. Furthermore, host genetic factors that affect cytokines may determine differences in the susceptibility to many diseases. In this review, we present the cytokine profiles and the main cytokine gene polymorphisms associated with resistance/susceptibility to H. pylori and discuss how such polymorphisms may influence infection/disease outcomes.

  12. Effects of fucosylated milk of goat and mouse on Helicobacter pylori binding to Lewis b antigen

    Institute of Scientific and Technical Information of China (English)

    Hong-Tao Xu; Ning Li; Lennart Hammarstr(o)m; Thomas Borén; Rolf Sj(o)str(o)m; Yao-Feng Zhao; Zheng-Xing Lian; Bao-Liang Fan; Zhi-Hui Zhao; Shu-Yang Yu; Yun-Ping Dai; Li-Li Wang; Hui-Ling Niu

    2004-01-01

    AIM: To evaluate the effects of animal milk containing fucosylated antigens on Helicobacter pylori (Hpylori) binding to Lewis b antigen.METHODS: A mammary gland expression vector containing human α1-3/4-fucosyltransferase cDNA sequences was constructed. Transient expression of human α1-3/4-fucosyltransferase cDNA in goat mammary cell and establishment of transgenic mice were performed. The adhesion inhibitory properties of milk samples were analyzed by using H pylori RESULTS: Goat milk samples were found to inhibit bacterial binding to Lewis b antigen. The highest inhibition was observed 42 h after injection of the plasmid. The binding activity of Hpylori to Lewis b antigen reduced mostly, by 83%, however milk samples from transgenic mice did not inhibit H pylori binding to Lewis b antigen.CONCLUSION: The use of "humanized" animal milk produced by the transgenic introduction of fucosylated antigen can perhaps provide an alternative therapy and preventive measure for H pylori infection.

  13. Relationship between full-length sequence characteristics of the vacA gene from high-cytotoxic and low-cytotoxic Helicobacter pylori in China and VacA activities%中国幽门螺杆菌强细胞毒株和弱细胞毒株vacA 基因全长序列特征与VacA活性的关系

    Institute of Scientific and Technical Information of China (English)

    杨泽民

    2011-01-01

    AIM: To evaluate the effect of vacA gene sequence variation on VacA activity by analyzing the full-length sequence of the vacA gene of high- and low-cytotoxic Helicobacter pylori (H. Pylori) strains isolated from China.METHODS: The full-length sequences of the vacA gene of four high- and four low-cytotoxic H. Pylori strains were retrieved from GenBank database and analyzed using three bioinformatic programs (DNAMAN, Lasergene 7.0 and MEGA 5.0).RESULTS: There existed significant sequence variations in the vacA gene among high- and low-cytotoxic H. Pylori strains isolated fromChina and a high-cytotoxic H. Pylori 60190 strain isolated from west country. These variations were mainly concentrated on the p55 domain of the vacA gene, resulting in transitions between hydrophobic and polar amino acids. Several insertion variations were detected in low-cytotoxic H. Pylori strains compared to the H. Pylori 60190 strain. High- and low-cytotoxic strains as well as strains isolated from China and west country-were clustered as different H. Pylori lineages.CONCLUSION: Sequence and insert variation in the vacA gene might be an important reason resulting in VacA activity difference among H. Pylori strains.%目的:探讨中国幽门螺杆菌(Helicobacter pylori,H.pylori )强细胞毒株和弱细胞毒株vacA 基因序列差异对其VacA活性的影响.方法:从GenBank数据库下载4个强细胞毒株和4个弱细胞毒株vacA 基因全长DNA和氨基酸序列,利用DNAMAN、lasergene 7.0、MEGA 5.0 3个生物信息学软件对其进行分析.结果:(1)中国H.pylori 强细胞毒株、弱细胞毒株和西方强细胞毒株60190株3者之间在vacA基因序列上都存在明显的差异,这些差异主要集中在vacA 基因p55结构域,表现为疏水性氨基酸与极性氨基酸之间的转换; (2)弱细胞毒株还存在多个插入变异位点; (3)强细胞毒株和弱细胞毒株,中国和西方分离株在系统发育树中分别聚类为不同的谱系.结论:vacA 基因

  14. Interplay of the Gastric Pathogen Helicobacter pylori with Toll-Like Receptors

    Directory of Open Access Journals (Sweden)

    Suneesh Kumar Pachathundikandi

    2015-01-01

    Full Text Available Toll-like receptors (TLRs are crucial for pathogen recognition and downstream signaling to induce effective immunity. The gastric pathogen Helicobacter pylori is a paradigm of persistent bacterial infections and chronic inflammation in humans. The chronicity of inflammation during H. pylori infection is related to the manipulation of regulatory cytokines. In general, the early detection of H. pylori by TLRs and other pattern recognition receptors (PRRs is believed to induce a regulatory cytokine or chemokine profile that eventually blocks the resolution of inflammation. H. pylori factors such as LPS, HSP-60, NapA, DNA, and RNA are reported in various studies to be recognized by specific TLRs. However, H. pylori flagellin evades the recognition of TLR5 by possessing a conserved N-terminal motif. Activation of TLRs and resulting signal transduction events lead to the production of pro- and anti-inflammatory mediators through activation of NF-κB, MAP kinases, and IRF signaling pathways. The genetic polymorphisms of these important PRRs are also implicated in the varied outcome and disease progression. Hence, the interplay of TLRs and bacterial factors highlight the complexity of innate immune recognition and immune evasion as well as regulated processes in the progression of associated pathologies. Here we will review this important aspect of H. pylori infection.

  15. Accuracy of Helicobacter pylori serology in two peptic ulcer populations and in healthy controls

    Institute of Scientific and Technical Information of China (English)

    Rolv-Ole Lindsetmo; Roar Johnsen; Tor Jac Eide; Tore Gutteberg; Hanne Haukland Husum; Arthur Revhaug

    2008-01-01

    AIM: To estimate the test characteristics of Helicobacter pylori (H pylori) serology and of C14-urea breath test (C14-UBT) in two different peptic ulcer populations and in community controls. Second, the aim was to explore the association between the level of Hpylori IgG antibodies and severity of inflammation as to active peptic ulceration in the same populations.METHODS: Vagotomized (n = 83), medically treated peptic ulcer patients (n = 73) and one reference group of community controls (n = 88) were gastroscoped.H pylori status was determined by histology, bacterial growth, C14-UBT and serology. Based on the updated Sydney System, cumulative scores from biopsies from the prepyloruos, incisura angularis, corpus and fundus were calculated.RESULTS: The prevalence of Hpylori infection varied from 70% to 79%. The C14-UBT had high accuracy compared to the serology test. The sensitivity of the serology test was good, but the specificity was low (41%-71%). The association between H pylori IgG antibodies and scores of gastric mucosal inflammation and current or previous peptic ulcer were weak.CONCLUSION: The accuracy of C14-UBT to diagnose Hpylori infection was good, and the clinical utility of a negative H pylori serology test was substantial, while the gain in clinical information of a positive test was meagre. Positive H pylori titres could not distinguish between subjects with or those without active peptic ulceration.

  16. Differentiation of Helicobacter pylori isolates by polymerase chain reaction-restriction fragment length polymorphism

    Institute of Scientific and Technical Information of China (English)

    SHI Li; SUN Yong; ZHANG Ya-li; ZHANG Zhen-shu; ZHOU Dian-yuan

    2002-01-01

    Objective: To investigate the association between the diversity of urease gene and urease activity of clinical isolates of Helicobacter pylori (H. pylori). Methods: Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) of urease gene and rapid urease activity test were used to study the urease activity of different clinical isolates of H. pylori. Results: H. pylori clinical isolates were divided into 4types according to their PCR-RFLP results of urease gene and urease activity. Type I , possessing strong urease activity (0. 11) and presented 1 fragment of 1.7 kb by PCR-RFLP, had close relations with gastric ulcer; type Ⅱ , with the weakest urease activity (0. 07) and 2 fragments (1.3 and 0. 4 kb respectively), was associated with duodenal bulb ulcer; type Ⅱ , with the strongest urease activity (0. 12) and 2 fragments (0. 4and 0. 17 kb) with or without 1 fragment (0. 23 or 0. 37 kb) , was responsible for gastritis; type Ⅳ, with weak urease activity (0. 09) and 2 fragments (1.5 and 0. 2 kb), was shown to be related to both gastric and duodenal bulb ulcers. Conclusion: The diversity of urease gene decides different urease activities of different clinical isolates of H. pylori, hence the different possibilities of pathogenesis due to this bacteria.

  17. Helicobacter pylori and Peptic Ulcers

    Centers for Disease Control (CDC) Podcasts

    2010-08-17

    In this podcast, CDC's Dr. David Swerdlow discusses the relationship between Helicobacter pylori and peptic ulcer disease and trends in hospitalization rates for peptic ulcer disease in the United States between 1998 and 2005.  Created: 8/17/2010 by National Center for Emerging and Zoonotic Infectious Diseases.   Date Released: 8/17/2010.

  18. Helicobacter pylori and Gastrointestinal Malignancies.

    Science.gov (United States)

    Venerito, Marino; Vasapolli, Riccardo; Rokkas, Theodoros; Malfertheiner, Peter

    2015-09-01

    Helicobacter pylori infection is the principal trigger of gastric carcinogenesis and gastric cancer (GC) and remains the third leading cause of cancer-related death in both sexes worldwide. In a big Japanese study, the risk of developing GC in patients with peptic ulcer disease who received H. pylori eradication therapy and annual endoscopic surveillance for a mean of 9.9 years was significantly lower after successful eradication therapy compared to the group with persistent infection (0.21%/year and 0.45%/year, respectively, p = .049). According to a recent meta-analysis, H. pylori eradication is insufficient in GC risk reduction in subjects with advanced precancerous conditions (i.e., intestinal metaplasia and dysplasia). A microsimulation model suggested screening smokers over the age of 50 in the U.S. for serum pepsinogens. This would allow to detect advanced gastric atrophy with endoscopic follow-up of subjects testing positive as a cost-effective strategy to reduce GC mortality. In a Taiwanese study, the anti-H. pylori IgG-based test-and-treat program had lower incremental cost-effectiveness ratios than that with (13)C-urea breath test in both sexes to prevent GC whereas expected years of life lost for GC were higher and the incremental cost-effectiveness ratios of test-and-treat programs were more cost-effective in young adults (30-69 years old) than in elders (>70 years old). With respect to gastrointestinal malignancies other than GC, a meta-analysis confirmed the inverse association between H. pylori infection and esophageal adenocarcinoma. In a Finnish study, H. pylori seropositivity was associated with an increased risk of biliary tract cancers (multivariate adjusted OR 2.63; 95% CI: 1.08-6.37), another meta-analysis showed a slightly increased rate of pancreatic cancer in patients with CagA-negative strains (OR: 1.30; 95% CI: 1.02-1.65), whereas current data suggest that the association between H. pylori and colorectal neoplasms may be population

  19. H pylori are associated with chronic cholecystitis

    Institute of Scientific and Technical Information of China (English)

    Dong-Feng Chen; Lu Hu; Ping Yi; Wei-Wen Liu; Dian-Chun Fang; Hong Cao

    2007-01-01

    AIM:To study whether H pylori are associated with chronic cholecystitis.METHODS:The subjects were divided into three groups:H pylori-infected cholecystitis group,H pylorinegative cholecystitis group and control group.Pathologic changes of the gallbladder were observed by optic and electronic microscopes and the levels of interleukin-1,6 and 8(IL-1,6 and 8)were detected by radioimmunoassay.RESULTS:Histological evidence of chronic cholecystitis including degeneration,necrosis,inflammatory cell infiltration,were found in the region where H pylori-colonized.Levels of IL-1,6 and 8 in gallbladder mucosa homogenates were significantly higher in H pylori-infected cholecystitis group than those in H pylori-negative cholecystitis group and control group.CONCLUSION:H pylori infection may be related to cholecystitis.

  20. Evaluation on antibiotic resistance of helicobacter pylori isolated from patients admitted to tooba medical center, Sari

    Directory of Open Access Journals (Sweden)

    Amin Talebi BezminAbadi

    2009-01-01

    Full Text Available (Received 17 March, 2009; Accepted 8 July, 2009AbstractBackground and purpose: Helicobacter pylori, which infect approximately one half of the world’s population, are an important risk factor in chronic gastritis, peptic ulcer disease, and gastric cancer. H. pylori eradication is now widely recommended as the most effective treatment of peptic ulcer disease. One of the most important reasons for treatment failure is H. pylori resistance to the antimicrobials usage in therapy. The aim of this study was to determine susceptibility patterns of H. pylori isolates in 6 routine anti-microbial agents in Northern Iran.Materials and methods: 125 patients from Tooba Medical Center in Sari with endoscopic evidence of dyspepsia complaints were used for obtaining gastric biopsies specimens. Biopsies were sent to the laboratory in thioglycolate broth (transport medium. Bacteria were primarily cultured on Columbia agar supplemented with 7% horse blood, 7% fetal calf serum. Urease, Catalase and Oxidase activities were used for H. pylori identification. Bacterial suspensions equivalent to 3 Mc. Farlands were spread on plates, along with antibiotic disks and placed in the diameter zone. Inhibition was measured after 3 days of incubation in micro-aerophilic condition.Results: H. pylori were isolated from 116(92.8% subjects, a total of 125 biopsy specimens. Resistance to metronidazole, amoxicillin, clarithromycin, tetracycline, furazolidone and ciprofloxacin were 71%, 35%, 25%, 9%, 24% and 25%, respectively. Multiple resistance (amoxicillin-clarithromycin-metronidazole were found in (65% of the isolates.Conclusion: Comparison of our data with previous results showed that prevalence of H. pylori resistance to clarithromycin, furazolidone and metronidazole has increased in Iran considerably. Resistance to amoxicillin in our study was too high in comparison with foreign studies. The present study demonstrates the need for continuous monitoring of the antimicrobial

  1. Dietary prevention of Helicobacter pylori-associated gastric cancer with kimchi.

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    Jeong, Migyeong; Park, Jong-Min; Han, Young-Min; Park, Kun Young; Lee, Don Haeng; Yoo, Joon-Hwan; Cho, Joo Young; Hahm, Ki-Baik

    2015-10-06

    To prove whether dietary intervention can prevent Helicobacter pylori-induced atrophic gastritis and gastric cancer, we developed cancer preventive kimchi (cpKimchi) through special recipe and administered to chronic H. pylori-initiated, high salt diet-promoted, gastric tumorigenesis mice model. H. pylori-infected C57BL/6 mice were administered with cpKimchi mixed in drinking water up to 36 weeks. Gross and pathological gastric lesions were evaluated after 24 and 36 weeks, respectively and explored underlying molecular changes to explain efficacies. Cancer preventive actions of anti-inflammation and anti-mutagenesis were compared between standard recipe kimchi (sKimchi) and special recipe cpKimchi in in vitro H. pylori-infected cell model. The erythematous and nodular changes, mucosal ulcerative and erosive lesions in the stomach were noted at 24th weeks, but cpKimchi administration significantly ameliorated. After 36th weeks, scattered nodular masses, some ulcers, and thin nodular gastric mucosa were noted in H. pylori-infected mice, whereas these gross lesions were significantly attenuated in cpKimchi group. On molecular analysis, significant expressions of COX-2 and IL-6, activated NF-κB and STAT3, increased apoptosis, and marked oxidative stresses were noted in H. pylori-infected group relevant to tumorigenesis, but these were all significantly attenuated in cpKimchi group. cpKimchi extracts imparted significant selective induction of apoptosis only in cancer cells, led to inhibition of H. pylori-induced proliferation, while no cytotoxicity through significant HO-1 induction in non-transformed gastric cells. In conclusion, daily dietary intake of cpKimchi can be an effective way either to rejuvenate H. pylori-atrophic gastritis or to prevent tumorigenesis supported with the concerted actions of anti-oxidative, anti-inflammatory, and anti-mutagenic mechanisms.

  2. HELICOBACTER PYLORI-RELATED GASTRITIS AND LYMPHOID TISSUE HYPERPLASIA IN THE AGED

    Institute of Scientific and Technical Information of China (English)

    高天; 陈晓宇; 胡梅洁

    2003-01-01

    Objective To examine the relationship between Helicobacter pylori-related gastritis and the development of lymphoid tissue hyperplasia in the antral mucosa and to pursue its evolution after eradication of H.pylori in the aged. Methods Gastric antral mucosa biopsy specimens for microscopic study were obtained from 101 chronic gastritis patients over 60 years old with H.pylori-positive in the period from 2000 to 2001, and meanwhile those from 124 H.pylori-positive chronic gastritis patients under the age of 60 served as controls. Four to six weeks after a course of anti-H.pylori therapy, biopsy specimens were again obtained. Lym-phoid follicles and aggregates were counted and other pathologic features were scored according to the updated Sydney System for classification of chronic gastritis. Results The prevalence and density of lymphoid follicles and aggregates were significantly lower in the aged as compared with those in the control group, being 36. 6%(37/101) and 0. 41 vs. 72. 5%(90/124) and 0. 81, respectively(P<0.0001). The prevalence and density of lymphoid follicles and aggregates correlated strongly with the activity and severity of gastric antral mucosal inflammation in both groups. Eradication of H.pylori resulted in a decrease in the prevalence and density of lymphoid follicles and aggregates in both groups, especially in the aged group. Conclusion The prevalence and density of lymphoid follicles and aggregates in gastric antral mucosal biopsies correlated closely with H.phlori infection in the aged, therefore, anti-H.pylori treatment would be of importance to the aged patients infected with H.pylori.

  3. 3rd Brazilian Consensus on Helicobacter pylori.

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    Coelho, Luiz Gonzaga; Maguinilk, Ismael; Zaterka, Schlioma; Parente, José Miguel; do Carmo Friche Passos, Maria; Moraes-Filho, Joaquim Prado P

    2013-04-01

    Signicant progress has been obtained since the Second Brazilian Consensus Conference on Helicobacter pylori Infection held in 2004, in São Paulo, SP, Brazil, and justify a third meeting to establish updated guidelines on the current management of H. pylori infection. The Third Brazilian Consensus Conference on H pylori Infection was organized by the Brazilian Nucleus for the Study of Helicobacter, a Department of the Brazilian Federation of Gastroenterology and took place on April 12-15, 2011, in Bento Gonçalves, RS, Brazil. Thirty-one delegates coming from the five Brazilian regions and one international guest, including gastroenterologists, pathologists, epidemiologists, and pediatricians undertook the meeting. The participants were allocated in one of the five main topics of the meeting: H pylori, functional dyspepsia and diagnosis; H pylori and gastric cancer; H pylori and other associated disorders; H pylori treatment and retreatment; and, epidemiology of H pylori infection in Brazil. The results of each subgroup were submitted to a final consensus voting to all participants. Relevant data were presented, and the quality of evidence, strength of recommendation, and level of consensus were graded. Seventy per cent and more votes were considered as acceptance for the final statement. This article presents the main recommendations and conclusions to guide Brazilian doctors involved in the management of H pylori infection.

  4. 3rd BRAZILIAN CONSENSUS ON Helicobacter pylori

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    Luiz Gonzaga Coelho

    2013-04-01

    Full Text Available Significant progress has been obtained since the Second Brazilian Consensus Conference on Helicobacter pylori Infection held in 2004, in São Paulo, SP, Brazil, and justify a third meeting to establish updated guidelines on the current management of H. pylori infection. The Third Brazilian Consensus Conference on H pylori Infection was organized by the Brazilian Nucleus for the Study of Helicobacter, a Department of the Brazilian Federation of Gastroenterology and took place on April 12-15, 2011, in Bento Gonçalves, RS, Brazil. Thirty-one delegates coming from the five Brazilian regions and one international guest, including gastroenterologists, pathologists, epidemiologists, and pediatricians undertook the meeting. The participants were allocated in one of the five main topics of the meeting: H pylori, functional dyspepsia and diagnosis; H pylori and gastric cancer; H pylori and other associated disorders; H pylori treatment and retreatment; and, epidemiology of H pylori infection in Brazil. The results of each subgroup were submitted to a final consensus voting to all participants. Relevant data were presented, and the quality of evidence, strength of recommendation, and level of consensus were graded. Seventy per cent and more votes were considered as acceptance for the final statement. This article presents the main recommendations and conclusions to guide Brazilian doctors involved in the management of H pylori infection.

  5. Helicobacter Pylori Seropostivity of Colon Cancer

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    F. Tugba Kos

    2014-03-01

    Full Text Available Aim: Until now many researches have showed that Helicobacter pylori infection may be etiological factor of colorectal cancer. The aim of current study was to investigate the frequency of H.pylori infection seropositivity of colorectal cancer patients and compare the clinicopathological features of H.pylori positive patients with negative ones. Material and Method: Seventy four colorectal patients were included in study. Retrospectively, patients clinical features, surgery history and pathological characteristics were screened. Patients group serum samples were collected. H.pylori Ig G level were quantitatively measured with ELISA method and levels above 5 arbU/ml were accepted as seropositive. Results: Patients median age was 60.5 ( range 26-83 and 56.8% (n=42 were male. H.pylori Ig G was positive in 37.8% (n=28 and negative in 62.2% (n=46 of patient group. H.pylori serpositive and negative patients median age of diagnosis were 56 and 64 respectively (p=0.01. There were no significant difference between H.pylori seropositive group when compared with negative group according to age, level of CEA and Ca 19-9, stage, lymph node involvement, perineural and vascular invasion, presence of polyps, differantion, localisation of tumours. Discussion: H.pylori seropositive patients were diagnosed at younger age. Association of this finding with etiology was confusing. Further studies with healthy controls may provide detailed information about whether H.pylori seropositivity is associated with colorectal cancer etiology.

  6. Helicobacter pylori filtrate impairs spatial learning and memory in rats and increases β-amyloid by enhancing expression of presenilin-2

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    Xiu-Lian eWang

    2014-04-01

    Full Text Available Helicobacter pylori (H.pylori infection is related with a high risk of Alzheimer’s Disease (AD, but the intrinsic link between H.pylori infection and AD development is still missing. In the present study, we explored the effect of H.pylori infection on cognitive function and β-amyloid production in rats. We found that intraperitoneal injection of H.pylori filtrate induced spatial learning and memory deficit in rats with a simultaneous retarded dendritic spine maturation in hippocampus. Injection of H.pylori filtrate significantly increased Aβ42 both in the hippocampus and cortex, together with an increased level of presenilin-2 (PS-2, one key component of γ-secretase involved in Aβ production. Incubation of H.pylori filtrate with N2a cells which over-express APP also resulted in increased PS-2 expression and Aβ42 overproduction. Injection of Escherichia coli (E.coli filtrate, another common intestinal bacterium, had no effect on cognitive function in rats and Aβ production in rats and cells. These data suggest a specific effect of H.pylori on cognition and Aβ production. We conclude that soluble surface fractions of H.pylori may promote Aβ42 formation by enhancing the activity of γ-secretase, thus induce cognitive impairment through interrupting the synaptic function.

  7. Genotyping analysis of Helicobacter pylori using multiple-locus variable-number tandem-repeats analysis in five regions of China and Japan

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    Zhang Jinyong

    2011-09-01

    Full Text Available Abstract Background H. pylori (Helicobacter pylori is the major causative agent of chronic active gastritis. The population of H. pylori shows a high genomic variability among isolates. And the polymorphism of repeat-units of genomics had participated the important process of evolution. Its long term colonization of the stomach caused different clinical outcomes, which may relate to the high degree of genetic variation of H. pylori. A variety of molecular typing tools have been developed to access genetic relatedness in H. pylori isolates. However, there is still no standard genotyping system of this bacterium. The MLVA (Multi-locus of variable number of tandem repeat analysis method is useful for performing phylogenetic analysis and is widely used in bacteria genotyping; however, there's little application in H. pylori analysis. This article is the first application of the MLVA method to investigate H. pylori from different districts and ethnic groups of China. Results MLVA of 12 VNTR loci with high discrimination power based on 30 candidates were performed on a collection of 202 strains of H. pylori which originated from five regions of China and Japan. Phylogenetic tree was constructed using MLVA profiles. 12 VNTR loci presented with high various polymorphisms, and the results demonstrated very close relationships between genotypes and ethnic groups. Conclusions This study used MLVA methodology providing a new perspective on the ethnic groups and distribution characteristics of H. pylori.

  8. Regulatory B Cell Function Is Suppressed by Smoking and Obesity in H. pylori-Infected Subjects and Is Correlated with Elevated Risk of Gastric Cancer.

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    Li, Guanggang; Wulan, Hasi; Song, Zongchang; Paik, Paul A; Tsao, Ming L; Goodman, Gary M; MacEachern, Paul T; Downey, Robert S; Jankowska, Anna J; Rabinowitz, Yaron M; Learch, Thomas B; Song, David Z; Yuan, Ji J; Zheng, Shihang; Zheng, Zhendong

    2015-01-01

    Helicobacter pylori infection occurs in more than half of the world's population and is the main cause for gastric cancer. A series of lifestyle and nutritional factors, such as tobacco smoking and obesity, have been found to elevate the risk for cancer development. In this study, we sought to determine the immunological aspects during H. pylori infection and gastric cancer development. We found that B cells from H. pylori-infected patients presented altered composition and function compared to uninfected patients. IL-10-expressing CD24+CD38+ B cells were upregulated in H. pylori-infected patients, contained potent regulatory activity in inhibiting T cell pro-inflammatory cytokine secretion, and responded directly to H. pylori antigen stimulation. Interestingly, in H. pylori-infected smoking subjects and obese subjects, the number of IL-10+ B cells and CD24+CD38+ B cells were reduced compared to H. pylori-infected asymptomatic subjects. Regulatory functions mediated by CD24+CD38+ B cells were also impaired. In addition, gastric cancer positive patients had reduced IL-10-producing B cell frequencies after H. pylori-stimulation. Altogether, these data suggest that in H. pylori-infection, CD24+CD38+ B cell is upregulated and plays a role in suppressing pro-inflammatory responses, possibly through IL-10 production, a feature that was not observed in smoking and obese patients.

  9. Tnfluence of various proton pump inhibitors on intestinal metaplasia in noneradicated Helicobacter pylori patients

    Institute of Scientific and Technical Information of China (English)

    Marinko Marusic; Zarko Babic; Mirjana Nesanovic; Mira Lucijanic-Mlinac,; Vesna Stajcar

    2005-01-01

    AIM: Intestinal metaplasia (IM) is more often found in patients with Helicobacter pylori(H pylori) infection, while eradication of H pylori results in significant reduction in the severity and activity of chronic gastritis. We aimed to determine in patients with unsuccessful eradication of H pylori the role of various proton pump inhibitors (PPIs)having different mechanisms in the resolution of IM.METHODS: We confirmed endoscopically and pathohistologically (Sydney classification) the IM in 335 patients with gastritis before and after medication for eradication of H pylori(Maastricht Protocol 2002). H pylori infection was determined by using histology, urease test and culture. Control endoscopy and histology were done after 30 d and thereafter (within 1 year). Unsuccessful eradication was considered if only one of the three tests (histology, urease and culture) was negative after therapy protocol. We used omeprazole, pantoprazole,lansoprazole in therapy protocols (in combination with two antibiotics).RESULTS: We found no significant difference in resolution of IM by using different PPI between the groups of eradicated and noneradicated patients (P<0.4821 and P<0.4388,respectively).CONCLUSION: There is no significant difference in resolution of intestinal metaplasia by different proton pump inhibitors.

  10. Review: Pharmacological ins and outs of medicinal plants against Helicobacter pylori: A review.

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    Zaidi, Syed Faisal; Muhammad, Jibran Sualeh; Usmanghani, Khan; Sugiyama, Toshiro

    2015-05-01

    Since Helicobacter pylori was discovered in 1980, it has been considered as a major cause in the pathogenesis of gastric ulcer, mucosa-associated lymphoid tissue (MALT) lymphomas, and gastric cancer. Eventually antibiotics were designed to eradicate this bacterium, which not only prevent peptic ulcer recurrence but also decrease the chances of developing gastric cancer. Propitious consequences of these antibiotic regimens and better hygienic conditions, particularly in developed countries, resulted in significant decline in the prevalence of H. pylori infection. However, persistent high H. pylori infection in developing countries, decreased patience compliance and emerging antibiotic resistance forced researchers to quest for novel candidates. Herbal medicines have always served as a leading source in drug discovery. Since time immemorial, herbs have been used to treat various disorders covering from minor illnesses as pain to life threatening conditions like cancer. Ample amount of studies from different parts of the world have shown promising activities of medicinal herbs not only against H. pylori but also associated disorders while employing in vitro, in vivo and clinical studies. In this review, these multiple pharmacological effects of medicinal plants and their chemical constituents will be discussed in relation to H. pylori not only to scientifically evaluate the beneficial effects of these medicinal plants but to also critically analyze their plausible role as chemo preventive agents against H. pylori-associated disorders.

  11. Helicobacter pylori: epidemiology and routes of transmission.

    Science.gov (United States)

    Brown, L M

    2000-01-01

    H. pylori is a common bacterium, and approximately 50 percent of the world's population has been estimated to be infected (198). Humans are the principal reservoir. The prevalence of H. pylori infection varies widely by geographic area, age, race, ethnicity, and SES. Rates appear to be higher in developing than in developed countries, with most of the infections occurring during childhood, and they seem to be decreasing with improvements in hygiene practices. H. pylori causes chronic gastritis and has been associated with several serious diseases of the gastrointestinal tract, including duodenal ulcer and gastric cancer. Since its "discovery" in 1982 by Warren and Marshall (1), H. pylori has been the topic of extensive research. A number of studies have used questionnaire components to investigate factors possibly related to the etiology of H. pylori infection. The majority of recent studies have not found tobacco use or alcohol consumption to be risk factors for H. pylori infection. Adequate nutritional status, especially frequent consumption of fruits and vegetables and of vitamin C, appears to protect against infection with H. pylori. In contrast, food prepared under less than ideal conditions or exposed to contaminated water or soil may increase the risk. Overall, inadequate sanitation practices, low social class, and crowded or high-density living conditions seem to be related to a higher prevalence of H. pylori infection. This finding suggests that poor hygiene and crowded conditions may facilitate transmission of infection among family members and is consistent with data on intrafamilial and institutional clustering of H. pylori infection. Understanding the route of H. pylori transmission is important if public health measures to prevent its spread are to be implemented. Iatrogenic transmission of H. pylori following endoscopy is the only proven mode. For the general population, the most likely mode of transmission is from person to person, by either the

  12. Helicobacter pylori Disrupts Host Cell Membranes, Initiating a Repair Response and Cell Proliferation

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    Hsueh-Fen Juan

    2012-08-01

    Full Text Available Helicobacter pylori (H. pylori, the human stomach pathogen, lives on the inner surface of the stomach and causes chronic gastritis, peptic ulcer, and gastric cancer. Plasma membrane repair response is a matter of life and death for human cells against physical and biological damage. We here test the hypothesis that H. pylori also causes plasma membrane disruption injury, and that not only a membrane repair response but also a cell proliferation response are thereby activated. Vacuolating cytotoxin A (VacA and cytotoxin-associated gene A (CagA have been considered to be major H. pylori virulence factors. Gastric cancer cells were infected with H. pylori wild type (vacA+/cagA+, single mutant (ΔvacA or ΔcagA or double mutant (ΔvacA/ΔcagA strains and plasma membrane disruption events and consequent activation of membrane repair components monitored. H. pylori disrupts the host cell plasma membrane, allowing localized dye and extracellular Ca2+ influx. Ca2+-triggered members of the annexin family, A1 and A4, translocate, in response to injury, to the plasma membrane, and cell surface expression of an exocytotic maker of repair, LAMP-2, increases. Additional forms of plasma membrane disruption, unrelated to H. pylori exposure, also promote host cell proliferation. We propose that H. pylori activation of a plasma membrane repair is pro-proliferative. This study might therefore provide new insight into potential mechanisms of H. pylori-induced gastric carcinogenesis.

  13. Novel epidermal growth factor receptor pathway mediates release of human β-defensin 3 from Helicobacter pylori-infected gastric epithelial cells.

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    Muhammad, Jibran S; Zaidi, Syed F; Zhou, Yue; Sakurai, Hiroaki; Sugiyama, Toshiro

    2016-04-01

    Persistent Helicobacter pylori (H. pylori) infection in hostile gastric mucosa can result in gastric diseases. Helicobacter pylori induces to express antimicrobial peptides from gastric epithelial cells, especially human β-defensin 3 (hBD3), as an innate immune response, and this expression of hBD3 is mediated by epidermal growth factor receptor (EGFR) activation. In this study, we found that phosphorylation of a serine residue of EGFR via transforming growth factor β-activated kinase-1 (TAK1), and subsequent p38α activation is essential for H. pylori-induced hBD3 release from gastric epithelial cells. We showed that this pathway was dependent on H. pylori type IV secretion system and was independent of H. pylori-derived CagA or peptidoglycan. H. pylori infection induced phosphorylation of serine residue of EGFR, and this phosphorylation was followed by internalization of EGFR; consequently, hBD3 was released at an early phase of the infection. In the presence of TAK1 or p38α inhibitors, synthesis of hBD3 was completely inhibited. Similar results were observed in EGFR-, TAK1- or p38α-knockdown cells. However, NOD1 knockdown in gastric epithelial cells did not inhibit hBD3 induction. Our study has firstly demonstrated that this novel EGFR activating pathway functioned to induce hBD3 at an early phase of H. pylori infection.

  14. Characterization of the Vacuolating Cytotoxin in Helicobacter pylori Strains Isolated from Iran

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    Akbar Oghalaie

    2010-01-01

    Full Text Available Objective: Helicobacter pylori (H. pylori cytotoxin and its heterogeneity amongst strains hasbeen closely linked to the varying infection-associated clinical outcomes. In order to determinethe decisive role of the vacuolating cytotoxin (vacA gene mosaicism in its corresponding geneexpression and phenotype, we aimed to characterize vacA alleles of different H. pylori strainsin addition to the resulting protein and its vacuolating activity in epithelial cell culture.Materials and Methods: vacA gene polymorphism was determined for 80 H. pylori strainsisolated from dyspeptic patients, using multiplex gene-specific polymerase chain reaction(PCR. VacA protein was detected by immuno-blotting assay using a polyclonal anti-VacAantibody. In vitro cytotoxicity assay was conducted on HeLa cells in order to evaluate thevacuolating cytotoxin activity.Results: Genotyping revealed the following strain distribution: 26 (32.5% s1m1, 35(43.8% s1m2, and 19 (23.8% s2m2 subtypes. Infection with s1m1 type strain was significantlyassociated with gastric cancer as compared to non-ulcer dyspepsia (p=0.005and peptic ulcer disease (p=0.008. A 95-kDa immuno-reactive band that represented thevacuolating toxin was demonstrated in SDS-PAGE analysis of concentrated culture filtrate(CCF of H. pylori strains. H. pylori CCFs induced HeLa cell vacuolation which correlatedwith the strain genotype; s1m1 strains demonstrated higher levels of vacuolation as comparedto s1m2 strains, whereas s2m2 strains showed no detectable cytotoxic activity.Conclusion: The current study confirmed the relatively high cytotoxic activity of s1m1type H. pylori strains which infect the majority of patients suffering from gastric cancer andmay be partly responsible for the pathogenesis of this mortal disease.

  15. Epidemiology of Helicobacter pylori and gastric cancer.

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    Kikuchi, Shogo

    2002-01-01

    Findings in epidemiological studies of the relationship between Helicobacter pylori and gastric cancer have been inconsistent: many studies have yielded a positive relationship, whereas several studies have shown no relationship. The inconsistency arises because of the occurrence of seroreversion during the period between the time that H. pylori exerts a carcinogenic effect and the time of blood sampling. When this seroreversion is taken into account, there is an epidemiologically positive association between H. pylori status and the risk for gastric cancer. In addition to the epidemiological evidence, experimental studies using Mongolian gerbils have shown that H. pylori infection elevates the risk for gastric cancer. It is concluded that H. pylori is a causal factor for gastric cancer. In the creation of preventive strategies against gastric cancer by the eradication of H. pylori, determination of the time at which H. pylori plays a role as a carcinogen is important. Three hypotheses have been proposed in regard to this timing: that H. pylori infection in childhood or the teenage years acts as a factor that produces precancerous lesions with irreversible damage in the gastric mucosa, that in adulthood it acts as an initiator, and also in adulthood, that it acts as a promoter. As these hypotheses are not mutually exclusive, the extent to which each hypothesis plays a part in explaining gastric carcinogenesis should be evaluated. Only a small proportion of subjects infected with H. pylori have gastric cancer during their lifetime. Interleukin-1 polymorphism, a host factor, and CagA, a virulence factor of H. pylori, are suspected to be risk factors for gastric cancer in subjects with H. pylori infection. Dietary factors, especially vitamin C, and patterns of precancerous lesions also seem to influence the relationship between H. pylori and gastric cancer. H. pylori seems to reduce the risk for esophageal and for some gastric cardia adenocarcinomas. This finding, as

  16. Ammonium Metabolism Enzymes Aid Helicobacter pylori Acid Resistance

    OpenAIRE

    2014-01-01

    The gastric pathogen Helicobacter pylori possesses a highly active urease to support acid tolerance. Urea hydrolysis occurs inside the cytoplasm, resulting in the production of NH3 that is immediately protonated to form NH4+. This ammonium must be metabolized or effluxed because its presence within the cell is counterproductive to the goal of raising pH while maintaining a viable proton motive force (PMF). Two compatible hypotheses for mitigating intracellular ammonium toxicity include (i) th...

  17. Helicobacter pylori colonization of the oral cavity: A milestone discovery.

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    Yee, John K C

    2016-01-14

    Over the past several years, the severity of Helicobacter pylori (H. pylori) infections has not significantly diminished. After successful eradication, the annual H. pylori recurrence rate is approximately 13% due to oral H. pylori infection. Established clinical diagnostic techniques do not identify an oral etiologic basis of H. pylori prior to gastric infection. There has been disagreement as to whether oral infection of H. pylori exists or not, with no definite conclusion. In medical practice, negative results with the urea breath test suggest that the stomach infection of H. pylori is cured in these patients. In fact, patients can present negative urea breath test results and yet exhibit H. pylori infection due to oral infection. The present paper provides evidence that H. pylori oral infection is nonetheless present, and the oral cavity represents a secondary site for H. pylori colonization.

  18. Current knowledge on alleviating Helicobacter pylori infections through the use of some commonly known natural products: bench to bedside

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    Malliga Raman Murali

    2014-09-01

    Full Text Available Helicobacter pylori, a spiral-shaped Gram-negative bacterium, has been classified as a class I carcinogen by the World Health Organization and recognized as the causative agent for peptic ulcers, duodenal ulcer, gastritis, mucosa-associated lymphoid tissue lymphomas, and gastric cancer. Owing to their alarming rate of drug resistance, eradication of H. pylori remains a global challenge. Triple therapy consisting of a proton pump inhibitor, clarithromycin, and either amoxicillin or metronidazole, is generally the recommended standard for the treatment of H. pylori infection. Complementary and alternative medicines have a long history in the treatment of gastrointestinal ailments and various compounds has been tested for anti-H. pylori activity both in vitro and in vivo; however, their successful use in human clinical trials is sporadic. Hence, the aim of this review is to analyze the role of some well-known natural products that have been tested in clinical trials in preventing, altering, or treating H. pylori infections. Whereas some in vitro and in vivo studies in the literature have demonstrated the successful use of a few potential natural products for the treatment of H. pylori-related infections, others indicate a need to consider natural products, with or without triple therapy, as a useful alternative in treating H. pylori-related infections. Thus, the reported mechanisms include killing of H. pylori urease inhibition, induction of bacterial cell damage, and immunomodulatory effect on the host immune system. Furthermore, both in vitro and in vivo studies have demonstrated the successful use of some potential natural products for the treatment of H. pylori-related infections. Nevertheless, the routine prescription of potential complementary and alternative medicines continues to be restrained, and evidence on the safety and efficacy of the active compounds remains a subject of ongoing debate.

  19. Helicobacter pylori Outer Membrane Protein 18 (Hp1125 Is Involved in Persistent Colonization by Evading Interferon-γ Signaling

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    Yuqun Shan

    2015-01-01

    Full Text Available Outer membrane proteins (OMPs can induce an immune response. Omp18 (HP1125 of H. pylori is a powerful antigen that can induce significant interferon-γ (IFN-γ levels. Previous studies have suggested that IFN-γ plays an important role in H. pylori clearance. However, H. pylori has multiple mechanisms to avoid host immune surveillance for persistent colonization. We generated an omp18 mutant (H. pylori 26695 and H. pylori SS1 strain to examine whether Omp18 interacts with IFN-γ and is involved in H. pylori colonization. qRT-PCR revealed that IFN-γ induced Omp18 expression. qRT-PCR and western blot analysis revealed reduced expressions of virulence factors CagA and NapA in H. pylori 26695 with IFN-γ treatment, but they were induced in the Δomp18 strain. In C57BL/6 mice infected with H. pylori SS1 and the Δomp18 strain, the Δomp18 strain conferred defective colonization and activated a stronger inflammatory response. Signal transducer phosphorylation and transcription 1 (STAT1 activator was downregulated by the wild-type strain but not the Δomp18 strain in IFN-γ-treated macrophages. Furthermore, Δomp18 strain survival rates were poor in macrophages compared to the wild-type strain. We concluded that H. pylori Omp18 has an important function influencing IFN-γ-mediated immune response to participate in persistent colonization.

  20. A novel chimeric flagellum fused with the multi-epitope vaccine CTB-UE prevents Helicobacter pylori-induced gastric cancer in a BALB/c mouse model.

    Science.gov (United States)

    Song, Hui; Lv, Xiaobo; Yang, Jue; Liu, Wei; Yang, Huan; Xi, Tao; Xing, Yingying

    2015-11-01

    Helicobacter pylori (H. pylori) infection causes peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue (MALT) lymphoma. The eradication of H. pylori might be an effective means of preventing gastric cancer. A dual-antigen epitope and dual-adjuvant vaccine called CTB-UE-CF (CCF) was constructed by combining a multi-epitope vaccine CTB-UE with a novel chimeric flagellum (CF) to simultaneously activate Toll-like receptor (TLR) 5-agonist activity and preserve the immunogenicity of H. pylori flagellum FlaA. The evaluation of efficacy to reduce H. pylori colonization was performed using BALB/c mice by oral immunization with a triple dose of this vaccine strain. Two weeks after the last immunization, mice were sacrificed to determine specific antibody levels and proinflammatory cytokine production. To determine the presence of H. pylori, we detected the number of H. pylori by real-time quantitative PCR (qPCR) and measured the urease activity in the gastric tissue. The results showed that the immunogenicity and mucosal immune responses of CCF performed significantly better than those of CTB-UE. This dual-antigen epitope and dual-adjuvant system might greatly contribute to the development of a safe and efficient therapeutic vaccine for humans against H. pylori infection.

  1. The Development of Urease Inhibitors: What Opportunities Exist for Better Treatment of Helicobacter pylori Infection in Children?

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    Hassan, Sherif T. S.; Šudomová, Miroslava

    2017-01-01

    Stomach infection with Helicobacter pylori (H. pylori) causes severe gastroduodenal diseases in a large number of patients worldwide. The H. pylori infection breaks up in early childhood, persists lifelong if not treated, and is associated with chronic gastritis and an increased risk of peptic ulcers and gastric cancer. In recent years, the problem of drug-resistant strains has become a global concern that makes the treatment more complicated and the infection persistent at higher levels when the antibiotic treatment is stopped. Such problems have led to the development of new strategies to eradicate an H. pylori infection. Currently, one of the most important strategies for the treatment of H. pylori infection is the use of urease inhibitors. Despite the fact that large numbers of molecules have been shown to exert potent inhibitory activity against H. pylori urease, most of them were prevented from being used in vivo and in clinical trials due to their hydrolytic instability, toxicity, and appearance of undesirable side effects. Therefore, it is crucial to focus attention on the available opportunities for the development of urease inhibitors with suitable pharmacokinetics, high hydrolytic stability, and free toxicological profiles. In this commentary, we aim to afford an outline on the current status of the use of urease inhibitors in the treatment of an H. pylori infection, and to discuss the possibility of their development as effective drugs in clinical trials. PMID:28054971

  2. A five-year follow-up study on the pathological changes of gastric mucosa after H.pylori eradication

    Institute of Scientific and Technical Information of China (English)

    周丽雅; 沈祖尧; 林三仁; 金珠; 丁士刚; 黄雪彪; 夏志伟; 郭慧兰; 刘建军; 曹世植

    2003-01-01

    Objectives To investigate the relationship between H.pylori infection, gastric cancer and other gastric diseases through the changes in gastric mucosa and the status of different gastric diseases within 5 years after H.pylori eradication in H.pylori-positive subjects in a high incidence region of gastric cancer. Methods One thousand and six adults were selected from the general population in Yantai, Shandong province, a high incidence region for gastric cancer in China. Gastroscopy and Campylobacter-like organism (CLO) testing were performed on all subjects. Biopsy samples from the gastric antrum and body were obtained for histology and assessment of H.pylori infection. All H.pylori-positive subjects were then randomly divided into two groups: treatment group receiving Omeprazole Amoxicillin Clarythromycin (OAC) triple therapy and placebo as controls. These subjects were endoscopically followed up in the second and fifth year. We compared the endoscopic appearance and histology of the biopsy specimens from the same site obtained at the first and last visits. Conclusions H.pylori eradication results in remarkable reduction in the severity and activity of chronic gastritis, marked resolution of intestinal metaplasia in the antrum. On the other hand, continuous H.pylori infection leads to progressive aggravation of atrophy and intestinal metaplasia.

  3. Helicobacter pylori infection and serum ferritin

    DEFF Research Database (Denmark)

    Berg, Gabriele; Bode, G; Blettner, M

    2001-01-01

    OBJECTIVE: Helicobacter pylori may possibly affect the iron metabolism by occult bleeding, impaired absorption of non-hem iron, and by scavenging hem iron or ferritin, as some studies have suggested. The aim of this study was to analyze the association between H. pylori infection and serum ferrit...

  4. Inflammation, immunity, and vaccines for Helicobacter pylori

    DEFF Research Database (Denmark)

    D'Elios, Mario M; Andersen, Leif P

    2009-01-01

    Helicobacter pylori infects almost half of the population worldwide and represents the major cause of gastroduodenal diseases, such as duodenal and gastric ulcer, gastric adenocarcinoma, autoimmune gastritis, and B-cell lymphoma of mucosa-associated lymphoid tissue. Helicobacter pylori induces...

  5. Helicobacter pylori and non-malignant diseases.

    Science.gov (United States)

    Furuta, Takahisa; Delchier, Jean-Charles

    2009-09-01

    It is well known that Helicobacter pylori infection is associated with many nonmalignant disorders such as gastritis, peptic ulcer, gastroesophageal reflux disease (GERD), gastric polyp, nonsteroidal anti-inflammatory drug (NSAID)/aspirin-induced gastric injury, and functional dyspepsia. In 2008, interesting articles on the association of H. pylori infection with these disorders were presented, some of which intended to reveal the mechanisms of inter-individual differences in response to H. pylori infection, and have demonstrated that genetic differences in host and bacterial factors as well as environmental factors account for these differences. A decline in the occurrence of peptic ulcer related to H. pylori was confirmed. An inverse relationship between H. pylori infection and GERD was also confirmed but the impact of gastric atrophy on the prevention of GERD remained debatable. For NSAID-induced gastric injury, eradication of H. pylori infection has been recommended. During this year, eradication of H. pylori infection was recommended for patients treated with antiplatelet therapy as well as aspirin and NSAID. It was also reported that for patients with functional dyspepsia, eradication of H. pylori offers a modest but significant benefit.

  6. Helicobacter Pylori and Gastric Cancer: Clinical Aspects

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    Zhi-Qiang Song

    2015-01-01

    Full Text Available Objective: Although Helicobacter pylori (H. pylori is considered as the main etiological factor for gastric cancer, the strategy of screening and treating the oncogenic bacterium is still controversial. The objective was to evaluate the status and progress of the cognition about the relationship between H. pylori infection and gastric cancer from a clinical aspect. Data Sources: The data used in this review were mainly from the PubMed articles published in English from 1984 to 2015. Study Selection: Clinical research articles were selected mainly according to their level of relevance to this topic. Results: Gastric cancer is the fifth most common malignancy and the third leading cause of cancer deaths worldwide. The main etiological factor for gastric cancer is H. pylori infection. About 74.7-89.0% gastric cancer was related to H. pylori infection. Up to date, some regional gastric cancer prevention programs including the detection and treatment of H. pylori infection are under way. Current data obtained from the randomized controlled trials suggest that population-based H. pylori screening and treatment is feasible and cost-effective in preventing gastric cancer; however, a population-based H. pylori eradication campaign would potentially lead to bacterial resistance to the corresponding antibiotics, as well as a negative impact on the normal flora. Conclusions: The important questions of feasibility, program costs, appropriate target groups for intervention, and the potential harm of mass therapy with antibiotics must first be answered before implementing any large-scale program.

  7. 具有拮抗幽门螺杆菌作用的植物乳杆菌特性研究%Biological characteristics of Lactobacillus plantarum with antagonistic activity against Helicobacter pylori

    Institute of Scientific and Technical Information of China (English)

    陈晓华; 肖苇苇; 田丰伟; 刘小鸣; 张灏; 陈卫

    2012-01-01

    Helicobacter pylori is a spiral-shaped, microaerophilic and Gram negative bacillus that causes chronic gastritis,peptic ulcer diseases and is suspected to be involved in the genesis of gastric cancer.The aim was to discuss the biological characteristics of Lactobacillus plantarum 18 with antagonistic activity against H.pylorilThe results showed that L.plantarum 18 could grow in the low acid conditions,survive in the simulated gastric juice,and inhibit the growth of H.pylori.Biological characteristics research of L.plantarum 18 showed that the logarithmic time was from 4th hour to 14th hour,the optimum growth pH was 5-7 ,the optimum growth temperature was 30-37℃, the optimum inoculated concentration was 1%-2% (V/V), and the tolerance level of bile salt was 0.2% (V/V).%幽门螺杆菌是螺旋形或是S形的微需氧革兰氏阴性菌,是慢性活动性胃炎、消化性溃疡发病的主要病因,并与胃恶性肿瘤(胃癌、胃粘膜相关淋巴样组织淋巴瘤)关系密切。本文探讨了具有拮抗幽门螺杆菌作用的植物乳杆菌的生物特性,结果表明L.plantarum18在低酸条件下可以生长,耐受pH2.5的人工胃液,能够抑制多种幽门螺杆菌的生长。该菌株生长比较快,4h进入生长对数期,14h后进入稳定期;最适生长pH为5-7,最适生长温度为30~37℃,最适接种量为1%-2%(V/V),可在0.2%的胆盐中生长。

  8. Effect of Byrsonima crassa and Phenolic Constituents on Helicobacter pylori-Induced Neutrophils Oxidative Burst

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    Wagner Vilegas

    2011-12-01

    Full Text Available Byrsonima crassa Niedenzu (Malpighiaceae is used in Brazilian folk medicine for the treatment of diseases related mainly to gastric ulcers. In a previous study, our group described the gastric protective effect of the methanolic extract from the leaves of B. crassa. The present study was carried out to investigate the effects of methanolic extract and its phenolic compounds on the respiratory burst of neutrophils stimulated by H. pylori using a luminol-based chemiluminescence assay as well as their anti-H. pylori activity. The suppressive activity on oxidative burst of H. pylori-stimulated neutrophils was in the order of methyl gallate > (+-catechin > methanol extract > quercetin 3-O-α-l-arabinopyranoside > quercetin 3-O-β-d-galactopyranoside > amentoflavone. Methyl gallate, compound that induced the highest suppressive activity with IC50 value of 3.4 µg/mL, did not show anti-H. pylori activity. B. crassa could be considered as a potential source of natural antioxidant in gastric ulcers by attenuating the effects on the damage to gastric mucosa caused by neutrophil generated reactive oxygen species, even when H. pylori displays its evasion mechanisms.

  9. Role of Helicobacter pylori in functional dyspepsia

    Institute of Scientific and Technical Information of China (English)

    Colm O'Morain

    2006-01-01

    The aetiology of dyspepsia is unknown in the majority of patients. Helicobacter pylori(H pylori) is the cause in a subset of patients. A non invasive test to assess the presence of H pylori is recommended in the management of patients under the age of 50 presenting to a family practitioner with dyspepsia. A urea breath test or a stool antigen test are the most reliable non invasive tests. Eradication of H pylori will reduce the risk to the patient with dyspepsia of developing a peptic ulcer, reduce the complication rate if prescribed nonsteroid anti-inflammatory drugs and later reduce the risk of gastric cancer. The recommended treatment for non ulcer dyspepsia associated with a H pylori infection should be a 10-d course of treatment with a PPI and two antibiotics. Treatment efficacy should be assessed four weeks after completing treatment with a urea breath test or a stool antigen test.

  10. Helicobacter pylori, Cancer, and the Gastric Microbiota.

    Science.gov (United States)

    Wroblewski, Lydia E; Peek, Richard M

    Gastric adenocarcinoma is one of the leading causes of cancer-related death worldwide and Helicobacter pylori infection is the strongest known risk factor for this disease. Although the stomach was once thought to be a sterile environment, it is now known to house many bacterial species leading to a complex interplay between H. pylori and other residents of the gastric microbiota. In addition to the role of H. pylori virulence factors, host genetic polymorphisms, and diet, it is now becoming clear that components of the gastrointestinal microbiota may also influence H. pylori-induced pathogenesis. In this chapter, we discuss emerging data regarding the gastric microbiota in humans and animal models and alterations that occur to the composition of the gastric microbiota in the presence of H. pylori infection that may augment the risk of developing gastric cancer.

  11. Helicobacter pylori virulence factors affecting gastric proton pump expression and acid secretion.

    Science.gov (United States)

    Hammond, Charles E; Beeson, Craig; Suarez, Giovanni; Peek, Richard M; Backert, Steffen; Smolka, Adam J

    2015-08-01

    Acute Helicobacter pylori infection of gastric epithelial cells and human gastric biopsies represses H,K-ATPase α subunit (HKα) gene expression and inhibits acid secretion, causing transient hypochlorhydria and supporting gastric H. pylori colonization. Infection by H. pylori strains deficient in the cag pathogenicity island (cag PAI) genes cagL, cagE, or cagM, which do not transfer CagA into host cells or induce interleukin-8 secretion, does not inhibit HKα expression, nor does a cagA-deficient strain that induces IL-8. To test the hypothesis that virulence factors other than those mediating CagA translocation or IL-8 induction participate in HKα repression by activating NF-κB, AGS cells transfected with HKα promoter-Luc reporter constructs containing an intact or mutated NF-κB binding site were infected with wild-type H. pylori strain 7.13, isogenic mutants lacking cag PAI genes responsible for CagA translocation and/or IL-8 induction (cagA, cagζ, cagε, cagZ, and cagβ), or deficient in genes encoding two peptidoglycan hydrolases (slt and cagγ). H. pylori-induced AGS cell HKα promoter activities, translocated CagA, and IL-8 secretion were measured by luminometry, immunoblotting, and ELISA, respectively. Human gastric biopsy acid secretion was measured by microphysiometry. Taken together, the data showed that HKα repression is independent of IL-8 expression, and that CagA translocation together with H. pylori transglycosylases encoded by slt and cagγ participate in NF-κB-dependent HKα repression and acid inhibition. The findings are significant because H. pylori factors other than CagA and IL-8 secretion are now implicated in transient hypochlorhydria which facilitates gastric colonization and potential triggering of epithelial progression to neoplasia.

  12. Five-day bismuth-free triple therapy for the eradication of Helicobacter pylori and reduction of duodenal ulcer relapse

    Energy Technology Data Exchange (ETDEWEB)

    Coelho, L.G.; Passos, M.C.; Chausson, Y.; Castro L de, P. (Gastroenterology, Nutrition and Digestive Surgery Unit, University Hospital, Federal University of Minas Gerais (Brazil))

    1991-08-01

    Previous studies have demonstrated that the eradication of Helicobacter pylori (H. pylori) is associated with a significant reduction of the rate of duodenal ulcer (DU) relapse. The aim of this study was to assess the long-term effect of a bismuth-free triple therapy on the eradication of H. pylori and reduction of DU relapse. After informed consent, 61 patients with endoscopically proven DU and H. pylori infection detected on 14C-urea breath test (BT) were included in the study. All patients received a combination of furazolidone, amoxicillin, and metronidazole, three times a day, for 5 days, in addition to eventual classical antiulcer agents prescribed by their attending physicians. BT was repeated after an interval of at least 60 days to evaluate H. pylori eradication. Endoscopy and another BT were performed again at 6.5 months after therapy to detect possible recurrences. Forty-eight patients completed the trial: 26 (54%) patients were negative for H. pylori at 6.5 months after the end of treatment, and 22 (46%) persisted H. pylori positive. Ninety-two percent of the patients in whom the bacteria were eradicated showed endoscopically healed ulcers and were asymptomatic, and two that were symptomatic presented only occasional pain not requiring therapy. Among the 22 patients who persisted H. pylori positive, six (27%) showed endoscopically active ulcers (p = 0.012) and eight (36%) patients continued to be symptomatic (p less than 0.01), and were still using antiulcer drugs (p = 0.002) 6.5 months after treatment. It is concluded that combined treatment with furazolidone, amoxicillin, and metronidazole for 5 days represents a well-tolerated, inexpensive, and effective therapeutic regime for the eradication of H. pylori and abolition of DU relapse in more than 50% of the patients during a follow-up period of 6.5 months.

  13. Isocitrate dehydrogenase of Helicobacter pylori potentially induces humoral immune response in subjects with peptic ulcer disease and gastritis.

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    M Abid Hussain

    Full Text Available BACKGROUND: H. pylori causes gastritis and peptic ulcers and is a risk factor for the development of gastric carcinoma. Many of the proteins such as urease, porins, flagellins and toxins such as lipo-polysaccharides have been identified as potential virulence factors which induce proinflammatory reaction. We report immunogenic potentials of isocitrate dehydrogenase (ICD, an important house keeping protein of H. pylori. METHODOLOGY/PRINCIPAL FINDINGS: Amino acid sequences of H. pylori ICD were subjected to in silico analysis for regions with predictably high antigenic indexes. Also, computational modelling of the H. pylori ICD as juxtaposed to the E. coli ICD was carried out to determine levels of structure similarity and the availability of surface exposed motifs, if any. The icd gene was cloned, expressed and purified to a very high homogeneity. Humoral response directed against H. pylori ICD was detected through an enzyme linked immunosorbent assay (ELISA in 82 human subjects comprising of 58 patients with H. pylori associated gastritis or ulcer disease and 24 asymptomatic healthy controls. The H. pylori ICD elicited potentially high humoral immune response and revealed high antibody titers in sera corresponding to endoscopically-confirmed gastritis and ulcer disease subjects. However, urea-breath-test negative healthy control samples and asymptomatic control samples did not reveal any detectable immune responses. The ELISA for proinflammatory cytokine IL-8 did not exhibit any significant proinflammatory activity of ICD. CONCLUSIONS/SIGNIFICANCE: ICD of H. pylori is an immunogen which interacts with the host immune system subsequent to a possible autolytic-release and thereby significantly elicits humoral responses in individuals with invasive H. pylori infection. However, ICD could not significantly stimulate IL8 induction in a cultured macrophage cell line (THP1 and therefore, may not be a notable proinflammatory agent.

  14. Evaluation of Helicobacter pylory colonization by serologic test (IgG and dyspepsia in volunteers from the countryside of Monte Negro, in the Brazilian western Amazon region Avaliação da colonização por Helicobacter pylori através de teste sorológico (IgG e de dispepsia em voluntários da população rural de Monte Negro (RO, região da Amazônia ocidental

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    Rafael Bernardon Ribeiro

    2010-08-01

    Full Text Available The present study intended to analyze the seroprevalence of Helicobacter pylori, IgG, and its relation to dyspepsia in a population from the western Amazon region. During the "Projeto Bandeira Científica", a University of São Paulo Medical School program, in Monte Negro's rural areas, state of Rondônia, 266 blood samples were collected from volunteers. The material was tested for IgG antibodies anti-Helicobacter pylori by ELISA method and the participants were also interviewed on dyspepsia, hygiene and social aspects. Participants aged between five and 81 years old (34 years on average, 149 (56% were female and 117 (44% male. We found 210 (78.9% positive, 50 (18.8% negative and six (2.3% undetermined samples. Dyspeptic complaints were found in 226 cases (85.2%. There was no statistical association between dyspepsia and positive serology for H. pylori. We concluded that the seroprevalence in all age categories is similar to results found in other studies conducted in developing countries, including those from Brazil. On the other hand, the seroprevalence found in Monte Negro was higher than that reported in developed countries. As expected, there was a progressive increase in the positivity for H. pylori in older age groups.Este trabalho tem por objetivo analisar a soroprevalência do Helicobacter pylori, IgG, em população rural da Amazônia, e sua correlação com queixa dispéptica. No Projeto Bandeira Científica da FMUSP, em Monte Negro - RO, foram coletadas 266 amostras sangüíneas nos assentamentos rurais do município. Foram pesquisados anticorpos da classe IgG dirigidos contra Helicobacter pylori pelo método ELISA e aplicados questionários sobre dispepsia, aspectos sociais e epidemiológicos. Os pacientes tinham idades entre cinco e 81 anos (média de 34 anos; 149 (56% do sexo feminino e 117 (44% do sexo masculino. Foram encontradas 210 (78.9% amostras positivas, 50 negativas (18.8% e seis indeterminadas (2.3%. A queixa de

  15. Virulence of water-induced coccoid Helicobacter pylori and its experimental infection in mice

    Institute of Scientific and Technical Information of China (English)

    Fei-Fei She; Jian-Yin Lin; Jun-Yan Liu; Cheng Huang; Dong-Hui Su

    2003-01-01

    AIM: To explore the virulence and the infectivity of coccoid Helicobacter ppylori(H.pylori) transformed from spiral form by exposure to sterile tap water.METHODS: Three strains of H.pylori, isolated from gastric biopsy specimens of confirmed peptic ulcer, were converted from spiral into coccoid form by exposure to sterile tap water.Both spiral and coccoid forms of H.pylori were tested for the urease activity, and the adherence to Hep-2 cells. The presence of flagella was examined under electron microscopy. In the experimental animal infection, the spiral and coccoid forms of H.pylori originated from the same strain F49 were inoculated intragastrically into BALB/c mice respectively four times at a 3-day interval. Half of the mice from each group were sacrificed at Day 21 and Day 28 after the last inoculation. Histology and H.pylori colonization were detected by urease test of gastric mucosa, cultures of H. pylori,and electron microscopy and so on.RESULTS: The urease activity and the ability of adherence to Hep-2 cells were found to be lower in coccoid H.pylori than that in its spiral form. For example, the transformation in strain F44 led to a significant decrease of the adherence rate and adherence index from 70.0±5.3 % to 30.2±3.5 %(P<0.01), and from 2.6±0.4 to 0.86±0.3 (P<0.01),respectively. The flagella of coccoid H.pylori were observed under electron microscope. In the experimental infection in mice, the positive rate of gastric mucosa urease test was 93.8 % (15/16) in the group infected by spiral H.pylori and 50 % (8/16) in the group infected by coccoid H. pylori,and the estimated coccoid H.pylori colony number was 1.75 vs0,56. The positive rates of H. pyloriculture were 87.5 %(14/16) in spiral H. pylori group and 68.8 % (11/16) in coccoid H.pylorigroup. There was no significant difference in either urease test or bacterial culture rate between the groups examined at Day 21 and Day 28 after inoculation. Electron microscopic examination of the samples

  16. Development of bacterial transglycosylase inhibitors as new antibiotics: moenomycin A treatment for drug-resistant Helicobacter pylori.

    Science.gov (United States)

    Tseng, Yen-Yu; Liou, Jyh-Ming; Hsu, Tsui-Ling; Cheng, Wei-Chieh; Wu, Ming-Shiang; Wong, Chi-Huey

    2014-06-01

    The problem of multidrug-resistant Helicobacter pylori requires new antibiotics development. We have evaluated a potential antibiotics, moenomycin A, which is classified as a phosphoglycolipid antibiotics that targets transglycosylase and is previously thought to be limited in Gram-positive bacteria. Herein, we report the activity of moenomycin A against multidrug-resistant H. pylori and the isolates from patients with different gastrointestinal diseases.

  17. Helicobacter pylori cholesteryl α-glucosides contribute to its pathogenicity and immune response by natural killer T cells.

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    Yuki Ito

    Full Text Available Approximately 10-15% of individuals infected with Helicobacter pylori will develop ulcer disease (gastric or duodenal ulcer, while most people infected with H. pylori will be asymptomatic. The majority of infected individuals remain asymptomatic partly due to the inhibition of synthesis of cholesteryl α-glucosides in H. pylori cell wall by α1,4-GlcNAc-capped mucin O-glycans, which are expressed in the deeper portion of gastric mucosa. However, it has not been determined how cholesteryl α-glucosyltransferase (αCgT, which forms cholesteryl α-glucosides, functions in the pathogenesis of H. pylori infection. Here, we show that the activity of αCgT from H. pylori clinical isolates is highly correlated with the degree of gastric atrophy. We investigated the role of cholesteryl α-glucosides in various aspects of the immune response. Phagocytosis and activation of dendritic cells were observed at similar degrees in the presence of wild-type H. pylori or variants harboring mutant forms of αCgT showing a range of enzymatic activity. However, cholesteryl α-glucosides were recognized by invariant natural killer T (iNKT cells, eliciting an immune response in vitro and in vivo. Following inoculation of H. pylori harboring highly active αCgT into iNKT cell-deficient (Jα18(-/- or wild-type mice, bacterial recovery significantly increased in Jα18(-/- compared to wild-type mice. Moreover, cytokine production characteristic of Th1 and Th2 cells dramatically decreased in Jα18(-/- compared to wild-type mice. These findings demonstrate that cholesteryl α-glucosides play critical roles in H. pylori-mediated gastric inflammation and precancerous atrophic gastritis.

  18. Helicobacter pylori Cholesteryl α-Glucosides Contribute to Its Pathogenicity and Immune Response by Natural Killer T Cells

    Science.gov (United States)

    Ito, Yuki; Vela, Jose Luis; Matsumura, Fumiko; Hoshino, Hitomi; Tyznik, Aaron; Lee, Heeseob; Girardi, Enrico; Zajonc, Dirk M.; Liddington, Robert; Kobayashi, Motohiro; Bao, Xingfeng; Bugaytsova, Jeanna; Borén, Thomas; Jin, Rongsheng; Zong, Yinong; Seeberger, Peter H.; Nakayama, Jun; Kronenberg, Mitchell; Fukuda, Minoru

    2013-01-01

    Approximately 10–15% of individuals infected with Helicobacter pylori will develop ulcer disease (gastric or duodenal ulcer), while most people infected with H. pylori will be asymptomatic. The majority of infected individuals remain asymptomatic partly due to the inhibition of synthesis of cholesteryl α-glucosides in H. pylori cell wall by α1,4-GlcNAc-capped mucin O-glycans, which are expressed in the deeper portion of gastric mucosa. However, it has not been determined how cholesteryl α-glucosyltransferase (αCgT), which forms cholesteryl α-glucosides, functions in the pathogenesis of H. pylori infection. Here, we show that the activity of αCgT from H. pylori clinical isolates is highly correlated with the degree of gastric atrophy. We investigated the role of cholesteryl α-glucosides in various aspects of the immune response. Phagocytosis and activation of dendritic cells were observed at similar degrees in the presence of wild-type H. pylori or variants harboring mutant forms of αCgT showing a range of enzymatic activity. However, cholesteryl α-glucosides were recognized by invariant natural killer T (iNKT) cells, eliciting an immune response in vitro and in vivo. Following inoculation of H. pylori harboring highly active αCgT into iNKT cell-deficient (Jα18−/−) or wild-type mice, bacterial recovery significantly increased in Jα18−/− compared to wild-type mice. Moreover, cytokine production characteristic of Th1 and Th2 cells dramatically decreased in Jα18−/− compared to wild-type mice. These findings demonstrate that cholesteryl α-glucosides play critical roles in H. pylori-mediated gastric inflammation and precancerous atrophic gastritis. PMID:24312443

  19. Cytopathic effects of toxogenic strains of Helicobacter pylori on different cell lines

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    K. Lakshmana Gowda

    2014-01-01

    Full Text Available Purpose: Many virulence factors are involved in the pathomechanism of infection caused by Helicobacter pylori. Toxins such as vacuolating cytotoxin, encoded by the vacA gene and the immunogenic protein cagA, encoded by the cagA gene (cytotoxin-associated gene are major factors conferring the property of virulence. The current study is aimed at isolation of H. pylori and separation of its toxin from antral biopsies of patients. Materials and Methods: The following cell lines were used to demonstrate the cytopathic effect (CPE of the separated toxin: African green monkey kidney (Vero, baby hamster kidney, human lung carcinoma (LLC-MK2, and human epithelial. Results: H. pylori was isolated from 27 out of 45 patients (60% selected for the study. CPE of H. pylori toxin was highly significant on Vero cells than other cell lines used as it reached a high dilution titer of toxin (1/16 in 13 isolated strains (48.15%. No significant difference in CPE of toxin in different dilutions was detected among other cell lines used in different groups. H. pylori toxin could be detected by sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis as a distinct band with a molecular weight ranging between 66 and 97 kDa and closely related to 87 kDa. Conclusion: H. pylori vacuolating cytotoxin plays a vital role in the pathogenesis of gastroduodenal diseases (gastritis, gastric ulcer, duodenal ulcer, and gastric cancer. The Vero cell lines were found to be the most suitable form of tissue culture when compared with other cell lines used in our study for demonstrating the activity of H. pylori toxin.

  20. Inhibitory effect of Raphanobrassica on Helicobacter pylori-induced gastritis in Mongolian gerbils.

    Science.gov (United States)

    Yamada, Takanori; Wei, Min; Toyoda, Takeshi; Yamano, Shoutaro; Wanibuchi, Hideki

    2014-08-01

    Helicobacter pylori (H. pylori) infection is well known to be associated with chronic gastritis and also development of gastric cancer. Raphanobrassica (RB) is an intergeneric hybrid of the genera Raphanus (radish) and Brassica (cabbages) containing appreciable amounts of glucoraphanin (GR) and glucoraphenin (GRe), which are actively hydrolyzed by the enzyme myrosinase to sulforaphane and sulforaphene, respectively. Both of these metabolites exert antimicrobial and anti-inflammatory activity. The purpose of the present study was to investigate the effect of two freeze-dried products of RB (RB1 and RB2) on H. pylori-induced gastritis in Mongolian gerbils. Six-week-old male Mongolian gerbils were inoculated orally with H. pylori (ATCC 43504), and 2weeks later were fed diets containing no additives or diets supplemented with 2% RB1 (containing both GR and GRe) or 2% RB2 (containing GR only) for 10weeks. In the RB1, but not the RB2 group, mononuclear cell infiltration, mRNA expression of IL-6, and cell proliferation in the gastric mucosa were significantly suppressed. These results indicate that RB1 containing both GR and GRe exerted significant inhibitory effects on H. pylori-induced gastritis in Mongolian gerbils apparently mediated via suppression of IL-6 expression and chronic inflammation.

  1. H pylori infection and reflux oesophagitis: A case-control study

    Institute of Scientific and Technical Information of China (English)

    Rahim Masjedizadeh; Eskandar Hajiani; Koorosh MoezArdalan; Saeed Samie; Mohammad-Javad Ehsani-Ardakani; Ali Daneshmand; Mohammad-Reza Zali

    2006-01-01

    AIM: To examine the relationship between H pylori and gastro-oesophageal reflux disease (GORD) in Iran.METHODS: In this study 51 GORD patients (referred to endoscopy at Taleghani hospital) were compared with 49 age-sex matched controls. Diagnosis of H pylori was made by gastric mucosal biopsy and rapid urease test (positive if the result of one or both diagnostic methods was positive). Updated Sydney system was used to report histopathological changes.RESULTS: The frequency of H pylori infection based on rapid urease test and histology was 88.2% (45) in patients and 77.6% (38) in controls, which showed no significant difference. The frequency of H pylori infection was significantly higher in the antrum than in the corpus and cardia. The mean activity, inflammation,and gastritis scores were also higher in the antrum of patients than in the antrum of controls. The mean scores were significantly higher in the corpus of controls than in the corpus of patients. Diffuse active gastritis was observed in a significantly larger number of controls,while the frequency of diffuse chronic gastritis was higher in patients. There was no significant difference in the frequency of other histological findings between patients and controls.CONCLUSION: H pylori infection cannot prevent GORD in this region.

  2. Cytotoxic T Cells in H. pylori-Related Gastric Autoimmunity and Gastric Lymphoma

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    Mathijs P. Bergman

    2010-01-01

    Full Text Available Helicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop gastric B-cell lymphoma, gastric autoimmunity, or other life threatening diseases, as gastric cancer or peptic ulcer. The type of host immune response against H. pylori, particularly the cytolytic effector functions of T cells, is crucial for the outcome of the infection. T cells are potentially able to kill a target via different mechanisms, such as perforins or Fas-Fas ligand interaction. In H. pylori-infected patients with gastric autoimmunity cytolytic T cells, that cross-recognize different epitopes of H. pylori proteins and H+K+-ATPase autoantigen, infiltrate the gastric mucosa and lead to gastric atrophy via long-lasting activation of Fas ligand-mediated appotosis and perforin-induced cytotoxicity. On the other hand, gastric T cells from MALT lymphoma exhibit defective perforin- and Fas-Fas ligand-mediated killing of B cells, with consequent abnormal help for B-cell proliferation, suggesting that deregulated and exhaustive H. pylori-induced T cell-dependent B-cell activation can support both the onset and the promotion of low-grade B-cell lymphoma.

  3. Effect of the oral intake of probiotic Pediococcus acidilactici BA28 on Helicobacter pylori causing peptic ulcer in C57BL/6 mice models.

    Science.gov (United States)

    Kaur, Baljinder; Garg, Neena; Sachdev, Atul; Kumar, Balvir

    2014-01-01

    Probiotic lactic acid bacteria are being proposed to cure peptic ulcers by reducing colonization of Helicobacter pylori within the stomach mucosa and by eradicating already established infection. In lieu of that, in vitro inhibitory activity of pediocin-producing probiotic Pediococcus acidilactici BA28 was evaluated against H. pylori by growth inhibition assays. Further, chronic gastritis was first induced in two groups of C57BL/6 mice by orogastric inoculation with H. pylori with polyethylene catheter, and probiotic P. acidilactici BA28 was orally administered to study the eradication and cure of peptic ulcer disease. H. pylori and P. acidilactici BA28 were detected in gastric biopsy and fecal samples of mice, respectively. A probiotic treatment with P. acidilactici BA28, which is able to eliminate H. pylori infection and could reverse peptic ulcer disease, is being suggested as a co-adjustment with conventional antibiotic treatment. The study provided an evidence of controlling peptic ulcer disease, by diet mod

  4. Human Lysozyme Synergistically Enhances Bactericidal Dynamics and Lowers the Resistant Mutant Prevention Concentration for Metronidazole to Helicobacter pylori by Increasing Cell Permeability

    Directory of Open Access Journals (Sweden)

    Xiaolin Zhang

    2016-10-01

    Full Text Available Metronidazole (MNZ is an effective agent that has been employed to eradicate Helicobacter pylori (H. pylori. The emergence of broad MNZ resistance in H. pylori has affected the efficacy of this therapeutic agent. The concentration of MNZ, especially the mutant prevention concentration (MPC, plays an important role in selecting or enriching resistant mutants and regulating therapeutic effects. A strategy to reduce the MPC that can not only effectively treat H. pylori but also prevent resistance mutations is needed. H. pylori is highly resistant to lysozyme. Lysozyme possesses a hydrolytic bacterial cell wall peptidoglycan and a cationic dependent mode. These effects can increase the permeability of bacterial cells and promote antibiotic absorption into bacterial cells. In this study, human lysozyme (hLYS was used to probe its effects on the integrity of the H. pylori outer and inner membranes using as fluorescent probe hydrophobic 1-N-phenyl-naphthylamine (NPN and the release of aspartate aminotransferase. Further studies using a propidium iodide staining method assessed whether hLYS could increase cell permeability and promote cell absorption. Finally, we determined the effects of hLYS on the bactericidal dynamics and MPC of MNZ in H. pylori. Our findings indicate that hLYS could dramatically increase cell permeability, reduce the MPC of MNZ for H. pylori, and enhance its bactericidal dynamic activity, demonstrating that hLYS could reduce the probability of MNZ inducing resistance mutations.

  5. Helicobacter pylori HP(2-20) induces eosinophil activation and accumulation in superficial gastric mucosa and stimulates VEGF-alpha and TGF-beta release by interacting with formyl-peptide receptors.

    Science.gov (United States)

    Prevete, N; Rossi, F W; Rivellese, F; Lamacchia, D; Pelosi, C; Lobasso, A; Necchi, V; Solcia, E; Fiocca, R; Ceppa, P; Staibano, S; Mascolo, M; D'Argenio, G; Romano, M; Ricci, V; Marone, G; De Paulis, A

    2013-01-01

    Eosinophils participate in the immune response against Helicobacter pylori, but little is known about their role in the gastritis associated to the infection. We recently demonstrated that the Hp(2-20) peptide derived from H. pylori accelerates wound healing of gastric mucosa by interacting with N-formyl peptide receptors (FPRs) expressed on gastric epithelial cells. The aim of the present study was to investigate whether eosinophils play a role in the repair of gastric mucosa tissue during H. pylori infection. Immuno-histochemistry and transmission electron microscopy were used to detect eosinophils in gastric mucosal biopsies. Eosinophil re-distribution occurred in the gastric mucosa of H. pylori-infected patients: their density did not change in the deep mucosal layer, whereas it increased in the superficial lamina propria just below the foveolar epithelium; eosinophils entered the epithelium itself as well as the lumen of foveolae located close to the area harboring bacteria, which in turn were also engulfed by eosinophils. The H. pylori-derived peptide Hp(2-20) stimulated eosinophil migration through the engagement of FPR2 and FPR3, and also induced production of VEGF-A and TGF-beta, two key mediators of tissue remodelling. We also demonstrate that Hp(2-20) in vivo induced eosinophil infiltration in rat gastric mucosa after injury brought about by indomethacin. This study suggests that eosinophil infiltrate could modulate the capacity of gastric mucosa to maintain or recover its integrity thereby shedding light on the role of eosinophils in H. pylori infection.

  6. Study of serum Helicobacter pylori soluble antigen

    Institute of Scientific and Technical Information of China (English)

    吴勤动; 朱永良

    2002-01-01

    Objective:to explore a new serological method for detecting Helicobacter pylori(H.pylori) infection.Methods:Serum soluble antigen of H.pylori was detected by using avidin-biotin ELISA technique to evaluate the status of H.pylori infection and for comparison with rapid urease test(RUT).histologic examination and serology,Results:The sensitivity,specificity,positive predictive value and negative predictive value were 77.46% ,91.07%,91.67% and 76.12%,respectively.The prevalence rate of werum H. pylori soluble antigen in 138 patients undergong endoscopy was similar to the rate obtained by 14 C-UBT methods(P>0.05).Conclusions:The detection of serum H.pylori soluble antigen(HpSAg) could be used as a new serological method which is accurate,and convenient,not affected by the memorizing raction of serum antibody;is more sensitive,more specific and suitable for dinical diagriosis,and evaluation of eradication and for follow-up of H.pylori as well as for detection in children and pregnant women.

  7. H pylori and host interactions that influence pathogenesis

    Institute of Scientific and Technical Information of China (English)

    Ellen J Beswick; Giovanni Suarez; Victor E Reyes

    2006-01-01

    H pylori is probably the most prevalent human pathogen worldwide. Since it was initially suggested in 1983 by Marshall and Warren to be implicated in gastritis and pepticulcer disease,H pylori has also been implicated in gastric carcinoma and was classified as a class I carcinogen. In the last two decades, a noteworthy body of research has revealed the multiple processes that this gram negative bacterium activates to cause gastroduodenal disease in humans. Most infections are acquired early in life and may persist for the life of the individual.While infected individuals mount an inflammatory response that becomes chronic, along with a detectable adaptive immune response, these responses are ineffective in clearing the infection. H pylori has unique features that allow it to reside within the harsh conditions of the gastric environment, and also to evade the host immune response. In this review, we discuss the various virulence factors expressed by this bacterium and how they interact with the host epithelium to influence pathogenesis.

  8. Virulence and potential pathogenicity of coccoid Helicobacter pylori induced by antibiotics

    Institute of Scientific and Technical Information of China (English)

    Fei Fei She; Dong Hui Su; Jian Yin Lin; Lin Ying Zhou

    2001-01-01

    AIM To explore the virulence and the potential pathogenicity of coccoid Helicobacter pylori (H. pylori) transformed from spiral form by exposure to antibiotic.METHODS Three strains of H. pylori, isolated from gastric biopsy specimens of confirmed peptic ulcer, were converted from spiral into coccoid from by exposure to metronidazole.Both spiral and coccoid form of H. pylori were tested for the urease activity, the adherence to Hep-2 cells and the vacuolating cytotoxicity to Hela cells, and the differences of the protein were analysed by SDS-PAGE and Western blot,The mutation of the genes including ureA, ureB,hpaA; vacA and cagA, related with virulence,was detected by means of PCR and PCR-SSCP.RESULTS In the coccoid H. pylori, the urease activity, the adherence to Hep-2 cells and the vacuolating cytotoxicity to Hela cells alldecreased. In strain F44, the rate and index of adherence reduced from 70.0% ± 5.3% to 33% ±5.1% and from 2.6 ±0.4 to 0.96 ±0.3 (P<0.01),respectively. The invasion of coccoid H. pylori into Hep-2 cell could be seen under electronmicroscope. SDS-PAGE showed that the content of the protein with the molecular weight over Mr74 000 decreased, and the hybriditional signal in band Mr 125 000 weakened, while the band Mr 110000 and Mr63000 strengthened in coccoid H. pylori as shown in Western blot. The results of PCR were all positive, and PCR-SSCP indicated that there may exist the point mutation in gene hpaA or vacA.CONCLUSION The virulence and the proteins with molecular weight over Mr74 000 in coccoid H. pylori decrease, but no deletion exists in amplification fragments from ureA, ureB, hpaA,vacA and cagA genes, suggesting that coccoid H. pylori may have potential pathogenicity.

  9. Adherence of Helicobacter pylori to the Gastric Mucosa

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    Marguerite Clyne

    1997-01-01

    Full Text Available Bacterial adhesion to the intestinal epithelium is a critical initial step in the pathogenesis of many enteric diseases. Helicobacter pylori is a duodenal pathogen that adheres to the gastric epithelium and causes gastritis and peptic ulceration. The mechanism by which H pylori causes disease has not yet been elucidated but adherence to the gastric mucosa is thought to be an important virulence determinant of the organism. What is known about adherence of H pylori to the gastric mucosa is summarized. Topics discussed are the mechanism of H pylori adherence; in vitro and in vivo models of H pylori infection; and adherence and potential adhesins and receptors for H pylori.

  10. Helicobacter pylori Seropositivity and Stool Antigen in Patients With Hyperemesis Gravidarum

    Directory of Open Access Journals (Sweden)

    2006-01-01

    Full Text Available The objective of this paper is to investigate whether Helicobacter pylori is an etiologic factor in hyperemesis gravidarum. Thirty one patients with hyperemesis gravidarum and twenty nine pregnant controls without hyperemesis gravidarum were included in this prospective study. All pregnant women were examined both for Helicobacter pylori serum immunoglobulin G antibodies (HpIgG Ab, showing chronic infection, and Helicobacter pylori stool antigens (HpSA, showing active gastrointestinal colonization. Chi-square and Student t tests were used accordingly for statistical analysis. Helicobacter pylori seropositivity was 67.7% in the patients with hyperemesis gravidarum and 79.3% in the control group ( χ 2 =1.02,P=.31 . HpSA was detected in 22.6% of patients with hyperemesis gravidarum, whereas 6.9% of patients in the control group. The difference was not statistically significant ( χ 2 =2.89,P=.08 . In this study, no relation was found between Helicobacter pylori and hyperemesis gravidarum. The low social status of women in both groups could be one of the reasons for the high prevalence of Hp infection.

  11. Helicobacter pylori infection and gastropathy: A comparison between Indonesian and Japanese patients

    Institute of Scientific and Technical Information of China (English)

    Murdani Abdullah; Hiroyuki Ohtsuka; Abdul Aziz Rani; Tadashi Sato; Ari F Syam; Masayuki A Fujino

    2009-01-01

    AIM: To compare the effects of Helicobacter pylori ( H pylori) infection on gastropathy between Indonesian and Japanese patients.METHODS: Biopsy specimens were obtained during upper gastrointestinal endoscopy from 167 subjects (125 Indonesians and 42 Japanese) with uninvestigated symptoms of dyspepsia. The specimens were analyzed for the presence of H pylori using urease analysis, histopathology, and cell culture. The grade and activity of gastritis was assessed using the updated Sydney system.RESULTS: The percentages of Indonesian and Japanese patients who were H pylori-positive at the antrum or body of the stomach were similar (68% and 59.5%, respectively; P = 0.316). Of those who were H pylori-positive, more Japanese patients than Indonesian patients had high levels of polymorphonuclear cells ( P = 0.001), mononuclear cells ( P = 0.013), glandular atrophy ( P = 0.000), and intestinal metaplasia ( P = 0.011) in both the antrum and body of the stomach.CONCLUSION: The grade of gastritis and prevalence of mucosal atrophy and intestinal metaplasia were higher in Japanese patients. The difference between Indonesian and Japanese patients was significant.

  12. Bacterial flora concurrent with Helicobacter pylori in the stomach of patients with upper gastrointestinal diseases

    Institute of Scientific and Technical Information of China (English)

    Yuan Hu; Li-Hua He; Di Xiao; Guo-Dong Liu; Yi-Xin Gu; Xiao-Xia Tao; Jian-Zhong Zhang

    2012-01-01

    AIM:To investigate the non-Helicobacter pylori (H.pylorl) bacterial flora concurrent with H.py/ori infection.METHODS:A total of 103 gastric biopsy specimens from H.py/ori positive patients were selected for bacterial culture.All the non-H.py/ori bacterial isolates were identified by matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS).RESULTS:A total of 201 non-H.py/ori bacterial isolates were cultivated from 67 (65.0%) of the 103 gastric samples,including 153 isolates identified successfully at species level and 48 at genus level by MALDI-TOF MS.The dominant species were Streptococcus,Neisseria,Rothia and Staphylococcus,which differed from the predominantly acid resistant species reported previously in healthy volunteers.The prevalence of non-H.pylori bacteria was higher in non-ulcer dyspepsia group than in gastric ulcer group (100% vs 42.9%,P < 0.001).Six bacterial species with urease activity (Staphylococcus epidermidis,Staphylococcus warneri,Staphylococcus capitis,Staphylococcus aureus,Brevibacterium spp.and Klebsiella pneumoniae) were also isolated.CONCLUSION:There is a high prevalence of the non-H.pylori bacteria concurrent with H.pylori infection,and the non-H.pylori bacteria may also play important as-yet-undiscovered roles in the pathogenesis of stomach disorders.

  13. The immunomodulatory properties of Helicobacter pylori confer protection against allergic and chronic inflammatory disorders

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    Anne eMüller

    2012-02-01

    Full Text Available Chronic infection with the gastric bacterial pathogen Helicobacter pylori causes gastritis and predisposes carriers to a high risk of developing gastric and duodenal ulcers, gastric cancer and gastric lymphoma, but has also recently been shown to protect against certain allergic and chronic inflammatory disorders. The immunomodulatory properties that allow the bacteria to persist for decades in infected individuals in the face of a vigorous, yet ultimately non-protective, innate and adaptive immune response may at the same time confer protection against allergies, asthma and inflammatory bowel diseases. Experimental evidence from mouse models suggests that H. pylori has evolved to skew the adaptive immune response towards immune tolerance rather than immunity, which promotes persistent infection on the one hand, and inhibits auto-aggressive and allergic T-cell responses on the other. Regulatory T-cells mediating peripheral immune tolerance have emerged as key cellular players in facilitating persistent infection as well as protection from allergies, in both observational studies in humans and experimental work in mice. Recent data suggest that H. pylori actively targets dendritic cells to promote tolerance induction. The findings discussed in this review raise the possibility of harnessing the immunomodulatory properties of H. pylori for the prevention and treatment of allergic and auto-immune diseases, and also provide new insights relevant for H. pylori-specific vaccine development.

  14. Multiple repeats of Helicobacter pylori CagA EPIYA-C phosphorylation sites predict risk of gastric ulcer in Iran.

    Science.gov (United States)

    Honarmand-Jahromy, Sahar; Siavoshi, Farideh; Malekzadeh, Reza; Sattari, Taher Nejad; Latifi-Navid, Saeid

    2015-12-01

    Biological activity of Helicobacter pylori oncoprotein CagA is determined by a diversity in the tyrosine phosphorylation motif sites. In the present study, the diversity and the type of the H. pylori CagA EPIYA motifs and their association with gastric ulcer (GU) and duodenal ulcer (DU) in Iranian dyspeptic patients were assessed. PCR amplification, sequencing, and bioinformatic analysis were performed to determine the pattern of CagA EPIYA motifs. Of 168 H. pylori cagA(+) strains, the frequency of ABC was 93.50%, ABCCC 5.40%, ABC + ABCCC 0.6% and ABCC 0.6%. There was no EPIYA-D segment. The ABCCC pattern of EPIYA motif was more frequent in the H. pylori isolates from GU (8/50, 16%) than in those from chronic gastritis (CG) (0/81, 0%) (P = 0). In contrast, The ABC pattern of EPIYA motif was less frequent in the H. pylori isolates from GU (41/50, 82%) than in those from CG (80/81, 98.80%) (Age-sex-adjusted odds ratio (OR) = 0.020, 95% CI = 0.002-0.259; P = 0.003). The distribution of the ABC motif was almost the same in H. pylori isolates from CG (98.80%) and DU diseases (97.30%). There was no significant association between the number of CagA EPIYA-C segment and DU (P > 0.05). We have proposed that CagA from Iranian H. pylori strains were Western type and all strains had active phosphorylation sites. The three EPIYA-C motifs of CagA were more frequently observed in the H. pylori strains from GU; thus it might be an important biomarker for predicting the GU risk in Iran.

  15. Proteomics-Based Identification and Analysis of Proteins Associated with Helicobacter pylori in Gastric Cancer.

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    Jianjiang Zhou

    Full Text Available Helicobacter pylori (H. pylori is a spiral-shaped Gram-negative bacterium that causes the most common chronic infection in the human stomach. Approximately 1%-3% of infected individuals develop gastric cancer. However, the mechanisms by which H. pylori induces gastric cancer are not completely understood. The available evidence indicates a strong link between the virulence factor of H. pylori, cytotoxin-associated gene A (CagA, and gastric cancer. To further characterize H. pylori virulence, we established three cell lines by infecting the gastric cancer cell lines SGC-7901 and AGS with cagA+ H. pylori and transfecting SGC-7901 with a vector carrying the full-length cagA gene. We detected 135 differently expressed proteins from the three cell lines using proteome technology, and 10 differential proteins common to the three cell lines were selected and identified by LC-MS/MS as well as verified by western blot: β-actin, L-lactate dehydrogenase (LDH, dihydrolipoamide dehydrogenase (DLD, pre-mRNA-processing factor 19 homolog (PRPF19, ATP synthase, calmodulin (CaM, p64 CLCP, Ran-specific GTPase-activating protein (RanGAP, P43 and calreticulin. Detection of the expression of these proteins and genes encoding these proteins in human gastric cancer tissues by real-time PCR (RT-qPCR and western blot revealed that the expression of β-ACTIN, LDH, DLD, PRPF19 and CaM genes were up-regulated and RanGAP was down-regulated in gastric cancer tissues and/or metastatic lymph nodes compared to peri-cancerous tissues. High gene expression was observed for H. pylori infection in gastric cancer tissues. Furthermore, the LDH, DLD and CaM genes were demethylated at the promoter -2325, -1885 and -276 sites, respectively, and the RanGAP gene was highly methylated at the promoter -570 and -170 sites in H. pylori-infected and cagA-overexpressing cells. These results provide new insights into the molecular pathogenesis and treatment targets for gastric cancer with H

  16. Helicobacter pylori infection in patients with autoimmune thrombocytopenic purpura

    Institute of Scientific and Technical Information of China (English)

    Erdal Kurtoglu; Ertugrul Kayacetin; Aysegul Ugur

    2004-01-01

    AIM: To compare the prevalence of Helicobacter pylori (Hpylori) infection in autoimmune thrombocytopenic purpura (AITP) patients with that of nonthrombocytopenic controls,and to evaluate the efficacy of the treatment in H pylori(+)and H pylori(-) AITP patients.METHODS: The prevalence of gastric H pylori infection in 38 adult AITP patients (29 female and 9 male; median age 27 years; range 18-39 years) who consecutively admitted to our clinic was investagated.RESULTS: H pylori infection was found in 26 of 38 AITP patients (68.5%). H pylori infection was found in 15 of 23control subjects (65.2%). The difference in H pylori infection between the 2 groups was not significant. Thrombocyte count of H pylori-positive AITP patients was significantly lower than that of H pylori-negative AITP patients (P<0.05).Thrombocyte recovery of H pylori-positive group was less than that of H pylori-negative group (P<0.05).CONCLUSION: H pylori infection should be considerecd in the treatment of AITP patients with H pylori infection.

  17. Eradication of Helicobacter pylori infection.

    Science.gov (United States)

    Wu, Tzung-Shiun; Hu, Huang-Ming; Kuo, Fu-Chen; Kuo, Chao-Hung

    2014-04-01

    Eradication of Helicobacter pylori infection has become an important issue recently, because this bacterial species cluster can cause many gastrointestinal diseases. Elevated antibiotic resistance is related to an increasing failure rate of H. pylori eradication. Standard triple therapy is still the first-line therapy; however, according to the Maastricht IV Consensus Report, it should be abandoned in areas of high clarithromycin resistance. Alternative first-line therapies include bismuth-containing quadruple therapy, sequential, concomitant, and hybrid therapies. Quinolone-based triple therapy may be considered as first-line therapy in areas of clarithromycin resistance >15-20% and quinolone resistance <10%. Unique second-line therapy is still unclear, and bismuth-containing quadruple therapy or levofloxacin-based triple therapy can be used as rescue treatment. Third-line therapy should be under culture guidance to select the most effective regimens (such as levofloxacin-based, rifabutin-based, or furazolidone-based therapies). Antibiotics resistance, patient compliance, and CYP 2C19 genotypes could influence the outcome. Clinicians should use antibiotics according to local reports.

  18. Treatment of Helicobacter pylori infection.

    LENUS (Irish Health Repository)

    O'Connor, Anthony

    2012-02-01

    This article aims to examine current best practice in the field reference to first-line, second-line, rescue and emerging treatment regimens for Helicobacter pylori eradication. The recommended first-line treatment in published guidelines in Europe and North American is proton pump inhibitor combined with amoxicillin and clarithromycin being the favoured regimen. Rates of eradication with this regimen however are falling alarmingly due to a combination of antibiotic resistance and poor compliance with therapy. Bismuth based quadruple therapies and levofloxacin based regimes have been shown to be effective second line regimens. Third-line options include regimes based on rifabutin or furazolidone, but susceptibility testing is the most rational option here, but is currently not used widely enough. Sequential therapy is promising but needs further study and validation outside of Italy. Although the success of first line treatments is falling, if compliance is good and a clear treatment paradigm adhered to, almost universal eradication rates can still be achieved. If compliance is not achievable, the problem of antibiotic resistance will continue to beset any combination of drugs used for H. pylori eradication.

  19. Transmission of Helicobacter pylori Infection

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    Giuseppina Oderda

    1999-01-01

    Full Text Available Helicobacter pylori infection is one of the most common bacterial infections worldwide. It is accepted as the major cause of chronic gastritis, peptic ulcer, carcinoma of the distal part of the stomach and gastric lymphoma. However, how and when the infection is acquired remain largely unknown. Identification of mode of transmission is vital for developing preventive measures to interrupt its spread, but studies focused on this issue are difficult to implement. From epidemiological studies, it is known that there are great differences in the prevalence of infection in different populations and in ethnic groups originating from high prevalence regions. This is likely related to inferior hygienic conditions and sanitation. In developing countries, infection occurs at a much earlier age. In developed countries, the prevalence of infection is related to poor socioeconomic conditions, particularly density of living. Humans seem to be the only reservoir of H pylori, which spread from person to person by oral-oral, fecal-oral or gastro-oral routes. Most infections are acquired in childhood, possibly from parents or other children living as close contacts. Infection from the environment or from animals cannot be entirely excluded.

  20. Binary and Tertiary Mixtures of Satureja hortensis and Origanum vulgare Essential Oils as Potent Antimicrobial Agents Against Helicobacter pylori.

    Science.gov (United States)

    Lesjak, Marija; Simin, Natasa; Orcic, Dejan; Franciskovic, Marina; Knezevic, Petar; Beara, Ivana; Aleksic, Verica; Svircev, Emilija; Buzas, Krisztina; Mimica-Dukic, Neda

    2016-03-01

    Essential oils possess strong antimicrobial activity, even against multiresistant Helicobacter pylori. Available therapies against H. pylori infection have multiple disadvantages, indicating a great need for a development of new therapeutics. The purpose of this study was to develop a potent natural product based anti-H. pylori formulation. First, anti-H. pylori activity of nine essential oils was determined, after which the most active oils were mixed in various ratios for further testing. Satureja hortensis, Origanum vulgare subsp. vulgare and O. vulgare subsp. hirtum essential oils expressed the highest activity (MIC = 2 μL mL(-1)). Their binary and ternary mixtures exhibited notably higher antimicrobial activity (MIC ≤ 2 μL mL(-1)). The most active was the mixture of S. hortensis and O. vulgare subsp. hirtum oils in volume ratio 2:1, which expressed 4 times higher activity than individual oils (MIC = 0.5 μL mL(-1)). According to GC-MS, both oils in the mixture were characterized by high content of phenols (48-73%), with carvacrol as the main carrier of antimicrobial activity. Presented in vitro study pointed out binary mixture of S. hortensis and O. vulgare subsp. hirtum essential oils in volume ratio 2:1 as promising candidate for further in vivo studies targeting H. pylori infection.

  1. Helicobacter Pylori Bacteremia: An Unusual Finding

    Science.gov (United States)

    De Luca, Concetta; Mancin, Annalisa; Calabrò, Maria; Daleno, Cristina; Ferrario, Antonella; Renzulli, Raffaella; Scuderi, Cristina; Casari, Erminia

    2016-01-01

    We report a case of Helicobacter pylori transient bacteremia in a woman with ulcerated antral gastric cancer. The patient was hospitalized for laparoscopy and subtotal gastrectomy. After surgery she developed fever (39°C) and was empirically treated with levofloxacin. Blood cultures, collected and sent immediately to Laboratory, were positive for a spiral Gram-negative bacterium. This isolate was identified as H. pylori and the specific susceptibility test was performed. One day after the fever was decreased but antibiotic treatment with levofloxacin was continued and it was maintained until discharge. In summary, H. pylori transient bacteremia may occur as a rare complication after stomach surgery. Further studies are necessary to elucidate the potential role of Helicobacter pylori presence in blood.

  2. Helicobacter pylori: Basic Mechanisms to Clinical Cure

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    ABR Thomson

    1995-01-01

    Full Text Available Since its rediscovery 10 years ago, Helicobacter pylori has reshaped our thinking about the course of peptic ulcer disease. Our approach to the patient with a duodenal ulcer has become one of attempting eradication therapy at the time of first diagnosis, in the hope of curing the ulcer disease. Gastric and duodenal ulceration are only two of the manifestations of this chronic antral infection; other complications of H pylori include gastritis, gastric cancer and possible maltomas. Therapy of H pylori infection is complicated and involves dual therapy with an antibiotic plus a protein pump inhibitor, such as omeprazole 20 mg bid plus amoxicillin 1 g bid for two weeks, triple or quadruple therapy with bismuth, two antibiotics and an H2-receptor antagonist. Vaccination against H pylori is on the far horizon.

  3. Distribution of Helicobacter pylori in north China

    Institute of Scientific and Technical Information of China (English)

    Yue-Hua Gong; Ying Wang; Yuan Yuan

    2005-01-01

    AIM: To compare the distribution of virulence-associatedgenotypes of Helicobacter pylori(H pylori) in two areas of north China with different gastric cancer risk and furthermore probe into the pathogenicity of the bacterium. METHODS: Gastric biopsies were taken from 355 subjects from Zhuanghe, a high risk area of gastric cancer, and 136 subjects from Shenyang, a low risk area of gastric cancer. A total of 149 H pylori strains isolated from these patients were studied by PCR for differences in the genotypes of cagA, vac A, and iceA.RESULTS: In patients with high risk for gastric cancer, higher frequencies of vacA s1 or s1m1b genotypes were found as compared to those from the low risk area. CONCLUSION: There is significantly different distribution of H pylori genotypes between Zhuanghe and Shenyang areas in north China.

  4. Spermine oxidase is a regulator of macrophage host response to Helicobacter pylori: enhancement of antimicrobial nitric oxide generation by depletion of spermine.

    Science.gov (United States)

    Chaturvedi, Rupesh; Asim, Mohammad; Barry, Daniel P; Frye, Jeanetta W; Casero, Robert A; Wilson, Keith T

    2014-03-01

    The gastric pathogen Helicobacter pylori causes peptic ulcer disease and gastric cancer. We have reported that in H. pylori-activated macrophages, nitric oxide (NO) derived from inducible NO synthase (iNOS) can kill the bacterium, iNOS protein expression is dependent on uptake of its substrate L-arginine (L-Arg), the polyamine spermine can inhibit iNOS translation by inhibiting L-Arg uptake, and inhibition of polyamine synthesis enhances NO-mediated bacterial killing. Because spermine oxidase (SMO), which back-converts spermine to spermidine, is induced in macrophages by H. pylori, we determined its role in iNOS-dependent host defense. SMO shRNA knockdown in RAW 264.7 murine macrophages resulted in a marked decrease in H. pylori-stimulated iNOS protein, but not mRNA expression, and a 90% reduction in NO levels; NO production was also inhibited in primary murine peritoneal macrophages with SMO knockdown. There was an increase in spermine levels after H. pylori stimulation that rapidly decreased, while SMO knockdown caused a greater increase in spermine that was sustained. With SMO knockdown, L-Arg uptake and killing of H. pylori by macrophages was prevented. The overexpression of SMO by transfection of an expression plasmid prevented the H. pylori-stimulated increase in spermine levels, and led to increased L-Arg uptake, iNOS protein expression and NO production, and H. pylori killing. In two human monocytic cell lines, U937 and THP-1, overexpression of SMO caused a significant enhancement of NO production with H. pylori stimulation. By depleting spermine, SMO can abrogate the inhibitory effect of polyamines on innate immune responses to H. pylori by enhancing antimicrobial NO production.

  5. Enhanced plasma ghrelin levels in Helicobacter pylori-colonized,interleukin-1-receptor type 1-homozygous knockout (IL-1R1-/-) mice

    Institute of Scientific and Technical Information of China (English)

    Yuka Abiko; Hidekazu Suzuki; Tatsuhiro Masaoka; Sachiko Nomura; Kumiko Kurabayashi; Hiroshi Hosoda; Kenji Kangawa; Toshifumi Hibi

    2005-01-01

    AIM: Ghrelin is an endogenous ligand for the growth hormone secretagogue receptor, and it plays a role in stimulating the growth hormone secretion, food intake,body weight gain and gastric motility. Eradication of Helicobacter pylori(H pylori) was shown to be associated with increase of the body weight. On the other hand, H pylori infection evokes the release of gastric IL-1β. The present study was designed to investigate the involvement of the gastric IL-1 signal in the ghrelin dynamics in H pyloricolonized mice.METHODS: Twelve-week-old female IL-1-receptor type 1-homozygous-knockout mice (IL-1R1-/-) and their wild-type littermates (WT) were orally inoculated with H pylori (Hp group), while other cohorts received oral inoculation of culture medium (Cont group). Thirteen weeks after the inoculation, the mice were examined. The plasma and stomach ghrelin levels and the gastric preproghrelin mRNA were measured.RESULTS: Although the WT mice with H pylori infection showed a significantly decreased body weight as compared with that of the animals without H pylori infection,H pylori infection did not influence the body weight of the IL-1R1-knockout (IL-1R1-/-) mice. In the H pylori-infected IL-1R1-/-mice, the total and active ghrelin levels in the plasma were significantly increased, and the gastric ghrelin level was decreased. No significant differences were noted in the gastric preproghrelin mRNA expression.CONCLUSION: Ghrelin secretion triggered by H pylori infection might be suppressed by IL-1β, the release of which is also induced by the infection, resulting in the body weight loss of mice with H pylori infection.

  6. Helicobacter pylori:Does it add to risk of coronary artery disease

    Institute of Scientific and Technical Information of China (English)

    Vishal; Sharma; Amitesh; Aggarwal

    2015-01-01

    Helicobacter pylori(H. pylori) is a known pathogen implicated in genesis of gastritis, peptic ulcer disease, gastric carcinoma and gastric lymphoma. Beyond the stomach, the organism has also been implicated in the causation of immune thrombocytopenia and iron deficiency anemia. Although an area of active clinical research, the role of this gram negative organism in causation of atherosclerosis and coronary artery disease(CAD) remains enigmatic. CAD is a multifactorial disease which results from the atherosclerosis involving coronaryarteries. The major risk factors include age, diabetes mellitus, smoking, hypertension and dyslipidemia. The risk of coronary artery disease is believed to increase with chronic inflammation. Various organisms like Chlamydia and Helicobacter have been suspected to have a role in genesis of atherosclerosis via causation of chronic inflammation. This paper focuses on available evidence to ascertain if the role of H. pylori in CAD causation has been proven beyond doubt and if eradication may reduce the risk of CAD or improve outcomes in these patients.

  7. Morphological and Cellular Features of Innate Immune Reaction in Helicobacter pylori Gastritis: A Brief Review.

    Science.gov (United States)

    Ieni, Antonio; Barresi, Valeria; Rigoli, Luciana; Fedele, Francesco; Tuccari, Giovanni; Caruso, Rosario Alberto

    2016-01-15

    Innate and adaptive immunity are both involved in acute and chronic inflammatory processes. The main cellular players in the innate immune system are macrophages, mast cells, dendritic cells, neutrophils, eosinophils, and natural killer (NK), which offer antigen-independent defense against infection. Helicobacter pylori (H. pylori) infection presents peculiar characteristics in gastric mucosa infrequently occurring in other organs; its gastric colonization determines a causal role in both gastric carcinomas and mucosa-associated lymphoid tissue lymphoma. In contrast, an active role for Epstein-Barr virus (EBV) has been identified only in 9% of gastric carcinomas. The aim of the present review is to discuss the role of cellular morphological effectors in innate immunity during H. pylori infection and gastric carcinogenesis.

  8. Preparation of epigallocatechin gallate-loaded nanoparticles and characterization of their inhibitory effects on Helicobacter pylori growth in vitro and in vivo

    Science.gov (United States)

    Lin, Yu-Hsin; Feng, Chun-Lung; Lai, Chih-Ho; Lin, Jui-Hsiang; Chen, Hao-Yun

    2014-08-01

    A variety of approaches have been proposed for overcoming the unpleasant side effects associated with antibiotics treatment of Helicobacter pylori (H. pylori) infections. Research has shown that epigallocatechin-3-gallate (EGCG), a major ingredient in green tea, has antibacterial activity for antiurease activity against H. pylori. Oral EGCG is not good because of its digestive instability and the fact that it often cannot reach the targeted site of antibacterial activity. To localize EGCG to H. pylori infection site, this study developed a fucose-chitosan/gelatin nanoparticle to encapsulate EGCG at the target and make direct contact with the region of microorganisms on the gastric epithelium. Analysis of a simulated gastrointestinal medium indicated that the proposed in vitro nanocarrier system effectively controls the release of EGCG, which interacts directly with the intercellular space at the site of H. pylori infection. Meanwhile, results of in vivo clearance assays indicated that our prepared fucose-chitosan/gelatin/EGCG nanoparticles had a significantly greater H. pylori clearance effect and more effectively reduced H. pylori-associated gastric inflammation in the gastric-infected mouse model than the EGCG solution alone.

  9. [Helicobacter pylori in the development of dental caries].

    Science.gov (United States)

    Moseeva, M V; Belova, E V; Vakhrushev, Ia M

    2010-01-01

    It is shown, that in patients with erosive and ulcer defects of gastroduodenal zone at settling Helicobacter pylori (Hp) in an oral cavity in 100% of cases caries develops at intensity 13.6 +/- 1.4 teeth. Produced Hp protease and ammonia cause disintegration connected to protein silica acids and reduce activity lysocim, worsening, thus, fluid and protective properties of a saliva. In the subsequent infringement of autopurification of a teeth results in accumulation of a dental strike where protease activity conditionally pathogenic microflora conducts to depolymerization and demineralization enamels of a teeth.

  10. Detection of Helicobacter pylori in Oral Lesions

    OpenAIRE

    Irani, Soussan; Monsef Esfahani, Alireza; Bidari Zerehpoush, Farahnaz

    2013-01-01

    Background and aims. Helicobacter pylori is a microaerophilic gram-negative spiral organism. It is recognized as the etiologic factor for peptic ulcers, gastric adenocarcinoma and gastric lymphoma. Recently, it has been isolated from dental plaque and the dorsum of the tongue. This study was designed to assess the association between H. pylori and oral lesions such as ulcerative/inflammatory lesions, squamous cell carcinoma (SCC) and primary lymphoma. Materials and methods. A total of 228 bio...

  11. Helicobacter pylori : migrations humaines et cancer gastrique

    OpenAIRE

    Breurec, Sébastien

    2011-01-01

    Helicobacter pylori is associated with severe gastroduodenal disorders but is also a bacterial genetic marker of human migrations. First, we provide evidence that distinct H. pylori genetic populations accompanied at least four ancient human migrations into Oceania and Southeast Asia: i) an expansion of Austronesian speaking people about 5000 years ago from Taiwan into Oceania, ii) a migration from India into Southeast Asia within the last 2000 years, iii) a migration of Austro-Asiatic speaki...

  12. Pleiotropic actions of Helicobacter pylori vacuolating cytotoxin, VacA.

    Science.gov (United States)

    Isomoto, Hajime; Moss, Joel; Hirayama, Toshiya

    2010-01-01

    Helicobacter pylori produces a vacuolating cytotoxin, VacA, and most virulent H. pylori strains secrete VacA. VacA binds to two types of receptor-like protein tyrosine phosphatase (RPTP), RPTPalpha and RPTPbeta, on the surface of host cells. VacA bound to RPTPbeta, relocates and concentrates in lipid rafts in the plasma membrane. VacA causes vacuolization, membrane anion-selective channel and pore formation, and disruption of endosomal and lysosomal activity in host cells. Secreted VacA is processed into p33 and p55 fragments. The p55 domain not only plays a role in binding to target cells but also in the formation of oligomeric structures and anionic membrane channels. Oral administration of VacA to wild-type mice, but not to RPTPbeta knockout mice, resulted in gastric ulcers, in agreement with the clinical effect of VacA. VacA with s1/m1 allele has more potent cytotoxic activity in relation to peptic ulcer disease and appears to be associated with human gastric cancer. VacA activates pro-apoptotic Bcl-2 family proteins, and induces apoptosis via a mitochondria-dependent pathway. VacA can disrupt other signal transduction pathways; VacA activates p38 MAPK, enhancing production of IL-8 and PGE(2), and PI3K/Akt, suppressing GSK-3beta activity. VacA has immunomodulatory actions on T cells and other immune cells, possibly contributing to the chronic infection seen with this organism. H. pylori virulence factors including VacA and CagA, which is encoded by cytotoxin-associated gene A, along with host genetic and environmental factors, constitute a complex network to regulate chronic gastric injury and inflammation, which is involved in a multistep process leading to gastric carcinogenesis.

  13. Regulation of tumour necrosis factor (TNF) induced apoptosis by soluble TNF receptors in Helicobacter pylori infection

    OpenAIRE

    Shibata, J; Goto, H.; Arisawa, T.; Niwa, Y.; Hayakawa, T.; Nakayama, A.; Mori, N.

    1999-01-01

    BACKGROUND—Tumour necrosis factor (TNF) is a predominant cytokine produced in the gastric mucosa of patients with Helicobacter pylori infection. TNF induces apoptosis in a variety of cells. The soluble TNF receptors (sTNF-Rs) can be divided into sTNF-RI and sTNF-RII, both of which inhibit TNF activity. However, their precise mechanisms remain unclear.
AIM—To investigate the role of sTNF-Rs in H pylori infection.
METHODS—In 40 patients, production of TNF and sTNF-Rs in gastric mucosa was measu...

  14. Dual Roles of Helicobacter pylori NapA in Inducing and Combating Oxidative Stress▿

    OpenAIRE

    Wang, Ge; Hong, Yang; Olczak, Adriana; Maier, Susan E.; Maier, Robert J.

    2006-01-01

    Neutrophil-activating protein (NapA) has been well documented to play roles in human neutrophil recruitment and in stimulating host cell production of reactive oxygen intermediates (ROI). A separate role for NapA in combating oxidative stress within H. pylori was implied by studies of various H. pylori mutant strains. Here, physiological analysis of a napA strain was the approach used to assess the iron-sequestering and stress resistance roles of NapA, its role in preventing oxidative DNA dam...

  15. Gastric angiogenesis and Helicobacter pylori infection Angiogénesis gástrica e infección por Helicobacter pylori

    Directory of Open Access Journals (Sweden)

    I. D. Pousa

    2006-06-01

    Full Text Available The formation of new blood vessels seen in conditions commonly associated with Helicobacter pylori (H. pylori infection, including gastritis, peptic ulcer, and gastric carcinoma, prompts consideration of a potential relationship between mucosal colonization by this organism and the angiogenic process. H. pylori directly or indirectly damages endothelial cells, which induces a number of changes in the microvasculature of the gastric mucosa. In H. pylori-associated conditions, that is, in gastritis, peptic ulcer and gastric carcinoma, there is an increased concentration of angiogenic factors, and subsequently a formation of new blood vessels. However, this early angiogenesis -which is activated to repair the gastric mucosa- is subsequently inhibited in patients with peptic ulcer, and ulcer healing is thus delayed. This may be due to the antiproliferative action of this organism on endothelial cells. While the angiogenic process becomes inhibited in infected patients with peptic ulcer, it remains seemingly active in those with gastritis or gastric cancer. This fact is in support of the notion suggested by various studies that peptic ulcer and gastric cancer are mutually excluding conditions. In the case of gastric cancer, neoangiogenesis would enhance nutrient and oxygen supply to cancer cells, and thus tumor growth and metastatic spread.

  16. Effects of killing Helicobacter pylori quadruple therapy on peptic ulcer: A randomized double-blind clinical trial

    Institute of Scientific and Technical Information of China (English)

    Li-Ying Feng; Xi-Xian Yao; Shu-Lin Jiang

    2005-01-01

    AIM: To study the therapeutic efficacy of a Chinese and Western integrated regimen, killing Helicobacter pylori quadruple therapy on H pylori-associated peptic ulcers(PU).METHODS: With prospective and double-blind controlled method, seventy-five active PU patients with H pylori infection were randomized to receive one of the following three regimens: (1) new triple therapy (group A:lansoprazole 30 mg qd, plus clarithromycin 250 mg bid,plus amoxycillin 500 mg tid, each for 10 d); (2) killing Hp quadruple therapy(group B: the three above drugs plus killing H pylori capsule 6 capsules bid for 4 wk) and (3)placebo(group C: gastropine 3 tablets bid for 4 wk).H pylori eradication and ulcer healing quality were evaluated under an endoscope 4 wk after treatment. The patients were followed up for 5 years.RESULTS: Both the healing rate of PU and H pylori eradication rate in group B were significantly higher than those in group C (100% and 96.4% vs 20% and 0%,respectively, P<0.005), but there was no significant difference compared to those in group A (88% and92%, P>0.05). The healing quality of ulcer in group B was superior to that in groups C and A (P<0.05). The recurrence rate of PU in group B (4%) was lower than that in group A (10%) and group C (100%, P<0.01).CONCLUSION: Killing Helicobacter pylori quadruple therapy can not only promote the eradication of H pylori and healing quality of ulcer but also reduce recurrence rate of ulcer.

  17. Changing epidemiology of Helicobacter pylori in Japan.

    Science.gov (United States)

    Inoue, Manami

    2017-03-01

    Helicobacter pylori (H. Pylori) is known as the most important cause of gastric cancer. The prevalence of H. pylori infection varies widely by geographic area, age, and socioeconomic status. In Japan, H. pylori infection has been highly correlated with the incidence rate of gastric cancer, and a reduction in H. pylori infection is therefore crucial for decreasing the incidence of gastric cancer, especially at the population level. Infection occurs during childhood, commonly before 5 years of age. In Japan, where gastric cancer has ranked as the most common cancer by incidence and mortality for the last several decades, the prevalence of H. pylori infection has dramatically declined by birth cohort effect, mainly due to improvements in the general hygiene environment in childhood. Older generations born before around 1950 show a high prevalence of around 80-90 %, decreasing with age to reach around 10 % or less in those born around the 1990s, and less than 2 % for children born after the year 2000. This change will have generational effects on gastric cancer prevention strategies, both primary and secondary. The risk-stratified approach to gastric cancer prevention should be considered in Japan and other countries which have similarly experienced rapid economic development.

  18. Study of serum Helicobacter pylori soluble antigen

    Institute of Scientific and Technical Information of China (English)

    吴勤动; 朱永良

    2002-01-01

    Objective: to explore a new serological method for detecting Helicobac ter pylori ( H. pylori ) infection. Methods: Serum soluble antigen of H. p ylor i was detected by using avidin-biotin ELISA technique to evaluate the status of H. pylori infection and for comparison with rapid urease test ( RUT ), histo logi c examination and serology. Results: The sensitivity, specificity, positive pred ictive value and negative predictive value were 77.46%, 91.07%, 91.67% a nd 76.12 %, respectively. The prevalence rate of serum H. pylori soluble antigen in 138 patients undergoing endoscopy was similar to the rate obtained by 14 C-UBT met hods ( P>0.05 ). Conclusions: The detection of serum H. pylori solub le antigen( HpSAg) could be used as a new serological method which is accurate, and convenie nt, not affected by the memorizing reaction of serum antibody; is more sensitive , m ore specific and suitable for clinical diagnosis, and evaluation of eradication and for follow-up of H. pylori as well as for detection in children and pre gnant women.

  19. Antiadhesion and anti-inflammation effects of noni (Morinda citrifolia) fruit extracts on AGS cells during Helicobacter pylori infection.

    Science.gov (United States)

    Huang, Hsin-Lun; Ko, Chien-Hui; Yan, Yeong-Yu; Wang, Chin-Kun

    2014-03-19

    Helicobacter pylori is a human gastric pathogen that adheres to host cells and injects cytotoxin-associated gene A (CagA) to induce interleukin-8 (IL-8), inducible nitric oxide (iNOS), and cyclooxygenase 2 (COX-2). Noni (Morinda citrifolia) is found to possess antibacteria, anti-inflammation, and antioxidation activities, but its effect on H. pylori infection is still unknown. Ethanol and ethyl acetate extracts of noni fruit were used in this study. The inhibitory effect on CagA and H. pylori-induced IL-8, iNOS, and COX-2 were determined. The coculture medium was collected for measuring neutrophil chemotaxis. Both extracts of noni fruit showed weak inhibition on H. pylori. Both ethanol and ethyl acetate extracts provided antiadhesion of H. pylori to AGS cells and down-regulation on the CagA, IL-8, COX-2, and iNOS expressions. Results also indicated both extracts relieved neutrophil chemotaxis. Noni fruit extracts down-regulated inflammatory responses during H. pylori infection, and the phenolic compounds play key role in antiadhesion.

  20. Effect of Helicobacter pylori infection on gastric mucosal pathologic change and level of nitric oxide and nitric oxide synthase

    Institute of Scientific and Technical Information of China (English)

    Yong-Fu Wang; Chun-Lin Guo; Li-Zhen Zhao; Guo-An Yang; Peng Chen; Hong-Kun Wang

    2005-01-01

    AIM: To investigate the level of nitric oxide (NO) and nitrous oxide synthase (NOS) enzyme and its effect on gastric mucosal pathologic change in patients infected with Helicobacter pylori (H pylori), and to study the pathogenic mechanism of H pylori.METHODS: The mucosal tissues of gastric antrum were taken by endoscopy, then their pathology, H pylori and anti-CagA-IgG were determined. Fifty H pyloripositive cases and 35 H pylori negative cases were randomly chosen.Serum level of NO and NOS was detected.RESULTS: One hundred and seven cases (71.33%) were anti-CagA-IgG positive in 150 H pyloripositive cases. The positive rate was higher especially in those with preneoplastic diseases, such as atrophy, intestinal metaplasia and dysplasia. The level of NO and NOS in positive group was higher than that in negative group, and apparently lower in active gastritis than in pre-neoplastic diseases such as atrophy, intestinal metaplasia and dysplasia.CONCLUSION: H pyloriis closely related with chronic gastric diseases, and type Ⅰ Hpylorimay be the real factor for Hpylori-related gastric diseases. Infection with H pylori can induce elevation of NOS, which produces NO.

  1. Identification of self-growth-inhibiting compounds lauric acid and 7-(Z)-tetradecenoic acid from Helicobacter pylori.

    Science.gov (United States)

    Yamashita, Shinpei; Igarashi, Masayuki; Hayashi, Chigusa; Shitara, Tetsuo; Nomoto, Akio; Mizote, Tomoko; Shibasaki, Masakatsu

    2015-06-01

    Helicobacter pylori growth medium is usually supplemented with horse serum (HS) or FCS. However, cyclodextrin derivatives or activated charcoal can replace serum. In this study, we purified self-growth-inhibiting (SGI) compounds from H. pylori growth medium. The compounds were recovered from porous resin, Diaion HP-20, which was added to the H. pylori growth medium instead of known supplements. These SGI compounds were also identified from 2,6-di-O-methyl-β-cyclodextrin, which was supplemented in a pleuropneumonia-like organisms broth. The growth-inhibiting compounds were identified as lauric acid (LA) and 7-(Z)-tetradecenoic acid [7-(Z)-TDA]. Although several fatty acids had been identified in H. pylori, these specific compounds were not previously found in this species. However, we confirmed that these fatty acids were universally present in the cultivation medium of the H. pylori strains examined in this study. A live/dead assay carried out without HS indicated that these compounds were bacteriostatic; however, no significant growth-inhibiting effect was observed against other tested bacterial species that constituted the indigenous bacterial flora. These findings suggested that LA and 7-(Z)-TDA might play important roles in the survival of H. pylori in human stomach epithelial cells.

  2. Improvement in symptoms after H2-receptor antagonist-based therapy for eradication of H pylori infection

    Institute of Scientific and Technical Information of China (English)

    2007-01-01

    AIM: To investigate the therapeutic effects of triple therapy combining lafutidine with clarithromycin and amoxicillin on H pylori infection and the resolution of gastroesophageal symptoms after eradication.METHODS: We conducted a randomized, multicenter,open-label controlled trial to compare the effectiveness of a triple therapy of lafutidine, clarithromycin, and amoxicillin (lafutidine group) with that of a triple therapy of lansoprazole, clarithromycin, and amoxicillin (lansoprazole group) in patients with H pylori infection. The study group comprised 22 patients with gastric ulcers and 18 patients with duodenal ulcers who had H pylori infection.RESULTS: H pylori eradication rates were similar in the lafutidine group (14/20, 70%) and the lansoprazole group (14/20, 70%). Gastroesophageal reflux and abdominal symptoms improved after eradication therapy in both groups, whereas abdominal discomfort, diarrhea,and constipation were unchanged. H pylori status had no apparent effect on improvement of gastroesophageal reflux or abdominal symptoms after treatment. Adverse events were similar in both groups.CONCLUSION: The triple therapy including lafutidine is equivalent to triple therapy including lansoprazole in terms of H pylori eradication rates and improvement in gastroesophageal reflux and abdominal symptoms.These results are attributed to the fact that lafutidine has strong, continuous antisecretory activity, unaffected by CYP2C19 polymorphisms.

  3. CXC chemokine CXCL12 tissue expression and circulating levels in peptic ulcer patients with Helicobacter pylori infection.

    Science.gov (United States)

    Bagheri, Vahid; Hassanshahi, Gholamhossein; Mirzaee, Vahid; Khorramdelazad, Hossein

    2016-09-01

    Helicobacter pylori (H. pylori) infection is among the most prevalent human infections. CXCL12 is a well-known CXC chemokine involved in inflammation and play major roles in angiogenesis. There is currently very limited data on the role of CXCL12 in peptic ulcer disease. Hence, we aimed to explore whether CXCL12 is involved in the pathogenesis of peptic ulcer induced by H. pylori. In this study, we enrolled 102 H. pylori-infected patients, including 51 with active ulcer (GA) and 51 with healing ulcer (GH). We also recruited 50 healthy subjects as control, which did not show any sign or symptoms of chronic inflammatory diseases, infection, or immune-related disorders. Endoscopy was performed to determine the stage of the disease. ELISA was used for detection of H. pylori infection and CXCL12 measurement. We also employed western blotting to detect CXCL12 in ulcerative lesions of H. pylori. Demographic data were also collected by questionnaire. Our results demonstrated that CXCL12 serum levels in GA group (151.8±18.31pg/mL) were significantly higher than those in GH (36.89±6.78pg/mL) and control groups (33.77±9.12pg/mL) (Pulcer. CXCL12 serum levels may also be used to distinguish between GA and GH phases of the disease.

  4. Early Attempts to Eradicate Helicobacter pylori after Endoscopic Resection of Gastric Neoplasm Significantly Improve Eradication Success Rates

    Science.gov (United States)

    Huh, Cheal Wung; Youn, Young Hoon; Jung, Da Hyun; Park, Jae Jun; Kim, Jie-Hyun; Park, Hyojin

    2016-01-01

    Purpose After endoscopic resection (ER) of gastric tumors, eradication of Helicobacter pylori (H. pylori) infection is advised to reduce metachronous recurrence. Optimal timing of such therapy (yet to be established) was investigated herein, examining early active and late scarring stages of post-ER iatrogenic ulcers. Materials and Methods Analysis included 514 patients who received proton-pump inhibitor (PPI)-based triple therapy for H. pylori eradication after ER for gastric neoplasms between January 2008 and June 2015. Clinicopathologic characteristics, particularly the timing of triple therapy, were used to compare eradication rates, assigning patients to early- (≤2 weeks), intermediate- (2–8 weeks), and late-phase (≥8 weeks) treatment groups. Results H. pylori eradication rates differed significantly by timing of triple therapy after ER (early, 90.0%; intermediate, 76.2%, late, 72.4%; p ulcer, and duration of therapeutic regimen. Early initiation of H. pylori eradication was also identified as a significant independent predictor of eradication success in multivariate analysis (Odds ratio = 3.67, 95% CI 2.18–6.16; p <.001). Conclusion In patients undergoing ER of gastric tumors, early post-ER attempts at eradication of H. pylori offer the best chance of eradication success. PMID:27588679

  5. Non-Viable Lactobacillus reuteri DSMZ 17648 (Pylopass™ as a New Approach to Helicobacter pylori Control in Humans

    Directory of Open Access Journals (Sweden)

    Andreas Busjahn

    2013-08-01

    Full Text Available Prevalence of infections by Helicobacter pylori, a pathogen involved in a number of gastrointestinal diseases, remains high in developing countries. Management of infections by eradication is not always an option. Lactobacillus reuteri (L. reuteri DSMZ17648 (Pylopass™/Lonza specifically co-aggregates H. pylori in vitro and was shown to reduce 13C urea breath test in vivo. In this pilot study, we tried to replicate previous findings in an independent sample and to evaluate effects of spray-drying vs. freeze-drying of cultures. A single-blinded, placebo-controlled study was done in 22 H. pylori positive, asymptomatic adults. H. pylori levels were determined by 13C-urea-breath method after 14 days of supplementation, as well as after 6, 12, and 24 weeks follow-up. In the test group, but not in the placebo group, a significant reduction of H. pylori was observed. For the first time, spray-dried cells of L. reuteri DSMZ17648 have been used in a human study and results are in line with the first study results, supplementing with freeze-dried material. This is of special interest as spray-drying results in dead cell material, meaning that the effect of L. reuteri must be independent of its probiotic activity. These results confirm the potential of Pylopass™ as a novel way to reduce the load of H. pylori.

  6. Effects of Helicobacter pylori eradication on atrophic gastritis and intestinal metaplasia: A 3-year follow-up study

    Institute of Scientific and Technical Information of China (English)

    Bin Lu; Ming-Tao Chen; Yi-Hong Fan; Yan Liu; Li-Na Meng

    2005-01-01

    AIM: To investigate the effect of H pylori eradication on atrophic gastritis and intestinal metaplasia (IM).METHODS: Two hundred and fifty-nine patients with atrophic gastritis in the antrum were included in the study, 154 patients were selected for H pylori eradication therapy and the remaining 105 patients served as untreated group. Gastroscopy and biopsies were performed both at the beginning and at the end of a 3-year follow-up study. Gastritis was graded according to the updated Sydney system.RESULTS: One hundred and seventy-nine patients completed the follow-up, 92 of them received H pylori eradication therapy and the remaining 87 H pyloriinfected patients were in the untreated group. Chronic gastritis, active gastritis and the grade of atrophy significantly decreased in H pylori eradication group (P<0.01). However, the grade of IM increased in H pylori -infected group (P<0.05).CONCLUSION: H pylori eradication may improve gastric mucosal inflammation, atrophy and prevent the progression of IM.

  7. Mutation of cytotoxin-associated gene A affects expressions of antioxidant proteins of Hellcobacter pylori

    Institute of Scientific and Technical Information of China (English)

    Zhi-Gang Huang; Guang-Cai Duan; Qing-Tang Fan; Wei-Dong Zhang; Chun-Hua Song; Xue-Yong Huang; Rong-Guang Zhang

    2009-01-01

    AIM: To determine if disruption of the cagA gene of Helicobacter pylori ( H pylori) has an effect on the expression of other proteins at proteome level.METHODS: Construction of a cagA knock out mutant Hp27_. cagA ( cagA-) via homologous recombinat ion wi th the wi ld- type st rain Hp27 ( cagA+) as a recipient was performed. The method of sonicat ion-urea-CHAPS-DTT was employed to extract bacterial proteins from both strains. Soluble proteins were analyzed by two-dimensional electrophoresis (2-DE). Images of 2-DE gels were digitalized and analyzed. Only spots that had a statistical significance in differential expression were selected and analyzed by matrix-assisted laser desorption/ionizationtime of flight mass spectrometry (MALDI-TOF-MS). Biological information was used to search protein database and identify the biological function of proteins. RESULTS: The proteome expressions between wild-type strain and isogenic mutant with the cagA gene knocked-out were compared. Five protein spots with high abundance in bacteria proteins of wild-type strains, down-regulated or absently expressed in bacteria proteins of mutants, were identified and analyzed. From a quantitative point of view, the identified proteins are related to the cagA gene and important antioxidant proteins of H pylori, including alkyl hydroperoxide reductase (Ahp), superoxide dismutase (SOD) and modulator of drug activity (Mda66), respectively, suggesting that cagA is important to maintain the normal activity of antioxidative stress and ensure H pylori persistent colonization in the host. CONCLUSION: cagA gene i s relevant to the expressions of antioxidant proteins of H pylori, which may be a novel mechanism involved in H pylori cagA pathogenesis.

  8. Predictive computational modeling of the mucosal immune responses during Helicobacter pylori infection.

    Directory of Open Access Journals (Sweden)

    Adria Carbo

    Full Text Available T helper (Th cells play a major role in the immune response and pathology at the gastric mucosa during Helicobacter pylori infection. There is a limited mechanistic understanding regarding the contributions of CD4+ T cell subsets to gastritis development during H. pylori colonization. We used two computational approaches: ordinary differential equation (ODE-based and agent-based modeling (ABM to study the mechanisms underlying cellular immune responses to H. pylori and how CD4+ T cell subsets influenced initiation, progression and outcome of disease. To calibrate the model, in vivo experimentation was performed by infecting C57BL/6 mice intragastrically with H. pylori and assaying immune cell subsets in the stomach and gastric lymph nodes (GLN on days 0, 7, 14, 30 and 60 post-infection. Our computational model reproduced the dynamics of effector and regulatory pathways in the gastric lamina propria (LP in silico. Simulation results show the induction of a Th17 response and a dominant Th1 response, together with a regulatory response characterized by high levels of mucosal Treg cells. We also investigated the potential role of peroxisome proliferator-activated receptor γ (PPARγ activation on the modulation of host responses to H. pylori by using loss-of-function approaches. Specifically, in silico results showed a predominance of Th1 and Th17 cells in the stomach of the cell-specific PPARγ knockout system when compared to the wild-type simulation. Spatio-temporal, object-oriented ABM approaches suggested similar dynamics in induction of host responses showing analogous T cell distributions to ODE modeling and facilitated tracking lesion formation. In addition, sensitivity analysis predicted a crucial contribution of Th1 and Th17 effector responses as mediators of histopathological changes in the gastric mucosa during chronic stages of infection, which were experimentally validated in mice. These integrated immunoinformatics approaches

  9. II Consenso Brasileiro sobre Helicobacter pylori Second Brazilian Consensus Conference on Helicobacter pylori infection

    Directory of Open Access Journals (Sweden)

    Luiz Gonzaga Vaz Coelho

    2005-06-01

    Full Text Available Avanços significativos ocorridos desde o Primeiro Consenso Brasileiro sobre H. pylori realizado em 1995, em Belo Horizonte, MG, justificam este segundo consenso. O evento foi organizado pela Federação Brasileira de Gastroenterologia e pelo Núcleo Brasileiro para Estudo do Helicobacter, sendo realizado em São Paulo nos dias 19 e 20 de junho de 2004. Contou com a participação das principais autoridades nacionais na área, a partir de lista elaborada pelas duas sociedades organizadoras do evento. Assim, participaram 36 delegados provenientes de 15 estados brasileiros, incluindo gastroenterologistas, patologistas, pediatras e microbiologistas. Os participantes foram alocados em um dos cinco sub-temas a serem contemplados no encontro, a saber: Helicobacter pylori e dispepsia funcional; Helicobacter pylori e AINEs; Helicobacter pylori e doença do refluxo gastroesofágico; tratamento Helicobacter pylori e retratamento Helicobacter pylori. Foi adotado como consensual as decisões que atingissem 70% ou mais de concordância entre os participantes. Os resultados foram apresentados em outubro de 2004 durante sessão especial da VI Semana Brasileira do Aparelho Digestivo, realizada em Recife, PE, e esta publicação apresenta o sumário das principais recomendações e conclusões do evento.Significant progress has been obtained since the First Brazilian Consensus Conference on H. pylori Infection held in 1995, in Belo Horizonte, MG, and justify a second meeting to establish updated guidelines on the current management of H. pylori infection. The Second Brazilian Consensus Conference on H. pylori Infection was organized by the Brazilian Federation of Gastroenterology and Brazilian Nucleus for the Study of Helicobacter and took place on June, 19-20, 2004 in São Paulo, SP. Thirty six delegates coming from 15 different Brazilian states including gastroenterologists, pathologists, microbiologists and pediatricians undertook the meeting. The

  10. Helicobacter pylori VacA suppresses Lactobacillus acidophilus-induced interferon beta signaling in macrophages via alterations in the endocytic pathway.

    Science.gov (United States)

    Weiss, Gudrun; Forster, Sam; Irving, Aaron; Tate, Michelle; Ferrero, Richard L; Hertzog, Paul; Frøkiær, Hanne; Kaparakis-Liaskos, Maria

    2013-06-11

    epithelium, remains elusive. Here we have shown that the H. pylori virulence factor VacA plays a key role by blocking the activation of innate cytokines induced by the probiotic Lactobacillus acidophilus in macrophages and suppresses the expression of key regulators required for the organization and dynamics of the intracellular cytoskeleton. Our results identify potential targets for the treatment of H. pylori infection and vaccination, since specific inhibition of the toxin VacA possibly allows the activation of an efficient immune response and thereby eradication of H. pylori in the host.

  11. Association Between Helycobacter Pylori Infection and Pathological Oral Manifestations

    Directory of Open Access Journals (Sweden)

    Carini Francesco

    2016-03-01

    Full Text Available Data from the literature are controversial regarding the presence of Helicobacter pylori (H. pylori in dental plaque and its association with gastric infection. One of the possible mechanisms suggested for re-infection is the recolonization with H. pylori from dental plaque. The purpose of this review was to determine whether dental plaque, poor oral hygiene, and periodontal disease were risk factors for H. pylori infection.

  12. Helicobacter pylori infection generates genetic instability in gastric cells

    DEFF Research Database (Denmark)

    Machado, Ana Manuel; Figueiredo, C.; Seruca, R.

    2010-01-01

    The discovery that Helicobacter pylori is associated with gastric cancer has led to numerous studies that investigate the mechanisms by which H. pylori induces carcinogenesis. Gastric cancer shows genetic instability both in nuclear and mitochondrial DNA, besides impairment of important DNA repair...... of the host, such as oxidative damage, methylation, chromosomal instability, microsatellite instability, and mutations. Interestingly, H. pylori infection generates genetic instability in nuclear and mitochondrial DNA. Based on the reviewed literature we conclude that H. pylori infection promotes gastric...

  13. Helicobacter pylori-coccoid forms and biofilm formation

    DEFF Research Database (Denmark)

    Andersen, Leif Percival; Rasmussen, Lone

    2009-01-01

    be detected by PCR in water supplies. There is no substantial evidence for viable H. pylori persisting in water supplies. Epidemiological studies suggest that environmental water is a risk factor for H. pylori infection when compared with tap water, and formation of H. pylori biofilm cannot be excluded....... Helicobacter pylori does not seem to take part in biofilm formation in the oral cavity even though the bacterium may be detected....

  14. Probiotics for the treatment of Helicobacter pylori infection in children

    OpenAIRE

    Pacifico, Lucia; Osborn, John Frederick; Bonci, Enea; Romaggioli, Sara; Baldini, Rossella; Chiesa, Claudio

    2014-01-01

    The combination of a proton pump inhibitor and two antibiotics (clarithromycin plus amoxicillin or metronidazole) has been the recommended first-line therapy since the first guidelines for Helicobacter pylori (H. pylori) infection in children were published. In recent years, the success of eradication therapies has declined, in part due to the development of H. pylori resistant strains. Alternative anti-H. pylori treatments are currently becoming more popular than the traditional eradication ...

  15. Extraintestinal manifestations of Helicobacter pylori: A concise review

    OpenAIRE

    Wong, Frank; Rayner-Hartley, Erin; Byrne, Michael F

    2014-01-01

    Helicobacter pylori (H. pylori) infection has been clearly linked to peptic ulcer disease and some gastrointestinal malignancies. Increasing evidence demonstrates possible associations to disease states in other organ systems, known as the extraintestinal manifestations of H. pylori. Different conditions associated with H. pylori infection include those from hematologic, cardiopulmonary, metabolic, neurologic, and dermatologic systems. The aim of this article is to provide a concise review of...

  16. Association Between Helycobacter Pylori Infection and Pathological Oral Manifestations

    Institute of Scientific and Technical Information of China (English)

    Carini Francesco; Samir Mallat; Cappello Francesco; Zummo Giovani; Jurjus Abdo; Tomasello Giovanni; Leone Angelo; Di Pasquale Roberto; Saniflippo Beatrice; Sinagra Emanuele; Damiani Provvidenza; Rosalyn Jurjus; Alice Gerges-Geagea; Inaya Hajj Hussein

    2016-01-01

    Data from the literature are controversial regarding the presence of Helicobacter pylori (H. pylori) in dental plaque and its association with gastric infection. One of the possible mechanisms suggested for re-infection is the recolonization with H. pylori from dental plaque. The purpose of this review was to determine whether dental plaque, poor oral hygiene, and periodontal disease were risk factors for H. pylori infection.

  17. Observation of efficacy of anti-helicobacter pylori chemotherapy combined with metronidazole and sulfuris cream on acne rosacea%抗幽门螺杆菌药物联合甲硫霜治疗酒渣鼻疗效观察

    Institute of Scientific and Technical Information of China (English)

    陈俊杰

    2013-01-01

    目的 探讨抗幽门螺杆菌(Hp)药物联合甲硫霜治疗酒渣鼻的疗效.方法 78例酒渣鼻患者随机分为两组,两组均外涂甲硫霜,3次/d.在此基础上,治疗组口服奥美拉唑、克拉霉素、替硝唑,两组疗程均为14 d,疗程结束判定疗效.结果 治疗组有效率为82.50%,对照组有效率为32.84%,两组有效率比较差异有统计学意义(χ2=16.96,P < 0.01).结论 抗Hp药物能显著提高治疗酒渣鼻的疗效.

  18. Furazolidone therapy for Helicobacter pylori: Is it effective and safe?

    Institute of Scientific and Technical Information of China (English)

    Vincenzo De Francesco; Enzo Ierardi; Cesare Hassan; Angelo Zullo

    2009-01-01

    Some aspects related with the use of furazolidone as a rescue therapy for Helicobacter pylori ( H pylori) infection should be remarked, especially regarding its potential oncologic risk. The inclusion of furazolidone in a treatment regimen for H pylori infection is, at least, controversial, and it does not appear to be safe.

  19. Helicobacter Pylori and the Prevention of Gastric Cancer

    Directory of Open Access Journals (Sweden)

    Terrence Sullivan

    2004-01-01

    Full Text Available BACKGROUND: Helicobacter pylori is an important cause of stomach cancer that infects a substantial proportion of the Canadian adult population. H pylori can be detected by noninvasive tests and effectively eradicated by medical treatment. Screening for and treatment of H pylori may represent a significant opportunity for preventive oncology.

  20. Antral atrophy, intestinal metaplasia, and preneoplastic markers in Mexican children with Helicobacter pylori-positive and Helicobacter pylori-negative gastritis.

    Science.gov (United States)

    Villarreal-Calderon, Rodolfo; Luévano-González, Arturo; Aragón-Flores, Mariana; Zhu, Hongtu; Yuan, Ying; Xiang, Qun; Yan, Benjamin; Stoll, Kathryn Anne; Cross, Janet V; Iczkowski, Kenneth A; Mackinnon, Alexander Craig

    2014-06-01

    Chronic inflammation and infection are major risk factors for gastric carcinogenesis in adults. As chronic gastritis is common in Mexican children, diagnosis of Helicobacter pylori and other causes of gastritis are critical for the identification of children who would benefit from closer surveillance. Antral biopsies from 82 Mexican children (mean age, 8.3 ± 4.8 years) with chronic gastritis (36 H pylori+, 46 H pylori-) were examined for gastritis activity, atrophy, intestinal metaplasia (IM), and immunohistochemical expression of gastric carcinogenesis biomarkers caudal type homeobox 2 (CDX2), ephrin type-B receptor 4 (EphB4), matrix metalloproteinase 3 (MMP3), macrophage migration inhibitory factor (MIF), p53, β-catenin, and E-cadherin. Atrophy was diagnosed in 7 (9%) of 82, and IM, in 5 (6%) of 82 by routine histology, whereas 6 additional children (7%) (3 H pylori+) exhibited aberrant CDX2 expression without IM. Significant positive correlations were seen between EphB4, MMP3, and MIF (Pgastritis.

  1. Iron status and Helicobacter pylori infection in symptomatic children: an international multi-centered study.

    Directory of Open Access Journals (Sweden)

    Dulciene Maria Magalhaes Queiroz

    Full Text Available OBJECTIVE: Iron deficiency (ID and iron deficiency anaemia (IDA are global major public health problems, particularly in developing countries. Whilst an association between H. pylori infection and ID/IDA has been proposed in the literature, currently there is no consensus. We studied the effects of H. pylori infection on ID/IDA in a cohort of children undergoing upper gastrointestinal endoscopy for upper abdominal pain in two developing and one developed country. METHODS: In total 311 children (mean age 10.7±3.2 years from Latin America--Belo Horizonte/Brazil (n = 125, Santiago/Chile (n = 105--and London/UK (n = 81, were studied. Gastric and duodenal biopsies were obtained for evaluation of histology and H. pylori status and blood samples for parameters of ID/IDA. RESULTS: The prevalence of H. pylori infection was 27.7% being significantly higher (p<0.001 in Latin America (35% than in UK (7%. Multiple linear regression models revealed H. pylori infection as a significant predictor of low ferritin and haemoglobin concentrations in children from Latin-America. A negative correlation was observed between MCV (r = -0.26; p = 0.01 and MCH (r = -0.27; p = 0.01 values and the degree of antral chronic inflammation, and between MCH and the degree of corpus chronic (r = -0.29, p = 0.008 and active (r = -0.27, p = 0.002 inflammation. CONCLUSIONS: This study demonstrates that H. pylori infection in children influences the serum ferritin and haemoglobin concentrations, markers of early depletion of iron stores and anaemia respectively.

  2. ASSESSMENT OF PATTERN OF ANTIMICROBIAL RESISTANCE OF HELICOBACTER PYLORI IN PATIENTS OF DYSPEPSIA OF RURAL AREA

    Directory of Open Access Journals (Sweden)

    Yogendra

    2015-08-01

    Full Text Available BACKGROUND : Helicobacter Pylori is a gastric pathogen that chronically infects more than half of the world's population. Unless treated, colonization usually persists lifelong. H. pylori infection represents a key factor in the etiology of various gastrointestinal diseases, ranging from chronic active gastritis without clinical symptoms to peptic ulceration, gastric adenocarcinoma, and gastric mucosa - associated lymphoid tissue lymphoma. Helicobacter pylori eradication rate varies in different parts of the world. This may be related to the regional difference in anti - microbial resistance that affects the outcome of therapy, genetic difference in the metabolism of the proton pump inhibitor, which can also alter the availability of anti - microbial in the stomach. The pattern of antimicrobial resistant of Helicobacter pylori has not been tested in this part of central India. In present study we have assessed the pattern of anti - microbial resistance of Helicobacter Pylori in patients of dyspepsia attending medicine opd , Department of Medicine, Dr. BRAM Hospital, Raipur (Chhattisgarh, India. METHODS: The present study was conducted in the Department of Medicine, Pt . J. N. M. Medical College, and Dr . BRAM Hospital Raipur (C.G. 60 patients attending medicine opd were subjected to upper gastrointestinal endoscopy. Multiple biopsy specimens taken from the gastric antrum. Rapid urease test were done. The biopsy specimen was inoculated in to culture media. The strains were subjected to antibiotic sensitivity test by disk diffusion method for metronidazole, tinidazole, Ornidazole, Clarithromycin, amoxicillin, tetracycline, furazolidone, ofloxacin and ciprofl oxacin. RESULT : The antibiotic resistance of H. Pylori in culture positive cases in our study showed 84.6%o of cases were resistant to Metronidazole, 38.5% to Tinidazole, 7.6%o to Ornidazole, 32.8% to Amoxicillin, 3.8% to Tetracycline, 19.2% to Clarithromycin, 11.5% to furazolidone, and 3

  3. Assessment of antibacterial effect of garlic in patients infected with Helicobacter pylori using urease breath test

    Science.gov (United States)

    Zardast, Mahmoud; Namakin, Kokab; Esmaelian Kaho, Jamil; Hashemi, Sarira Sadat

    2016-01-01

    Objective: Helicobacter pylori (H. pylori) is the most common pathogenic bacteria in the stomach. The aim of the current study was to explore the effect of oral garlic administration on bacterial urease activity inside the stomach and its contribution to the treatment of H. pylori infection. Materials and Methods: In this clinical trial, 15 patients were studied quantitatively with Urease Breath Test (UBT). The patients with gastrointestinal symptoms and a positive serum H. pylori IgG were enrolled. UBT was performed for each patient in three sessions as follows: at the beginning of the study, an initial UBT was performed based on which, the positive cases entered the study and the negative ones were excluded. Second UBT was done three days later in patients who were not receiving any treatment and were considered as the control, whereas the third UBT was performed three days after prescribing two medium-sized cloves of garlic (3 g) with their meal, twice a day (at noon and in the evening). The collected data were analyzed using ANOVA and Bonferroni tests and the significance level was set at p<0.05. Results: the mean UBT significantly differed before and after treatment with garlic cloves, being significantly lower after garlic consumption. No meaningful difference was observed in the mean UBT without garlic consumption between the first and second steps. Conclusion: Raw garlic has anti-bacterial effects against H. pylori residing in the stomach and may be prescribed along with routine drugs for the treatment of gastric H. pylori infection. PMID:27761418

  4. The molecular phylogenetic analysis based on the relationship between signature sequences of vacA gene types from Helicobacter pylori in China and VacA activities%中国幽门螺杆菌vacA基因型标签序列与VacA活性关系的分子系统发育分析

    Institute of Scientific and Technical Information of China (English)

    杨泽民; 何震宇; 陈伟强

    2012-01-01

    Objective To analyze the molecular phylogenetic relationships among s,m and i regions amino acid sequences of vacA gene from China H. pylori stains, and its effect on Vac A activities. Methods All VacA full-length amino acid sequences from China H. pylori stains were downloaded from GenBank database. The s, m and i regions amino acid sequences of vacA gene, and VacA full-length amino acid sequences were analyzed by ClustalX 2.0 and MEGA 5.05 software .and its molecular phylogeny trees were also constructed. Results All vacA gene types of no and low cytotoxin strain from China H. pylori were s1/ m2/il,while all high cytotoxin strain were sl/ml/il,except for chimeric ml - m2 H. pylori strain,ch2. The si type was strongly related to il type. Molecular phylogenetic analysis showed the s,m and i regions amino acid sequences of vacA gene from China H. pylori stains indicated obviously geography specificity. The VacA high and no/low cytotoxin stains could be completely classified by the molecular phylogeny tree of m region,while s and i region not. Conclusion The m region amino acid of vacA might be better to as virulence marker of VacA for China H. pylori.%目的 探讨中国幽门螺杆菌vacA基因s、m和i区氨基酸序列分子系统发育关系及其对VacA活性的影响.方法 从GenBank数据库中下载所有中国幽门螺杆菌VacA全长氨基酸序列,利用ClustalX 2.0和MEGA 5.05软件对vacA基因s、m和i区氨基酸序列及VacA全长氨基酸序列进行生物信息学分析,构建分子系统发育树.结果 中国幽门螺杆菌无毒弱毒株vacA基因型全为s1/m2/i1型,而强毒株除Ch2菌株为m1 -m2杂合型之外,全为s1/m1/i1型,s1型和i1型强相关.分子系统发育分析显示,中国幽门螺杆菌vacA基因s、m和i区氨基酸序列都呈现明显的地理特异性,其中m区分子系统发育树能够将VacA强毒株和无毒弱毒株分开,而s和i区分子系统发育树则不能将两者完全分开.结论 vacA基因m区氨基

  5. Diagnosis of Helicobacter pylori infection and diseases associated with Helicobacter pylori by Helicobacter pylori outer membrane proteins

    Institute of Scientific and Technical Information of China (English)

    Zheng Jiang; Ai-Long Huang; Xiao-Hong Tao; Pi-Long Wang

    2004-01-01

    AIM: To examine the serological response of patients with upper gastrointestinal diseases and Helicobocter pylori(Hpylori)infection to two H pylori outer membrane proteins (OMPs)(Mr18 000 and Mr26 000) acquired by gene recombinanttechnique, and to determine the diagnostic significance of serological tests derived from these OMPs.METHODS: Recombinant vectors encoding the two H pylori OMPs were used to transform and express in BL21 (DE3)E. coli. After purification with Ni2+-NTA agarose resin, colloid gold kits were prepared with purified recombinant proteins to detect H pylori infection and H pylori-associated diseases by the immunity-marker technology. We selected 150 patients with H pyloriinfection and digestive symptoms without previous treatment, induding chronic gastritis (n = 60), duodenal ulcer (n = 30), gastric ulcer (n = 30), and gastric cancer (n = 30).As controls, 33 H pylori-negative healthy volunteers were also recruited. Serum samples were collected from all subjects, and the antibodies to specific proteins of H pylori were tested with the colloid gold test kits. The sensitivity,specificity and accuracy of the colloid gold tests were evaluated, by using the combination of standard diagnostic methods (13C urea breath test and bacteria culture) and classic enzyme-linked immunosorbent assay (ELISA) as reference.RESULTS: After purification with Ni2+-NTA agarose resin,the purity of recombinant fusion proteins was about 95%.The recombinant fusion proteins were recognized by the specific monoclonal antibodies against the two H pylori OMPs,as demonstrated by the ELISA. Of the 150 serum samples from patients infected with H pylori 141 (94.0%) responded positively to the recombinant protein with Mr26 000, while the seropositive rates were 95.0%, 96.7%, 96.7% and 90.0%for patients with H pylori-associated chronic gastritis,duodenal ulcer, gastric ulcer, and gastric cancer respectively.The sensitivity, specificity, and accuracy of the colloid gold kit with Mr26 000

  6. Comparison of IL-6, IL-8 Concentrations in H. pylori- and non-H. pylori-associated Gastritis

    Directory of Open Access Journals (Sweden)

    Gontar Alamsyah Siregar

    2014-12-01

    Full Text Available BACKGROUND: Helicobacter pylori is a non-invasive microorganism causing intense gastric mucosal inflammatory and immune reaction. The gastric mucosal levels of the proinflammatory cytokines Interleukin 6 (IL-6 and IL-8 have been reported to be increased in H. pylori infection, but the serum levels in H. pylori infection is still controversial. The purpose of this study was to investigate the serum levels of IL-6 and IL-8 in H. pylori infection. METHODS: A cross sectional study was done on eighty consecutive gastritis patients admitted to endoscopy units at Adam Malik General Hospital and Permata Bunda Hospital, Medan, Indonesia from May-October 2014. Histopathology was performed for the diagnosis of gastritis. Rapid urease test for diagnosis of H. pylori infection. Serum samples were obtained to determine circulating IL-6 and IL-8. Univariate and bivariate analysis (independent t test were done. RESULTS: There were 41.25% patients infected with H. pylori. Circulatory IL-6 levels were significantly higher in H. pylori-infected patients compared to H. pylori negative, but there were no differences between serum levels of IL-8 in H. pylori positive and negative patients. CONCLUSIONS: The immune response to H. pylori promotes systemic inflammation, which was reflected in an increased level of serum IL-6. Serum levels of IL-8 were not significantly different between H. pylori positive and negative. KEYWORDS: Helicobacter pylori, gastritis, IL-6, IL-8, cytokine.

  7. Helicobacter Pylori and Gastric Cancer: Clinical Aspects

    Institute of Scientific and Technical Information of China (English)

    Zhi-Qiang Song; Li-Ya Zhou

    2015-01-01

    Objective: Although Helicobacterpylori (H.pylori) is considered as the main etiological factor for gastric cancer, the strategy of screening and treating the oncogenic bacterium is still controversial.The objective was to evaluate the status and progress of the cognition about the relationship between H.pylori infection and gastric cancer from a clinical aspect.Data Sources: The data used in this review were mainly from the PubMed articles published in English from 1984 to 2015.Study Selection: Clinical research articles were selected mainly according to their level of relevance to this topic.Results: Gastric cancer is the fifth most common malignancy and the third leading cause of cancer deaths worldwide.The main etiological factor for gastric cancer is H.pylori infection.About 74.7-89.0% gastric cancer was related to H.pylori infection.Up to date, some regional gastric cancer prevention programs including the detection and treatment of H.pylori infection are under way.Current data obtained from the randomized controlled trials suggest that population-based H.pylori screening and treatment is feasible and cost-effective in preventing gastric cancer;however, a population-based H.pylori eradication campaign would potentially lead to bacterial resistance to the corresponding antibiotics, as well as a negative impact on the normal flora.Conclusions: The important questions of feasibility, program costs, appropriate target groups for intervention, and the potential harm of mass therapy with antibiotics must first be answered before implementing any large-scale program.

  8. Helicobacter pylori Antibiotic Resistance: Trends Over Time

    Directory of Open Access Journals (Sweden)

    Raymond G Lahaie

    2000-01-01

    Full Text Available Resistance to antibiotics can be a major problem in the treatment of bacterial infections. As the use of antibiotics increases, bacterial resistance to these agents is rising and in many cases is responsible for the failure of treatment regimens. Although the treatment of Helicobacter pylori infection requires the use of more than one antibiotic to obtain adequate eradication rates, the efficacy of the currently used antibiotic combinations has been shown to be decreased by resistance to one of the antibiotics. The use of antibiotics in regimens for the treatment of H pylori is increasing in many countries, including Canada. This increase is both in the use of these antibiotics alone for the treatment of nongastrointestinal infections and in their use in association with proton pump inhibitors for the treatment of H pylori infection. In several European and Asian countries, where resistance to antibiotics is being monitored, it has been demonstrated that H pylori resistance to metronidazole and to clarithromycin increased throughout the 1990s. Thus far, the data available in Canada do not show increased resistance to either of these antibiotics. As for other antibiotics used in the treatment of H pylori infection, such as tetracycline and amoxicillin, the rate of resistance to these agents is still very low and does not constitute a significant problem. Because the efficacy of the regimens used in the treatment of H pylori infection is compromised by resistance to the antibiotics used, it is important that H pylori resistance rates in Canada and throughout the world continue to be monitored. Only with such reliable data can the most optimal regimens be recommended.

  9. Agglutination of Helicobacter pylori coccoids by lectins

    Institute of Scientific and Technical Information of China (English)

    Mar Mar Khin; Jie Song Hua; Hah Cong Ng; Bow Ho; Torkel Wadstrorr

    2000-01-01

    AIM To study the agglutination pattern of Helicobacter pylori coccoid and spiral forms.METHODS Assays of agglutination and agglutination inhibition were applied using fifteen commercial lectins. RESULTS Strong agglutination was observed with mannose-specific Concanavalin A (Con A ),fucose-specific Tetragonolobus purpureas ( Lotus A ) and N-acetyl glucosamine-specific Triticum vulgaris (WGA) lectins. Mannose and fucose specific lectins were reactive with all strains of H. pylori coccoids as compared to the spirals. Specific carbohydrates, glycoproteins and mucin were shown to inhibit H. pylori lectin-agglutination reactions. Pre-treatment of the bacterial cells with formalin and sulphuric acid did not alter the agglutination patterns with lectins. However, sodium periodate treatment of bacterial cells were shown to inhibit agglutination reaction with Con A, Lotus A and WGA lectins. On the contrary, enzymatic treatment of coccoids and spirals did not show marked inhibition of H. pylori-lectin agglutination. Interestingly, heating of H.pylori cells at 60℃ for 1 hour was shown to augment the agglutination with all of the lectins tested. CONCLUSION The considerable differences in lectin agglutination patterns seen among the two differentiated forms of H. pylori might be attributable to the structural changes during theevents of morphological transformation,resulting in exposing or masking some of the sugar residues on the cell surface. Possibility of various sugar residues on the cell wall of the coccoids may allow them to bind to different carbohydrate receptors on gastric mucus and epithelial cells. The coccoids with adherence characteristics like the spirals could aid in the pathogenic process of Helicobacter infection.This may probably lead to different clinical outcome of H. pylori associated gastroduodenal disease.

  10. A C-Terminal Coiled-Coil Region of CagL is Responsible for Helicobacter Pylori-Induced Il-8 Expression.

    Science.gov (United States)

    Wiedemann, Tobias; Hofbaur, Stefan; Loell, Eva; Rieder, Gabriele

    2016-09-29

    Interleukin-8 (IL-8) is a potent neutrophil-activating chemokine which triggers the infiltration and migration of neutrophils into areas of bacterial infection. Helicobacter pylori-infected patient studies as well as animal models have revealed that H. pylori type I strains carrying an intact cytotoxin-associated gene pathogenicity island (cag-PAI) with a functional type IV secretion system (T4SS) induce IL-8 expression and secretion in gastric mucosa. This gastric mucosal IL-8 expression correlates with severe histological changes due to H. pylori infection. In the present study, we explored a new recognition pattern on the bacterial adhesion protein CagL inducing IL-8 expression in H. pylori-infected host cells. To analyze the secreted IL-8 concentration, we performed IL-8 enzyme-linked immunosorbent assay (ELISA). To investigate the H. pylori-induced IL-8 expression on the transcriptional level, we transiently transfected gastric epithelial cells (AGS) with a human IL-8 luciferase reporter construct. The results of this study demonstrate that specifically the C-terminal coiled-coil region of the H. pylori CagL protein, a protein described to be located on the tip of the T4SS-pilus, is responsible for several in vitro observations: 1) H. pylori-induced IL-8 secretion via the transforming growth factor (TGF)-α activated epidermal growth factor-receptor (EGF-R) signaling pathway; 2) H. pylori-induced elongation of the cells, a typical CagA-induced phenotype; and 3) the bridging of the T4SS to its human target cells. This novel bacterial-host recognition sequence allows a new insight into how H. pylori induces the inflammatory response in gastric epithelial cells and facilitates the development of precancerous conditions.

  11. A C-Terminal Coiled-Coil Region of CagL is Responsible for Helicobacter Pylori-Induced Il-8 Expression

    Science.gov (United States)

    Wiedemann, Tobias; Hofbaur, Stefan; Loell, Eva; Rieder, Gabriele

    2016-01-01

    Interleukin-8 (IL-8) is a potent neutrophil-activating chemokine which triggers the infiltration and migration of neutrophils into areas of bacterial infection. Helicobacter pylori-infected patient studies as well as animal models have revealed that H. pylori type I strains carrying an intact cytotoxin-associated gene pathogenicity island (cag-PAI) with a functional type IV secretion system (T4SS) induce IL-8 expression and secretion in gastric mucosa. This gastric mucosal IL-8 expression correlates with severe histological changes due to H. pylori infection. In the present study, we explored a new recognition pattern on the bacterial adhesion protein CagL inducing IL-8 expression in H. pylori-infected host cells. To analyze the secreted IL-8 concentration, we performed IL-8 enzyme-linked immunosorbent assay (ELISA). To investigate the H. pylori-induced IL-8 expression on the transcriptional level, we transiently transfected gastric epithelial cells (AGS) with a human IL-8 luciferase reporter construct. The results of this study demonstrate that specifically the C-terminal coiled-coil region of the H. pylori CagL protein, a protein described to be located on the tip of the T4SS-pilus, is responsible for several in vitro observations: 1) H. pylori-induced IL-8 secretion via the transforming growth factor (TGF)-α activated epidermal growth factor-receptor (EGF-R) signaling pathway; 2) H. pylori-induced elongation of the cells, a typical CagA-induced phenotype; and 3) the bridging of the T4SS to its human target cells. This novel bacterial-host recognition sequence allows a new insight into how H. pylori induces the inflammatory response in gastric epithelial cells and facilitates the development of precancerous conditions. PMID:27766167

  12. Efficacy of omeprazole and amoxicillin with either clarithromycin or metronidazole on eradication of Helicobacter pylori in Chinese peptic ulcer patients

    Institute of Scientific and Technical Information of China (English)

    Wei-Hao Sun; Han Su; Xi-Long Ou; Da-Zhong Cao; Qian Yu; Ting Yu; Jin-Ming Hu; Feng Zhu; Yun-Liang Sun; Xi-Ling Fu

    2005-01-01

    AIM: One-week triple therapy with proton pump inhibitors, clarithromycin and amoxicillin has recently been proposed as the first-line treatment for Helicobacter pylori(H pylori) infection; however, data regarding the effects of this regimen in China are scarce. The aim of this prospective and randomized study was to compare the efficacy of clarithromycin and metronidazole when they were combined with omeprazole and amoxicillin on eradication of H pylori and ulcer healing in Chinese peptic ulcer patients.METHODS: A total of 103 subjects with H pylori-positive peptic ulcer were randomly divided into two groups, and accepted triple therapy with omeprazole 20 mg, amoxicillin 1 000 mg and either clarithromycin 500 mg (OAC group,n = 58) or metronidazole 400 mg (OAM group, n = 45).All drugs were given twice daily for 7 d. Patients with active peptic ulcer were treated with omeprazole 20 mg daily for 2-4 wk after anti-H pylori therapy. Six to eight weeks after omeprazole therapy, all patients underwent endoscopies and four biopsies (two from the antrum and two others from the corpus of stomach) were taken for rapid urease test and histological analysis (with modified Giemsa staining) to examine H pylori. Successful eradication was defined as negative results from both examination methods.RESULTS: One hundred patients completed the entire course of therapy and returned for follow-up. The eradication rate of H pylori for the per-protocol analysis was 89.3% (50/56) in OAC group and 84.1% (37/44) in OAM group. Based on the intention-to-treat analysis, the eradication rate of H pylori was 86.2% (50/58) in OAC group and 82.2% (37/45) in OAM group. There were no significant differences in eradication rates between the two groups on either analysis. The active ulcer-healing rate was 96.7% (29/30) in OAC group and 100% (21/21)in OAM group (per-protocol analysis, P>0.05). Six patients in OAC group (10.3%) and five in OAM group (11.1%)reported adverse events (P>0.05).CONCLUSION

  13. Helicobacter pylori induces in-vivo expansion of human regulatory T cells through stimulating interleukin-1β production by dendritic cells.

    Science.gov (United States)

    Mitchell, P J; Afzali, B; Fazekasova, H; Chen, D; Ali, N; Powell, N; Lord, G M; Lechler, R I; Lombardi, G

    2012-12-01

    Helicobacter pylori is one of the most common infections in the world. Despite inciting inflammation, immunological clearance of the pathogen is often incomplete. CD4(+) CD25(hi) forkhead box protein 3 (FoxP3(+)) regulatory T cells (T(regs)) are potent suppressors of different types of immune responses and have been implicated in limiting inflammatory responses to H. pylori. Investigating the influence of H. pylori on T(reg) function and proliferation, we found that H. pylori-stimulated dendritic cells (DCs) induced proliferation in T(regs) and impaired their suppressive capability. This effect was mediated by interleukin (IL)-1β produced by H. pylori-stimulated DCs. These data correlated with in-vivo observations in which H. pylori(+) gastric mucosa contained more T(regs) in active cell division than uninfected stomachs. Inciting local proliferation of T(regs) and inhibiting their suppressive function may represent a mechanism for the chronic gastritis and carcinogenesis attributable to H. pylori.

  14. [Peptic Ulcer Disease Associated with Helicobacter pylori Infection].

    Science.gov (United States)

    Yeo, Se-Hwan; Yang, Chang-Hun

    2016-06-25

    Although the global prevalence of peptic ulcer disease (PUD) is decreasing, PUD is still one of the most common upper gastrointestinal diseases in the world due to Helicobacter pylori infection and increased use of non-steroidal anti-inflammatory drugs. In Korea, the prevalence of H. pylori infection is also declining, but it is still the major cause of PUD. The outcomes of H. pylori infection are caused by imbalances between bacterial virulence factors, host factors, and environmental influences. In this review, we describe the prevalence trends of H. pylori infection in Korea, the mechanism of H. pylori infection-related PUD, and treatment strategies.

  15. Helicobacter pylori Infection and atherosclerosis: a systematic review.

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    Reza Karbasi-Afshar

    2015-02-01

    Full Text Available Helicobacter pylori (H. pylori is a spiral-shaped gram negative bacterium that naturally colonizes the human gastric epithelium. In recent years, large evidence has come to the literature strongly proposing causal link between H. pylori and extra gastric disorders. Cardiovascular system is one of the extra gastric organs that can be affected by H. pylori infection. The first evidence suggestive of such an association comes from seroepidemiological evaluations, but histopathological and eradication studies have strongly confirmed existence of a causal association between H. pylori infection and cardiovascular events.

  16. Innate immune responses to Helicobacter pylori infection: an overview.

    Science.gov (United States)

    Patel, Milan K; Trombly, Melanie I; Kurt-Jones, Evelyn A

    2012-01-01

    Innate immune receptors detect Helicobacter pylori infection and trigger downstream signaling events that result in the production of cytokines and interferon-β. This chapter gives an overview of the receptors and their roles in responding to H. pylori infection and details the downstream signaling events. The tools that have been developed to study the innate immune response to H. pylori are also discussed. Understanding the immune response to H. pylori is critical to develop better treatments for H. pylori-induced disease states including gastric malignancies and cancer.

  17. Horizontal versus familial transmission of Helicobacter pylori.

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    Sandra Schwarz

    2008-10-01

    Full Text Available Transmission of Helicobacter pylori is thought to occur mainly during childhood, and predominantly within families. However, due to the difficulty of obtaining H. pylori isolates from large population samples and to the extensive genetic diversity between isolates, the transmission and spread of H. pylori remain poorly understood. We studied the genetic relationships of H. pylori isolated from 52 individuals of two large families living in a rural community in South Africa and from 43 individuals of 11 families living in urban settings in the United Kingdom, the United States, Korea, and Colombia. A 3,406 bp multilocus sequence haplotype was determined for a total of 142 H. pylori isolates. Isolates were assigned to biogeographic populations, and recent transmission was measured as the occurrence of non-unique isolates, i.e., isolates whose sequences were identical to those of other isolates. Members of urban families were almost always infected with isolates from the biogeographic population that is common in their location. Non-unique isolates were frequent in urban families, consistent with familial transmission between parents and children or between siblings. In contrast, the diversity of H. pylori in the South African families was much more extensive, and four distinct biogeographic populations circulated in this area. Non-unique isolates were less frequent in South African families, and there was no significant correlation between kinship and similarity of H. pylori sequences. However, individuals who lived in the same household did have an increased probability of carrying the same non-unique isolates of H. pylori, independent of kinship. We conclude that patterns of spread of H. pylori under conditions of high prevalence, such as the rural South African families, differ from those in developed countries. Horizontal transmission occurs frequently between persons who do not belong to a core family, blurring the pattern of familial

  18. Clinical Significance of Helicobacter Pylori in Children with Idiopathic Thrombocytopenic Purpura%幽门螺杆菌在儿童特发性血小板减少性紫癜中的临床意义

    Institute of Scientific and Technical Information of China (English)

    唐瑛; 王书春; 王鲁娟; 刘永; 王海英; 王占聚

    2013-01-01

    This study was aimed to investigate the clinic significance of helicobacter pylori (HP) in children with idiopathic thrombocytopenic purpura( ITP). The infection of HP in 92 ITP children was determined by 13C-Urea Breath Test, the same test was also performed on 66 healthy children. The 68 children infected with HP were randomly divided into 2 groups: single drug group treated only with corticosteroid and; combined drug group treated with corticosteroid and anti-helicobacter pylori treatment. The results showed that 68 patients infected with HP were found in 92 ITP children(74. 7% ), 26 patients infected with HP were observed in 66 healthy children (39.4% ), which was lower than that in ITP children (74.7% , P<0.05). After anti-helicobacterpylori therapy, the total effective rate and cure rate of ITP patients increased respectively from 73.5% to 94.1 % , and the total recurrence rate( 17.0% ) was much lower than single drug group( 47. 1% , P < 0. 05). Otherwise, after therapy the platelet count in both two groups increased continuously, and at the same time point, the platelet count in snti-helicobacterium pylori group was higher than that in the single drug group(P < 0. 05). It is concluded that the ITP children have a higher infection rate of HP, which may be involved in the pathogenesis of ITP. Anti-helicobacterium pylori therapy would help to improve the therapeutic efficacy and reduce the recurrence of ITP children.%本研究旨在探讨幽门螺杆菌(helicobacter pylori,HP)在儿童特发性血小板减少性紫癜(ITP)中的临床意义.用13C尿素呼气试验检测92例ITP儿童患者的感染情况,并检测66名健康儿童作为对照组.将ITP患儿中68例阳性者随机分为2组:复合用药治疗组34例,应用糖皮质激素+抗菌治疗;单药治疗组34例,用糖皮质激素治疗.结果表明:ITP患儿HP的感染率为74.7%,明显高于对照组(39.4%)(P<0.05).ITP患儿经治疗后,单药治疗组的总有效率(73.5

  19. Treatment of Helicobacter Pylori in Children

    Directory of Open Access Journals (Sweden)

    F Famouri

    2014-04-01

    Full Text Available Childrenwith Helicobacter infection need treatment. The aim of treatment is elimination of H.Pylori. Most patients with this infection are asymptomatic and without peptic disease. Treatment and management of these patients are controversy. Conventional Treatment: The best treatment for H. pylori eradication regimens should have cure rates of at least 80%, be without major side effects, and induce minimal bacterial resistance. Antibiotics alone have not achieved this. Luminal acidity influences both the effectiveness of some antimicrobial agents and the survival of the bacteri; thus antibiotics have been combined with acid suppression such as proton pump inhibitors (PPIs, bismuth, or H2 antagonists. The “classic” regimen is treatment twice daily for 7 days with a PPI and clarithromycin plus either amoxicillin or metronidazole Bismuth has been used in the treatment of peptic ulcer disease and 1 part o quadruple therapy for H.Pylori but compliance of children for it is low.   Sequential Therapy  Sequential therapyinvolves dual therapy with a PPI and amoxicillin for 5 days followed sequentially by clarithromycin, Tinidazole and omeperazole for 5 days or other triple therapy for 7 days. This treatment has had 97% efficacy.   Adjunctive Therapies A number of studies have showed the potential benefits of probiotic therapy in H. pylori treatment regimens.Consumption of these drugs accompanied with other medications increase H.Pylori eradication.    

  20. Helicobacter pylori: prospettive per un vaccino

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    Giuseppe Del Giudice

    2003-09-01

    Full Text Available Helicobacter pylori causes one of the most widespread infections worldwide: it affects more than 50% of the human population, and is responsible for serious gastric pathologies such as chronic gastritis, peptic ulcer, atrophic gastritis and, in some individuals, gastric cancer. Current treatments with antibiotics are efficacious, but encounters several drawbacks at the level of compliance, side effects, antibiotic resistance, etc.The availability of vaccines could contribute in reducing the burden of H. pylori associated diseases. Several bacterial antigens have been identified as virulence factors and proposed as potential vaccine candidates. Some of these antigens have been tested in experimental animal models of challenge with H. pylori. The experiments in animals have shown that prophylactic and therapeutic vaccination against H. pylori is indeed feasible. Several open questions still remain concerning the understanding of the host-microbe relationship and the quality of the immune response which should be induced in order to confer protective immunity in man.The answers to these questions will be crucial in helping the preparation of appropriate vaccine formulations able to efficaciously protect humans both prophylactically and therapeutically. A few clinical trials have been carried out so far with still limited results. Other trials in humans are in progress and are planned for the next few years.The final hope is that these new vaccines will show the expected efficacy against H. pylori and will permit the elimination of this pathogen which has cohabited with humans for more than 100,000 years.

  1. Lipopolysaccharide Structure and Biosynthesis in Helicobacter pylori.

    Science.gov (United States)

    Li, Hong; Liao, Tingting; Debowski, Aleksandra W; Tang, Hong; Nilsson, Hans-Olof; Stubbs, Keith A; Marshall, Barry J; Benghezal, Mohammed

    2016-12-01

    This review covers the current knowledge and gaps in Helicobacter pylori lipopolysaccharide (LPS) structure and biosynthesis. H. pylori is a Gram-negative bacterium which colonizes the luminal surface of the human gastric epithelium. Both a constitutive alteration of the lipid A preventing TLR4 elicitation and host mimicry of the Lewis antigen decorated O-antigen of H. pylori LPS promote immune escape and chronic infection. To date, the complete structure of H. pylori LPS is not available, and the proposed model is a linear arrangement composed of the inner core defined as the hexa-saccharide (Kdo-LD-Hep-LD-Hep-DD-Hep-Gal-Glc), the outer core composed of a conserved trisaccharide (-GlcNAc-Fuc-DD-Hep-) linked to the third heptose of the inner core, the glucan, the heptan and a variable O-antigen, generally consisting of a poly-LacNAc decorated with Lewis antigens. Although the glycosyltransferases (GTs) responsible for the biosynthesis of the H. pylori O-antigen chains have been identified and characterized, there are many gaps in regard to the biosynthesis of the core LPS. These limitations warrant additional mutagenesis and structural studies to obtain the complete LPS structure and corresponding biosynthetic pathway of this important gastric bacterium.

  2. Can Helicobacter pylori infection influence human reproduction?

    Science.gov (United States)

    Moretti, Elena; Figura, Natale; Collodel, Giulia; Ponzetto, Antonio

    2014-05-21

    Helicobacter pylori (H. pylori) infection could be associated with extra-digestive diseases. Here, we report the evidences concerning the decrease in reproductive potential occurring in individuals infected by H. pylori, especially by strains expressing CagA. This infection is more prevalent in individuals with fertility disorders. Infected women have anti-H. pylori antibodies in cervical mucus and follicular fluid that may decrease sperm motility and cross react immunologically with spermatozoa, conceivably hampering the oocyte/sperm fusion. Infection by CagA positive organisms enhances the risk of preeclampsia, which is a main cause of foetus death. These findings are supported by the results of experimental infections of pregnant mice, which may cause reabsorption of a high number of foetuses and alter the balance between Th1 and Th2 cell response. Infected men have decreased sperm motility, viability and numbers of normally shaped sperm and augmented systemic levels of inflammatory cytokines, such as tumor necrosis factor-α, which may damage spermatozoa. In countries where parasitic infestation is endemic, detrimental effects of infection upon spermatozoa may not occur, because the immune response to parasites could determine a switch from a predominant Th1 type to Th2 type lymphocytes, with production of anti-inflammatory cytokines. In conclusion, the evidences gathered until now should be taken into consideration for future studies aiming to explore the possible role of H. pylori infection on human reproduction.

  3. Vacuolating cytotoxin A (VacA) - A multi-talented pore-forming toxin from Helicobacter pylori.

    Science.gov (United States)

    Junaid, Muhammad; Linn, Aung Khine; Javadi, Mohammad Bagher; Al-Gubare, Sarbast; Ali, Niaz; Katzenmeier, Gerd

    2016-08-01

    Helicobacter pylori is associated with severe and chronic diseases of the stomach and duodenum such as peptic ulcer, non-cardial adenocarcinoma and gastric lymphoma, making Helicobacter pylori the only bacterial pathogen which is known to cause cancer. The worldwide rate of incidence for these diseases is extremely high and it is estimated that about half of the world's population is infected with H. pylori. Among the bacterial virulence factors is the vacuolating cytotoxin A (VacA), which represents an important determinant of pathogenicity. Intensive characterization of VacA over the past years has provided insight into an ample variety of mechanisms contributing to host-pathogen interactions. The toxin is considered as an important target for ongoing research for several reasons: i) VacA displays unique features and structural properties and its mechanism of action is unrelated to any other known bacterial toxin; ii) the toxin is involved in disease progress and colonization by H. pylori of the stomach; iii) VacA is a potential and promising candidate for the inclusion as antigen in a vaccine directed against H. pylori and iv) the vacA gene is characterized by a high allelic diversity, and allelic variants contribute differently to the pathogenicity of H. pylori. Despite the accumulation of substantial data related to VacA over the past years, several aspects of VacA-related activity have been characterized only to a limited extent. The biologically most significant effect of VacA activity on host cells is the formation of membrane pores and the induction of vacuole formation. This review discusses recent findings and advances on structure-function relations of the H. pylori VacA toxin, in particular with a view to membrane channel formation, oligomerization, receptor binding and apoptosis.

  4. N-acetylcysteine, a novel treatment for Helicobacter pylori infection.

    Science.gov (United States)

    Huynh, Hien Quoc; Couper, Richard T L; Tran, Cuong D; Moore, Lynette; Kelso, Richard; Butler, Ross N

    2004-01-01

    N-Acetylcysteine (NAC), being both a mucolytic agent and a thiol-containing antioxidant, may affect the establishment and maintenance of H. pylori infection within the gastric mucus layer and mucosa. Agar and broth dilution susceptibility tests determined the MIC of H. pylori strain SSI to NAC. H. pylori load in SSI strain-infected C57BL mice was determined as colony forming units per gram of gastric tissue. Gastritis assessment was scored and gastric surface hydrophobicity was determined by contact angle measurement. MICs of NAC were 5 to 10 and 10 to 15 mg/ml using the agar dilution and broth dilution methods, respectively. NAC (120 mg per day for 14 days) reduced the H. pylori load in mice by almost 1 log compared with sham treatment. Pretreatment with NAC (40 mg/day) also significantly reduced the H. pylori load but did not prevent H. pylori colonization. Both H. pylori infection and NAC reduced the surface hydrophobicity of murine gastric mucosa. No significant differences were observed in the gastritis scores of H. felis- or H. pylori-infected mice receiving either NAC or sham treatments. This study demonstrates that NAC inhibits the growth of H. pylori in both agar and broth susceptibility tests and in H. pylori-infected mice. NAC did not alter the severity of H. pylori- or H. felis-induced gastritis.

  5. Current Therapy for Helicobacter pylori Infection in Children and Adolescents

    Directory of Open Access Journals (Sweden)

    Benjamin D Gold

    1999-01-01

    Full Text Available Helicobacter pylori infects approximately 50% of the world’s population and is a definitive cause of gastroduodenal disease (ie, gastritis, duodenal and gastric ulcers in children and adults. Four consensus conferences held around the globe have brought together clinicians, scientists, epidemiologists and health care economists to discuss the role of the gastric pathogen H pylori in human gastroduodenal disease. At each of these conferences, the overriding objective was to reach a consensus on the development of practical guidelines for the diagnosis and treatment of H pylori-infected individuals. However, it was not until the Canadian H pylori Consensus Conference, held in November 1997, that the issues of H pylori infection in children were addressed. Therapies for H pylori infection in children, presented in part at the First Canadian Paediatric H pylori Consensus Conference, held in Victoria, British Columbia, November 1998, are reviewed in this paper.

  6. Transcriptional profiling of type II toxin-antitoxin genes of Helicobacter pylori under different environmental conditions: identification of HP0967-HP0968 system

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    MIGUEL A DE LA CRUZ

    2016-11-01

    Full Text Available Helicobacter pylori is a Gram-negative bacterium that colonizes the human gastric mucosa and is responsible for causing peptic ulcers and gastric carcinoma. The expression of virulence factors allows the persistence of H. pylori in the stomach, which results in a chronic, sometimes uncontrolled inflammatory response. Type II toxin-antitoxin systems have emerged as important virulence factors in many pathogenic bacteria. Three type II toxin-antitoxin (TA systems have previously been identified in the genome of H. pylori 26695: HP0315-HP0316, HP0892-HP0893, and HP0894-HP0895. Here we characterized a heretofore undescribed type II TA system in H. pylori, HP0967-HP0968, which is encoded by the bicistronic operon hp0968-hp0967 and belongs to the Vap family. The predicted HP0967 protein is a toxin with ribonuclease activity whereas HP0968 is an antitoxin that binds to its own regulatory region. We found that all type II TA systems were expressed in H. pylori during early stationary growth phase, and differentially expressed in the presence of urea, nickel, and iron, although the hp0968-hp0967 pair was the most affected under these environmental conditions. Transcription of hp0968-hp0967 was strongly induced in a mature H. pylori biofilm and when the bacteria interacted with AGS epithelial cells. Kanamycin and chloramphenicol considerably boosted transcription levels of all the four type II TA systems. The hp0968-hp0967 TA system was the most frequent among 317 H. pylori strains isolated from all over the world. This study is the first report on the transcription of type II TA genes in H. pylori under different environmental conditions. Our data show that the HP0967 and HP0968 proteins constitute a bona fide type II TA system in H. pylori, whose expression is regulated by environmental cues, which are relevant in the context of infection of the human gastric mucosa.

  7. Analysis of T4SS-induced signaling by H. pylori using quantitative phosphoproteomics

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    Frithjof eGlowinski

    2014-07-01

    Full Text Available Helicobacter pylori is a Gram-negative bacterial pathogen colonizing the human stomach. Infection with H. pylori causes chronic inflammation of the gastric mucosa and may lead to peptic ulceration and/or gastric cancer. A major virulence determinant of H. pylori is the type IV secretion system (T4SS, which is used to inject the virulence factor CagA into the host cell, triggering a wide range of cellular signaling events. Here, we used a phosphoproteomic approach to investigate tyrosine signaling in response to host-pathogen interaction, using stable isotope labeling in cell culture (SILAC of AGS cells to obtain a differential picture between multiple infection conditions. Cells were infected with wild type H. pylori P12, a P12ΔCagA deletion mutant, and a P12ΔT4SS deletion mutant to compare signaling changes over time and in the absence of CagA or the T4SS. Tryptic peptides were enriched for tyrosine (Tyr phosphopeptides and analysed by nano-LC-Orbitrap MS. In total, 58 different phosphosites were found to be regulated following infection. The majority of phosphosites identified were kinases of the MAPK familiy. CagA and the T4SS were found to be key regulators of Tyr phosphosites. Our findings indicate that CagA primarily induces activation of ERK1 and integrin linked factors, whereas the T4SS primarily modulates JNK and p38 activation.

  8. The Effect of Cholecystectomy on the Histology of Antrum and Helicobacter Pylori Colonization

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    Hüseyin Özer

    2013-07-01

    Full Text Available Aim: Notwithstanding cholecystectomy’s being the standard cure for symptomatic gallbladder stones, it might as well trigger changes that result in the increase of duodenogastric reflux and the emergence of relevant clinic and laboratorial data. The aim of this thesis is to explore the effect of cholecystectomy on the duodenogastric reflux, histopathologic changes in the antral mucosa and Helicobacter pylori colonization. Material and Method: This prospective research is based upon data collected from 45 patients (28 of them being female and 17 of them being male patients with an average age of 50.9, who would undergo cholecystectomic surgery. Upper gastrointestinal endoscopy has been performed on patients before the operation and at least two months after the operation in order to examine the existence of bile in the stomach. The tissues removed from the antrum during these endoscopic biopsies have been examined to spot the histopathologic changes and the existence of Helicobacter pylori in the mucosa (chronic gastritis, activation findings, and intestinal metaplasia. Results: Duodenogastric reflux, chronic gastritis, and intestinal metaplasia have been observed to increase significantly after cholecystectomy (p<0.001 for duodenogastric reflux and chronic gastritis, p<0.05 for intestinal metaplasia. On the other hand, no significant data have been attained in terms of activation findings and the existence of H.pylori before and after the operation. Discussion: Although cholecystectomy cause duodenogastric reflux and histopathologic changes in the antrum, it does not affect  H.pylori colonization.

  9. Helicobacter pylori's cholesterol uptake impacts resistance to docosahexaenoic acid.

    Science.gov (United States)

    Correia, Marta; Casal, Susana; Vinagre, João; Seruca, Raquel; Figueiredo, Ceu; Touati, Eliette; Machado, José C

    2014-05-01

    Helicobacter pylori colonizes half of the world population and is associated with gastric cancer. We have previously demonstrated that docosahexaenoic acid (DHA), an n-3 polyunsaturated fatty acid known for its anti-inflammatory and antitumor effects, directly inhibits H. pylori growth in vitro and in mice. Nevertheless, the concentration of DHA shown to reduce H. pylori mice gastric colonization was ineffective in vitro. Related to the auxotrophy of H. pylori for cholesterol, we hypothesize that other mechanisms, in addition to DHA direct antibacterial effect, must be responsible for the reduction of the infection burden. In the present study we investigated if DHA affects also H. pylori growth, by reducing the availability of membrane cholesterol in the epithelial cell for H. pylori uptake. Levels of cholesterol in gastric epithelial cells and of cholesteryl glucosides in H. pylori were determined by thin layer chromatography and gas chromatography. The consequences of epithelial cells' cholesterol depletion on H. pylori growth were assessed in liquid cultures. We show that H. pylori uptakes cholesterol from epithelial cells. In addition, DHA lowers cholesterol levels in epithelial cells, decreases its de novo synthesis, leading to a lower synthesis of cholesteryl glucosides by H. pylori. A previous exposition of H. pylori to cholesterol influences the bacterium response to the direct inhibitory effect of DHA. Overall, our results suggest that a direct effect of DHA on H. pylori survival is modulated by its access to epithelial cell cholesterol, supporting the notion that cholesterol enhances the resistance of H. pylori. The cholesterol-dependent resistance of H. pylori to antimicrobial compounds raises new important aspects for the development of new anti-bacterial strategies.

  10. Evolutionary dynamics of insertion sequences in Helicobacter pylori.

    Science.gov (United States)

    Kalia, Awdhesh; Mukhopadhyay, Asish K; Dailide, Giedrius; Ito, Yoshiyki; Azuma, Takeshi; Wong, Benjamin C Y; Berg, Douglas E

    2004-11-01

    Prokaryotic insertion sequence (IS) elements behave like parasites in terms of their ability to invade and proliferate in microbial gene pools and like symbionts when they coevolve with their bacterial hosts. Here we investigated the evolutionary history of IS605 and IS607 of Helicobacter pylori, a genetically diverse gastric pathogen. These elements contain unrelated transposase genes (orfA) and also a homolog of the Salmonella virulence gene gipA (orfB). A total of 488 East Asian, Indian, Peruvian, and Spanish isolates were screened, and 18 and 14% of them harbored IS605 and IS607, respectively. IS605 nucleotide sequence analysis (n = 42) revealed geographic subdivisions similar to those of H. pylori; the geographic subdivision was blurred, however, due in part to homologous recombination, as indicated by split decomposition and homoplasy tests (homoplasy ratio, 0.56). In contrast, the IS607 populations (n = 44) showed strong geographic subdivisions with less homologous recombination (homoplasy ratio, 0.2). Diversifying selection (ratio of nonsynonymous change to synonymous change, >1) was evident in approximately 15% of the IS605 orfA codons analyzed but not in the IS607 orfA codons. Diversifying selection was also evident in approximately 2% of the IS605 orfB and approximately 10% of the IS607 orfB codons analyzed. We suggest that the evolution of these elements reflects selection for optimal transposition activity in the case of IS605 orfA and for interactions between the OrfB proteins and other cellular constituents that potentially contribute to bacterial fitness. Taken together, similarities in IS elements and H. pylori population genetic structures and evidence of adaptive evolution in IS elements suggest that there is coevolution between these elements and their bacterial hosts.

  11. Treatment of Helicobacter pylori infection 2011.

    LENUS (Irish Health Repository)

    O'Connor, Anthony

    2012-02-01

    This article reviews the literature published pertaining to Helicobacter pylori eradication over the last year. The general perception among clinicians and academics engaged in research on H. pylori has been that eradication rates for first-line therapies are falling, although some data published this year have cast doubt on this. The studies published this year have therefore focussed on developing alternative strategies for the first-line eradication of H. pylori. In this regard, clear evidence now exists that both levofloxacin and bismuth are viable options for first-line therapy. The sequential and "concomitant" regimes have also been studied in new settings and may have a role in future algorithms also. In addition, data have emerged that the probiotic Saccharomyces boulardii may be a useful adjunct to antibiotic therapy. Other studies promote individualized therapies based on host polymorphisms, age, and other such demographic factors.

  12. Helicobacter pylori vaccine: from past to future.

    Science.gov (United States)

    Agarwal, Kanishtha; Agarwal, Shvetank

    2008-02-01

    Helicobacter pylori infection is highly prevalent worldwide and is an important cause of gastritis, peptic ulcer disease, gastric mucosa-associated lymphoid tissue lymphoma (MALToma), and gastric adenocarcinoma. Infection is usually acquired during childhood and tends to persist unless treated. Because eradication requires treatment with multidrug regimens, prevention of initial infection by a suitable vaccine is attractive. Although immunization with H pylori protein subunits has been encouraging in animals, similar vaccine trials in humans have shown adjuvant-related adverse effects and only moderate effectiveness. Newer immunization approaches (use of DNA, live vectors, bacterial ghosts, and microspheres) are being developed. Several questions about when and whom to vaccinate will need to be appropriately answered, and a cost-effective vaccine production and delivery strategy will have to be useful for developing countries. For this review, we searched MEDLINE using the Medical Subject Heading (MeSH) terms Helicobacter pylori and vaccines for articles in English from 1990 to 2007.

  13. Recent "omics" advances in Helicobacter pylori.

    Science.gov (United States)

    Berthenet, Elvire; Sheppard, Sam; Vale, Filipa F

    2016-09-01

    The development of high-throughput whole genome sequencing (WGS) technologies is changing the face of microbiology, facilitating the comparison of large numbers of genomes from different lineages of a same organism. Our aim was to review the main advances on Helicobacter pylori "omics" and to understand how this is improving our knowledge of the biology, diversity and pathogenesis of H. pylori. Since the first H. pylori isolate was sequenced in 1997, 510 genomes have been deposited in the NCBI archive, providing a basis for improved understanding of the epidemiology and evolution of this important pathogen. This review focuses on works published between April 2015 and March 2016. Helicobacter "omics" is already making an impact and is a growing research field. Ultimately these advances will be translated into a routine clinical laboratory setting in order to improve public health.

  14. Helicobacter pylori upregulates Nanog and Oct4 via Wnt/β-catenin signaling pathway to promote cancer stem cell-like properties in human gastric cancer.

    Science.gov (United States)

    Yong, Xin; Tang, Bo; Xiao, Yu-Feng; Xie, Rui; Qin, Yong; Luo, Gang; Hu, Chang-Jiang; Dong, Hui; Yang, Shi-Ming

    2016-05-01

    Helicobacter pylori (H. pylori) infection is considered a major risk factor for gastric cancer. CagA behaves as a major bacterial oncoprotein playing a key role in H. pylori-induced tumorigenesis. Cancer stem cells (CSCs) are believed to possess the ability to initiate tumorigenesis and promote progression. Although studies have suggested that cancer cells can exhibit CSC-like properties in the tumor microenvironment, it remains unclear whether H. pylori infection could induce the emergence of CSC-like properties in gastric cancer cells and, the underlying mechanism. Here, gastric cancer cells were co-cultured with a CagA-positive H. pylori strain or a CagA isogenic mutant strain. We found that H. pylori-infected gastric cancer cells exhibited CSC-like properties, including an increased expression of CSC specific surface markers CD44 and Lgr5, as well as that of Nanog, Oct4 and c-myc, which are known pluripotency genes, and an increased capacity for self-renewal, whereas these properties were not observed in the CagA isogenic mutant strain-infected cells. Further studies revealed that H. pylori activated Wnt/β-catenin signaling pathway in a CagA-dependent manner and that the activation of this pathway was dependent upon CagA-positive H. pylori-mediated phosphorylation of β-catenin at the C-terminal Ser675 and Ser552 residues in a c-met- and/or Akt-dependent manner. We further demonstrated that this activation was responsible for H. pylori-induced CSC-like properties. Moreover, we found the promoter activity of Nanog and Oct4 were upregulated, and β-catenin was observed to bind to these promoters during H. pylori infection, while a Wnt/β-catenin inhibitor suppressed promoter activity and binding. Taken together, these results suggest that H. pylori upregulates Nanog and Oct4 via Wnt/β-catenin signaling pathway to promote CSC-like properties in gastric cancer cells.

  15. Helicobacter pylori: From Bench to Bedside

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    N Chiba

    1997-01-01

    Full Text Available With the exponential increase in research in the field of Helicobacter pylori a paradigm shift has occurred. It is now recognized that H pylori is a chronic infection of the stomach causing inflammation. Some patients remain asymptomatic, while others may develop dyspepsia, duodenal or gastric ulcer, gastric cancer or a mucosa-associated lymphoid tissue lymphoma. However, the role of H pylori in contributing to nonulcer dyspepsia or nonsteroidal anti-inflammatory drug gastropathy remains controversial. An effective vaccine against H pylori is years away. Major interest has focused on the questions "who should be investigated and therefore treated" and "what is the latest gold standard for eradication of H pylori"? In Europe, guidelines have been developed to help the practitioner answer these important questions. Canadian guidelines will soon be available. For persons with known peptic ulcer disease there should be unequivocal acceptance that the good clinical practice of eradicating H pylori will result in substantial savings in health care expenses. The original 'classical triple therapy' (bismuth, metronidazole and tetracycline [BMT] has now been surpassed by the combination of a proton pump inhibitor (PPI plus two antibiotics (metronidazole plus clarithromycin; amoxicillin plus clarithromycin; or amoxicillin plus metronidazole, each given twice a day for one week. In Canada, the regimen of omeprazole plus one antibiotic (amoxicillin or clarithromycin was approved recently but gives an eradication rate that is lower than the current target of 90%. According to the European (Mäastricht recommendations, if a single treatment attempt with PPI plus two antibiotics fails, PPI plus BMT is recommended.

  16. Giardia lamblia and Helicobater pylori Coinfection

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    R Shafie

    2009-03-01

    Full Text Available "nBackground: Giardia lamblia and Helicobacter pylori are two flagellate microorganisms that grow in duodenum and stom­ach. The aim of this study was to evaluate the prevalence of them in patients with dyspepsia and other GI disorders. "nMethods: In this cross-sectional study, co-infection of above-mentioned agents was investigated in a group of 130 patients [me­dian age of 40 yr (range=11-79 including 76 males (58.8%] with dyspepsia using three methods of duodenal aspiration sam­ple, duodenal biopsy samples and evaluation of stool samples."nResults: : From 105 patients (59 males, 46 females, median age 40 years, range 11-79 entering this study from 3 hospitals, 4 patients (3.8% had G. lamblia and 61 patients (58% had H. pylori. All 4 patients infected by Giardia had also H. pylori infec­tion. Tenesmus (3 out of 4 patients was the most common symptom in patients with H. pylori infection (48 out of 61 pa­tients was reflux. Other symptoms in patients infected with both organisms (4 patients included diarrhea (2 cases, weight loss (2 cases, and loss of appetite (1 case but no report of vomiting."nConclusion: In patients co-infected with Giardia, H.pylori differentiation by physical examination is not possible. So in those patients with positive Rapid Urease Test (RUT, stool examination for Giardia detection is recommended. In addition, met­ronidazole (broad spectrum, anti-protozoal drug can be useful in H. pylori infection.

  17. Endoscopic faces of Helicobacter Pylori infection

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    Geanina Spulber

    2015-08-01

    Full Text Available Introduction: The infection caused by H. pylori appears secondary after a bacterial colonization of the stomach and the initial portion of the small bowel. H. pylori –infected patients can develop gastritis, peptic ulcer, stomach cancer or MALT lymphoma. H. pylori infection is defined by WHO like a type I carcinogen, its role in gastric carcinogenesis being supported by the greatest researchers. Objectives: In this study our purpose was to determine the endoscopic appearances in H. pylori infection quoted in medical literature until now and the frequency of their appearance in our group of interest. Materials and methods: In this study it was made an analytic study in which it was realized a retrospective cohort investigation at the Emergency Central Military and University Hospital “Dr. Carol Davila” Bucharest, gastroenterology branch –endoscopic department between 18.12.2012- 21.08.2013 on 1694 patients between 18 and 92 years old, with the medium age of 55 years old. As a diagnostic method for H. pylori infection we used superior digestive endoscopy during which were taken biopsies and it was made a fast urease test. Results: Regarding the variation of the endoscopic aspects at the population of study, we have found gastritis with all its aspects (which was Sidney classified in the biggest percentage meaning 59.3% of the cases, followed with a percentage of 18.8% by those without any endoscopic abnormality, and then in 10,33% of the cases we have found peptic ulcer. With a smaller percentage, under 10%, we have found duodenitis at 8.67% of this patients, and finally the most severe lesions represented by gastric cancer and lymphoma were found at 2,7% of the H.pylori infected patients.

  18. Gene expression profiling in gastric mucosa from Helicobacter pylori-infected and uninfected patients undergoing chronic superficial gastritis.

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    Ze-Min Yang

    Full Text Available Helicobacter pylori infection reprograms host gene expression and influences various cellular processes, which have been investigated by cDNA microarray using in vitro culture cells and in vivo gastric biopsies from patients of the Chronic Abdominal Complaint. To further explore the effects of H. pylori infection on host gene expression, we have collected the gastric antral mucosa samples from 6 untreated patients with gastroscopic and pathologic confirmation of chronic superficial gastritis. Among them three patients were infected by H. pylori and the other three patients were not. These samples were analyzed by a microarray chip which contains 14,112 cloned cDNAs, and microarray data were analyzed via BRB ArrayTools software and Ingenuity Pathways Analysis (IPA website. The results showed 34 genes of 38 differentially expressed genes regulated by H. pylori infection had been annotated. The annotated genes were involved in protein metabolism, inflammatory and immunological reaction, signal transduction, gene transcription, trace element metabolism, and so on. The 82% of these genes (28/34 were categorized in three molecular interaction networks involved in gene expression, cancer progress, antigen presentation and inflammatory response. The expression data of the array hybridization was confirmed by quantitative real-time PCR assays. Taken together, these data indicated that H. pylori infection could alter cellular gene expression processes, escape host defense mechanism, increase inflammatory and immune responses, activate NF-κB and Wnt/β-catenin signaling pathway, disturb metal ion homeostasis, and induce carcinogenesis. All of these might help to explain H. pylori pathogenic mechanism and the gastroduodenal pathogenesis induced by H. pylori infection.

  19. Helicobacter pylori CagA: from pathogenic mechanisms to its use as an anti-cancer vaccine

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    Markus eStein

    2013-10-01

    Full Text Available Helicobacter pylori colonizes the gastric mucosa of more than 50% of the human population, causing chronic inflammation, which however is largely asymptomatic. Nevertheless, H. pylori-infected subjects can develop chronic gastritis, peptic ulcer, gastric mucosa-associated lymphoid tissue (MALT lymphoma, and gastric cancer. Chronic exposure to the pathogen and its ability to induce epithelial-to-mesenchymal transition (EMT through the injection of CagA into gastric epithelial cells may be key triggers of carcinogenesis. By deregulating cell-cell and cell-matrix interactions as well as DNA methylation, histone modifications, expression of micro RNAs, and resistance to apoptosis, EMT can actively contribute to early stages of the cancer formation. Host response to the infection significantly contributes to disease development and the concomitance of particular genotypes of both pathogen and host may turn into the most severe outcomes. T regulatory cells (Treg have been recently demonstrated to play an important role in H. pylori-related disease development and at the same time the Treg-induced tolerance has been proposed as a possible mechanism that leads to less severe disease. Efficacy of antibiotic therapies of H. pylori infection has significantly dropped. Unfortunately, no vaccine against H. pylori is currently licensed, and protective immunity mechanisms against H. pylori are only partially understood. In spite of promising results obtained in animal models of infection with a number of vaccine candidates, few clinical trials have been conducted so far and with no satisfactory outcomes. However, prophylactic vaccination may be the only means to efficiently prevent H. pylori-associated cancers.

  20. 3rd Brazilian consensus on Helicobacter pylori 3º Consenso Brasileiro para Estudo do Helicobacter pylori

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    Luiz Gonzaga Coelho

    Full Text Available Significant progress has been obtained since the Second Brazilian Consensus Conference on Helicobacter pylori Infection held in 2004, in São Paulo, SP, Brazil, and justify a third meeting to establish updated guidelines on the current management of H. pylori infection. The Third Brazilian Consensus Conference on H pylori Infection was organized by the Brazilian Nucleus for the Study of Helicobacter, a Department of the Brazilian Federation of Gastroenterology and took place on April 12-15, 2011, in Bento Gonçalves, RS, Brazil. Thirty-one delegates coming from the five Brazilian regions and one international guest, including gastroenterologists, pathologists, epidemiologists, and