PCR detection of Helicobacter pylori in string-absorbed gastric juice.

Science.gov (United States)

Domínguez-Bello, M G; Cienfuentes, C; Romero, R; García, P; Gómez, I; Mago, V; Reyes, N; Gueneau de Novoa, P

2001-04-20

Molecular methods for detection of Helicobacter pylori infection have been shown to be highly sensitive in gastric biopsies and cultures. The objective of this work was to compare PCR detection of H. pylori DNA in string-absorbed gastric juice and in gastric biopsies. The study was performed in 47 dyspeptic adult patients undergoing endoscopy, and infection was detected by amplification of a segment of H. pylori ureA gene. Of the 29 patients positive in biopsy analysis, 23 (79%) were also positive in the gastric string. PCR analysis of gastric strings is a sensitive and safe procedure to detect H. pylori when endoscopy is not indicated, and may be of great clinical and epidemiological usefulness in determining effectiveness of eradication therapies, typing virulence genes and detecting antibiotic resistance mutations.

Oral and gastric Helicobacter pylori: effects and associations.

Science.gov (United States)

Veiga, Nélio; Pereira, Carlos; Resende, Carlos; Amaral, Odete; Ferreira, Manuela; Nelas, Paula; Chaves, Claudia; Duarte, João; Cirnes, Luis; Machado, José Carlos; Ferreira, Paula; Correia, Ilídio J

2015-01-01

This study consisted in the comparison of the prevalence of Helicobacter pylori (H. pylori) present in the stomach and in saliva of a sample of Portuguese adolescents and the assessment of the association between H. pylori infection with socio-demographic variables and prevalence of dental caries. A cross-sectional study was designed including a sample of 447 adolescents aged 12 to 19 years old, attending a public school in Sátão, Portugal. A questionnaire about socio-demographic variables and oral health behaviors was applied. Gastric H. pylori infection was determined using the urease breath test (UBT). Saliva collection was obtained and DNA was extracted by Polymerase Chain Reaction (PCR) in order to detect the presence of oral H. pylori. The prevalence of gastric H. pylori detected by UBT was 35.9%. Within the adolescents with a gastric UBT positive, only 1.9% were positive for oral H. pylori. The presence of gastric H. pylori was found to be associated with age (>15years, Odds ratio (OR)=1.64, 95%CI=1.08-2.52), residence area (urban, OR=1.48, 95%CI=1.03-2.29) and parents´ professional situation (unemployed, OR=1.22, 95%CI=1.02-1.23). Among those with detected dental caries during the intra-oral observation, 37.4% were positive for gastric H. pylori and 40.2% negative for the same bacterial strain (p=0.3). The oral cavity cannot be considered a reservoir for infection of H. pylori. Gastric H. pylori infection was found to be associated with socio-demographic variables such as age, residence area and socioeconomic status.

Oral and gastric Helicobacter pylori: effects and associations.

Directory of Open Access Journals (Sweden)

Nélio Veiga

Full Text Available This study consisted in the comparison of the prevalence of Helicobacter pylori (H. pylori present in the stomach and in saliva of a sample of Portuguese adolescents and the assessment of the association between H. pylori infection with socio-demographic variables and prevalence of dental caries.A cross-sectional study was designed including a sample of 447 adolescents aged 12 to 19 years old, attending a public school in Sátão, Portugal. A questionnaire about socio-demographic variables and oral health behaviors was applied. Gastric H. pylori infection was determined using the urease breath test (UBT. Saliva collection was obtained and DNA was extracted by Polymerase Chain Reaction (PCR in order to detect the presence of oral H. pylori.The prevalence of gastric H. pylori detected by UBT was 35.9%. Within the adolescents with a gastric UBT positive, only 1.9% were positive for oral H. pylori. The presence of gastric H. pylori was found to be associated with age (>15years, Odds ratio (OR=1.64, 95%CI=1.08-2.52, residence area (urban, OR=1.48, 95%CI=1.03-2.29 and parents´ professional situation (unemployed, OR=1.22, 95%CI=1.02-1.23. Among those with detected dental caries during the intra-oral observation, 37.4% were positive for gastric H. pylori and 40.2% negative for the same bacterial strain (p=0.3.The oral cavity cannot be considered a reservoir for infection of H. pylori. Gastric H. pylori infection was found to be associated with socio-demographic variables such as age, residence area and socioeconomic status.

Unique mechanism of Helicobacter pylori for colonizing the gastric mucus.

Science.gov (United States)

Yoshiyama, H; Nakazawa, T

2000-01-01

Helicobacter pylori is a human gastric pathogen causing chronic infection. Urease and motility using flagella are essential factors for its colonization. Urease of H. pylori exists both on the surface and in the cytoplasm, and is involved in neutralizing gastric acid and in chemotactic motility. H. pylori senses the concentration gradients of urea in the gastric mucus layer, then moves toward the epithelial surface by chemotactic movement. The energy source for the flagella movement is the proton motive force. The hydrolysis of urea by the cytoplasmic urease possibly generates additional energy for the flagellar rotation in the mucus gel layer.

Prevalence Of Helicobacter pylori In Gastric Biopsies Of Patients ...

African Journals Online (AJOL)

The prevalence of Helicobacter pylori infection as seen at the University of Benin Teaching Hospital (UBTH) Benin City Nigeria was 16% which was significant using the students T-test (P<0.05). Eighty one gastric biopsy specimens received in the microbiology laboratory were cultured on chocolate agar. Of the H. pylori ...

Prevention of Gastric Cancer: Eradication of Helicobacter Pylori and Beyond

Directory of Open Access Journals (Sweden)

Tetsuya Tsukamoto

2017-08-01

Full Text Available Although its prevalence is declining, gastric cancer remains a significant public health issue. The bacterium Helicobacter pylori is known to colonize the human stomach and induce chronic atrophic gastritis, intestinal metaplasia, and gastric cancer. Results using a Mongolian gerbil model revealed that H. pylori infection increased the incidence of carcinogen-induced adenocarcinoma, whereas curative treatment of H. pylori significantly lowered cancer incidence. Furthermore, some epidemiological studies have shown that eradication of H. pylori reduces the development of metachronous cancer in humans. However, other reports have warned that human cases of atrophic metaplastic gastritis are already at risk for gastric cancer development, even after eradication of these bacteria. In this article, we discuss the effectiveness of H. pylori eradication and the morphological changes that occur in gastric dysplasia/cancer lesions. We further assess the control of gastric cancer using various chemopreventive agents.

Gastric microbiota and carcinogenesis: the role of non-Helicobacter pylori bacteria: a systematic review

Directory of Open Access Journals (Sweden)

Emanuel Dias-Jácome

Full Text Available Background and aim: Helicobacter pylori is the strongest risk factor for gastric cancer. However, recent advances in DNA sequencing technology have revealed a complex microbial community in the stomach that could also contribute to the development of gastric cancer. The aim of this study was to present recent scientific evidence regarding the role of non-Helicobacter pylori bacteria in gastric carcinogenesis. Methods: A systematic review of original articles published in PubMed in the last ten years related to gastric microbiota and gastric cancer in humans was performed. Results: Thirteen original articles were included. The constitution of gastric microbiota appears to be significantly affected by gastric cancer and premalignant lesions. In fact, differences in gastric microbiota have been documented, depending on Helicobacter pylori status and gastric conditions, such as non-atrophic gastritis, intestinal metaplasia and cancer. Gastric carcinogenesis can be associated with an increase in many bacteria (such as Lactobacillus coleohominis, Klebsiella pneumoniae or Acinetobacter baumannii as well as decrease in others (such as Porphyromonas spp, Neisseria spp, Prevotella pallens or Streptococcus sinensis. However, there is no conclusive data that confirms if these changes in microbiota are a cause or consequence of the process of carcinogenesis. Conclusions: Even though there is limited evidence in humans, microbiota differences between normal individuals, pre-malignant lesions and gastric cancer could suggest a progressive shift in the constitution of gastric microbiota in carcinogenesis, possibly resulting from a complex cross-talk between gastric microbiota and Helicobacter pylori. However, further studies are needed to elucidate the specific role (if any of different microorganisms.

Gastric microbiota and carcinogenesis: the role of non-Helicobacter pylori bacteria - A systematic review.

Science.gov (United States)

Dias-Jácome, Emanuel; Libânio, Diogo; Borges-Canha, Marta; Galaghar, Ana; Pimentel-Nunes, Pedro

2016-09-01

Helicobacter pylori is the strongest risk factor for gastric cancer. However, recent advances in DNA sequencing technology have revealed a complex microbial community in the stomach that could also contribute to the development of gastric cancer. The aim of this study was to present recent scientific evidence regarding the role of non-Helicobacter pylori bacteria in gastric carcinogenesis. A systematic review of original articles published in PubMed in the last ten years related to gastric microbiota and gastric cancer in humans was performed. Thirteen original articles were included. The constitution of gastric microbiota appears to be significantly affected by gastric cancer and premalignant lesions. In fact, differences in gastric microbiota have been documented, depending on Helicobacter pylori status and gastric conditions, such as non-atrophic gastritis, intestinal metaplasia and cancer. Gastric carcinogenesis can be associated with an increase in many bacteria (such as Lactobacillus coleohominis, Klebsiella pneumoniae or Acinetobacter baumannii) as well as decrease in others (such as Porphyromonas spp, Neisseria spp, Prevotella pallens or Streptococcus sinensis). However, there is no conclusive data that confirms if these changes in microbiota are a cause or consequence of the process of carcinogenesis. Even though there is limited evidence in humans, microbiota differences between normal individuals, pre-malignant lesions and gastric cancer could suggest a progressive shift in the constitution of gastric microbiota in carcinogenesis, possibly resulting from a complex cross-talk between gastric microbiota and Helicobacter pylori. However, further studies are needed to elucidate the specific role (if any) of different microorganisms.

Effect on Helicobacter pylori eradication therapy against gastric cancer in Japan.

Science.gov (United States)

Tsuda, Momoko; Asaka, Masahiro; Kato, Mototsugu; Matsushima, Rumiko; Fujimori, Kenji; Akino, Kozo; Kikuchi, Shogo; Lin, Yingsong; Sakamoto, Naoya

2017-10-01

In Japan, there have been approximately 50 000 deaths from gastric cancer annually for over 40 years with little variation. It has been reported that most gastric cancers in Japan are caused by Helicobacter pylori infection. H. pylori eradication therapy was approved for patients with chronic gastritis by the Japanese national health insurance scheme in February 2013 for patients with an endoscopic diagnosis of chronic gastritis is positive for H. pylori. We examined the effect on gastric cancer death rate 4 years after expansion of health insurance coverage. We conducted an epidemiological study and analyzed trends in prescription for H. pylori eradication therapy. We used the electronic medical claims database from Hokkaido, Japan to evaluate the impact of expansion of national health insurance coverage for H. pylori eradication therapy on deaths from gastric cancer. Data on deaths from gastric cancer were obtained from the Japanese Ministry of Health, Labour and Welfare and the Cancer Statistics in Japan (2015). Analysis of electronic claims records was performed using the National Database, mainly focusing on Hokkaido. Prescriptions for H. pylori eradication therapy and the number of patients treated for gastric cancer were also extracted from the Hokkaido database. Approximately 1.5 million prescriptions for H. pylori eradication therapy were written annually. Gastric cancer deaths fell each year: 48 427 in 2013, 47 903 in 2014, 46 659 in 2015, and 45 509 in 2016, showing a significant decrease after expansion of insurance coverage for H. pylori eradication therapy (Ppylori eradication therapy increased markedly after approval of the gastritis indication by the national health insurance scheme and was associated with a significant decrease in gastric cancer deaths. © 2017 The Authors. Helicobacter Published by John Wiley & Sons Ltd.

Prevalence of Helicobacter Pylori in Gastric Fluid in the Surgical Patient

National Research Council Canada - National Science Library

Mc

1998-01-01

Helicobacter pylori is a bacterium that infects the human gastric mucosa. It is well established as a primary factor in peptic ulcer disease and has been implicated in the pathogenesis of gastric adenocarcinoma...

Cholesterol-α-glucosyltransferase gene is present in most Helicobacter species including gastric non-Helicobacter pylori helicobacters obtained from Japanese patients.

Science.gov (United States)

Kawakubo, Masatomo; Horiuchi, Kazuki; Matsumoto, Takehisa; Nakayama, Jun; Akamatsu, Taiji; Katsuyama, Tsutomu; Ota, Hiroyoshi; Sagara, Junji

2018-02-01

Non-Helicobacter pylori helicobacters (NHPHs) besides H. pylori infect human stomachs and cause chronic gastritis and mucosa-associated lymphoid tissue lymphoma. Cholesteryl-α-glucosides have been identified as unique glycolipids present in H. pylori and some Helicobacter species. Cholesterol-α-glucosyltransferase (αCgT), a key enzyme for the biosynthesis of cholesteryl-α-glucosides, plays crucial roles in the pathogenicity of H. pylori. Therefore, it is important to examine αCgTs of NHPHs. Six gastric NHPHs were isolated from Japanese patients and maintained in mouse stomachs. The αCgT genes were amplified by PCR and inverse PCR. We retrieved the αCgT genes of other Helicobacter species by BLAST searches in GenBank. αCgT genes were present in most Helicobacter species and in all Japanese isolates examined. However, we could find no candidate gene for αCgT in the whole genome of Helicobacter cinaedi and several enterohepatic species. Phylogenic analysis demonstrated that the αCgT genes of all Japanese isolates show high similarities to that of a zoonotic group of gastric NHPHs including Helicobacter suis, Helicobacter heilmannii, and Helicobacter ailurogastricus. Of 6 Japanese isolates, the αCgT genes of 4 isolates were identical to that of H. suis, and that of another 2 isolates were similar to that of H. heilmannii and H. ailurogastricus. All gastric NHPHs examined showed presence of αCgT genes, indicating that αCgT may be beneficial for these helicobacters to infect human and possibly animal stomachs. Our study indicated that NHPHs could be classified into 2 groups, NHPHs with αCgT genes and NHPHs without αCgT genes. © 2017 John Wiley & Sons Ltd.

Helicobacter pylori gastritis

International Nuclear Information System (INIS)

Urban, B.A.; Fishman, E.K.; Kuhlman, J.E.; Jones, B.

1990-01-01

This paper reports on the CT scans of patients with Helicobacter pylori (formerly Campylobacter pylori) infection and histologic gastritis reviewed to determine if the inflammatory changes can mimic the CT appearance of gastric neoplasm. Records were obtained of 288 consecutive cases of biopsy-confirmed. Helicobacter pylori gastritis, spanning a 21-month period from July 1988 to March 1990. Abdominal CT scans had been performed in 70 of these cases and were retrospectively reviewed. RESULTS: Seven of the 70 cases of confirmed Helicobacter pylori gastritis were suggestive of malignancy on CT

Asymptomatic gastric heterotopia in the rectum with Helicobacter pylori infection.

Science.gov (United States)

Swatek, Jarosław; Wronecki, Lech; Ciechanek, Roman; Szumiło, Justyna

2015-12-01

Gastric heterotopia is very rare in the rectum - less than 50 cases have been reported so far. Only in six of them Helicobacter pylori has been observed in heterotopic mucosa. We report a case of a 58-year-old woman with asymptomatic gastric heterotopia in the rectum, incidentally revealed during colonoscopy as a small, sessile polyp. The presence of H. pylori was confirmed by immunohistochemistry. This finding supports the opinion that H. pylori may pass along the gastrointestinal tract in a viable form and that the fecal-oral route of transmission is possible.

No Helicobacter pylori, no Helicobacter pylori-associated peptic ulcer disease

NARCIS (Netherlands)

Tytgat, G. N.

1995-01-01

Virtually all duodenal ulcers (DUs) and the vast majority of gastric ulcers (GUs) are the consequence of Helicobacter pylori-associated inflammation. In DUs, the inflammation is maximal in the antrum and is associated with gastric metaplasia in the bulb. Gastrin homeostasis is disturbed by H. pylori

Treatment of Helicobacter pylori infection favourably affects gastric mucosal superoxide dismutases

NARCIS (Netherlands)

Götz, J. M.; Thio, J. L.; Verspaget, H. W.; Offerhaus, G. J.; Biemond, I.; Lamers, C. B.; Veenendaal, R. A.

1997-01-01

Excessive production of reactive oxygen metabolites (ROMs) by phagocytic cells is thought to contribute to the mucosal pathology of Helicobacter pylori infection. Previously, H pylori infection was shown to have a differential effect on some gastric mucosal scavenger enzymes of ROMs-namely,

Apigenin has anti-atrophic gastritis and anti-gastric cancer progression effects in Helicobacter pylori-infected Mongolian gerbils.

Science.gov (United States)

Kuo, Chao-Hung; Weng, Bi-Chuang; Wu, Chun-Chieh; Yang, Sheau-Fang; Wu, Deng-Chang; Wang, Yuan-Chuen

2014-02-12

Apigenin, one of the most common flavonoids, is abundant in celery, parsley, chamomile, passionflower, and other vegetables and fruits. Celery is recognized as a medicinal vegetable in Oriental countries to traditionally treat inflammation, swelling, blood pressure, serum lipid, and toothache. In this study, we investigated apigenin treatment effects on Helicobacter pylori-induced atrophic gastritis and gastric cancer progression in Mongolian gerbils. Five to eight-week-old Mongolian gerbils were inoculated with Helicobacter pylori for four weeks without (atrophic gastritis group) or with N'-methyl-N'-nitro-N-nitroso-guanidine (MNNG) (gastric cancer group) in drinking water, and were then rested for two weeks. During the 7th-32th (atrophic gastritis group) or the 7th-52th (gastric cancer group) weeks, they were given various doses (0-60 mg/kgbw/day) of apigenin. At the end of the 32th (atrophic gastritis group) or the 52th (atrophic gastritis group) week, all Mongolian gerbils were sacrificed using the CO2 asphyxia method. The histological changes of Helicobacter pylori colonization, neutrophil and monocyte infiltrations, and atrophic gastritis in both atrophic gastritis and gastric cancer Mongolian gerbils were examined using immunohistochemistry stain and Sydney System scoring. Apigenin treatments (30-60 mg/kgbw/day) effectively decreased atrophic gastritis (atrophic gastritis group) and dysplasia/gastric cancer (gastric cancer group) rates in Mongolian gerbils. Apigenin treatment (60 mg/kgbw/day) significantly decreased Helicobacter pylori colonization and Helicobacter pylori-induced histological changes of neutrophil and monocyte infiltrations and atrophic gastritis in both atrophic gastritis and gastric cancer Mongolian gerbils. Apigenin has the remarkable ability to inhibit Helicobacter pylori-induced atrophic gastritis and gastric cancer progression as well as possessing potent anti-gastric cancer activity. Copyright © 2013 Elsevier Ireland Ltd. All rights

Evidence of helicobacter pylori infection in dental plaque and gastric mucosa

International Nuclear Information System (INIS)

Siddiq, M.; Haseeb-ur-Rehman; Mahmood, A.

2004-01-01

Objective: To determine the presence of Helicobacter pylori (H. pylori) in dental plaque of individuals suffering from H. pylori associated gastric disease. Patients and Methods: Patients presenting with symptoms/signs of chronic gastritis were included in the study. Specimens of dental plaque and gastric biopsy were collected from all the patients. The dental plaque specimen was processed for helicourease test and the gastric biopsy specimens were processed both for the helicourease test and histopathology. Results: Out of all patients studied (n=52), 32 (61.53%) were positive for helicourease test with gastric biopsy while 48 (92.30%) were positive with dental plaque. The histopathology of gastric biopsy showed H. pylori associated chronic active gastritis in 42 (80.76%) patients. Eight (15.38%) patients showed chronic active gastritis which was not associated with H. pylori while in 2 (3.84%) patients the gastric biopsy specimen was unremarkable. Conclusion: Majority of the patients have possible H. pylori colonization in dental plaque while about two-thirds have H. pylori associated chronic active gastritis. Oral cavity may be the first place for colonization and then the infection involves the gastric mucosa. (author)

Helicobacter pylori infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer

OpenAIRE

Zhang, Chuan; Yamada, Nobutaka; Wu, Yun-Lin; Wen, Min; Matsuhisa, Takeshi; Matsukura, Norio

2005-01-01

AIM: To evaluate the histological features of gastric mucosa, including Helicobacter pylori infection in patients with early gastric cancer and endoscopically found superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer.

Host pathogen interactions in Helicobacter pylori related gastric cancer

Science.gov (United States)

Chmiela, Magdalena; Karwowska, Zuzanna; Gonciarz, Weronika; Allushi, Bujana; Stączek, Paweł

2017-01-01

Helicobacter pylori (H. pylori), discovered in 1982, is a microaerophilic, spiral-shaped gram-negative bacterium that is able to colonize the human stomach. Nearly half of the world's population is infected by this pathogen. Its ability to induce gastritis, peptic ulcers, gastric cancer and mucosa-associated lymphoid tissue lymphoma has been confirmed. The susceptibility of an individual to these clinical outcomes is multifactorial and depends on H. pylori virulence, environmental factors, the genetic susceptibility of the host and the reactivity of the host immune system. Despite the host immune response, H. pylori infection can be difficult to eradicate. H. pylori is categorized as a group I carcinogen since this bacterium is responsible for the highest rate of cancer-related deaths worldwide. Early detection of cancer can be lifesaving. The 5-year survival rate for gastric cancer patients diagnosed in the early stages is nearly 90%. Gastric cancer is asymptomatic in the early stages but always progresses over time and begins to cause symptoms when untreated. In 97% of stomach cancer cases, cancer cells metastasize to other organs. H. pylori infection is responsible for nearly 60% of the intestinal-type gastric cancer cases but also influences the development of diffuse gastric cancer. The host genetic susceptibility depends on polymorphisms of genes involved in H. pylori-related inflammation and the cytokine response of gastric epithelial and immune cells. H. pylori strains differ in their ability to induce a deleterious inflammatory response. H. pylori-driven cytokines accelerate the inflammatory response and promote malignancy. Chronic H. pylori infection induces genetic instability in gastric epithelial cells and affects the DNA damage repair systems. Therefore, H. pylori infection should always be considered a pro-cancerous factor. PMID:28321154

Helicobacter pylori stool antigen test (HpSA) for the diagnosis of gastric infection

International Nuclear Information System (INIS)

Faruqui, A.N.; Majid, U.; Ahmed, L.; Khalil, M.; Hussan, M.U.

2007-01-01

To determine the accuracy of Helicobacter pylori Stool Antigen test (HpSA), compared with endoscopic histopathology for the diagnosis of gastric Helicobecter pylori infection. A total of 50 patients underwent endoscopy for gastric antral mucosal tissue biopsy for histopathology of H.pylori and advised for HpSA. Patient's information including age, gender, past history, presenting signs and symptoms, results of HpSA and histopathology were recorded. Sensitivity analysis was performed to calculate sensitivity, specificity, and predictive values of HpSA. Among 50 patients, 48% males and 52% females (M: F 1: 1.08), a total of 27 (54%) were true positive while 20 (40%) were true negative. Two patients were false negative and only one was false positive. Sensitivity of HpSA was, therefore, 93.1%, specificity 95% and positive and negative predictive values were 96.42% and 90.9% respectively. Helicobacter pylori stool antigen was an accurate and reliable test for the diagnosis of gastric H. pylori infection. (author)

Molecular mimicry between Helicobacter pylori antigens and H+, K+ --adenosine triphosphatase in human gastric autoimmunity

NARCIS (Netherlands)

Amedei, Amedeo; Bergman, Mathijs P.; Appelmelk, Ben J.; Azzurri, Annalisa; Benagiano, Marisa; Tamburini, Carlo; van der Zee, Ruurd; Telford, John L.; Vandenbroucke-Grauls, Christina M. J. E.; D'Elios, Mario M.; del Prete, Gianfranco

2003-01-01

Autoimmune gastritis and Helicobacter pylori-associated gastric atrophy develop through similar mechanisms involving the proton pump H+,K+-adenosine triphosphatase as autoantigen. Here, we report that H. pylori-infected patients with gastric autoimmunity harbor in vivo-activated gastric CD4+ T cells

Development of gastric cancer associated with Helicobacter pylori infection.

Science.gov (United States)

Sugiyama, Toshiro

2004-09-01

Helicobacter pylori infection is associated with histological gastritis, gastric atrophy, gastric cancer and mucosa-associated lymphoid tissue lymphoma in the stomach. However, gastric cancer only develops in a minority of infected individuals. Such clinical diversity is caused by variations in the interactions between H. pylori pathogenicity, host susceptibility, and environmental factors. Based on evidence from three prospective epidemiological studies, the International Agency for Research on Cancer and the World Health Organization (IARC/WHO) concluded in 1994 that H. pylori has a causal linkage to gastric carcinogenesis and is a definite carcinogen in humans. Two large-scale, prospective, epidemiological studies have recently been reported in Japan and have confirmed that H. pylori infection constitutes a high risk factor for the development of gastric cancer, at least in males. In order to obtain evidence that eradication of H. pylori leads to a reduction in the occurrence of gastric cancer, reversibility of precancerous lesions, gastric atrophy or intestinal metaplasia should be proven after eradication treatment. A biopsy specimen from the lesser curvature of the corpus is the most sensitive for evaluating the regression of gastric atrophy on histology, and the evaluation needs be conducted at least 13 months after treatment. In a Mongolian gerbil model with or without low-dose chemical carcinogens, it has been demonstrated that H. pylori can lead to the development of gastric cancer. Experimental studies have elucidated that virulence factors of H. pylori interact with gastric epithelial cell signaling related to carcinogenesis. The cag pathogenicity island (cagPAI) is a major virulence gene cluster; it encodes the type IV secretion machinery system forming a cylinder-like structure. The CagA protein is translocated into target cells via this secretion system and induces a hummingbird phenotype, a growth factor-like effect. The other gene products are

Helicobacter pylori eradication and gastric cancer: when is the horse out of the barn?

NARCIS (Netherlands)

de Vries, A. C.; Kuipers, E. J.; Rauws, E. A. J.

2009-01-01

Helicobacter pylori infection is a major risk factor for gastric cancer development. Therefore, H. pylori eradication may be an important approach in the prevention of gastric cancer. However, long-term data proving the efficacy of this approach are lacking. This report describes two patients who

Human Gastric Mucosal Hydrophobicity Does dot Decrease with Helicobacter Pylori Infection or Chronological Age

Directory of Open Access Journals (Sweden)

Mohammed S Al-Marhoon

2005-01-01

Full Text Available BACKGROUND AND AIMS: Infection with cytotoxin-associated gene A (cagA Helicobacter pylori is associated with severe gastric diseases. Previous studies in humans have reported a decreased gastric hydrophobicity with H pylori infection. The aim of the present study was to differentiate between the effect of cagA+ and cagA- strains on gastric mucus hydrophobicity.

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...

Helicobacter pylori eradication: gastric cancer prevention.

Science.gov (United States)

Leontiadis, Grigorios I; Ford, Alexander Charles

2015-12-01

The principal effect of Helicobacter pylori infection is lifelong chronic gastritis, affecting up to 20% of younger adults but 50% to 80% of adults born in resource-rich countries before 1950. We conducted a systematic overview, aiming to answer the following clinical question: What are the effects of H pylori eradication treatment on the risk of developing gastric cancer? We searched: Medline, Embase, The Cochrane Library, and other important databases up to July 2014 (Clinical Evidence reviews are updated periodically; please check our website for the most up-to-date version of this review). At this update, searching of electronic databases retrieved 208 studies. After deduplication and removal of conference abstracts, 166 records were screened for inclusion in the overview. Appraisal of titles and abstracts led to the exclusion of 124 studies and the further review of 42 full publications. Of the 42 full articles evaluated, one systematic review was added at this update. We performed a GRADE evaluation for two PICO combinations. In this systematic overview, we categorised the efficacy for one intervention based on information about the effectiveness and safety of H pylori eradication treatment for the prevention of gastric cancer.

History of Helicobacter pylori, duodenal ulcer, gastric ulcer and gastric cancer.

Science.gov (United States)

Graham, David Y

2014-05-14

Helicobacter pylori (H. pylori) infection underlies gastric ulcer disease, gastric cancer and duodenal ulcer disease. The disease expression reflects the pattern and extent of gastritis/gastric atrophy (i.e., duodenal ulcer with non-atrophic and gastric ulcer and gastric cancer with atrophic gastritis). Gastric and duodenal ulcers and gastric cancer have been known for thousands of years. Ulcers are generally non-fatal and until the 20th century were difficult to diagnose. However, the presence and pattern of gastritis in past civilizations can be deduced based on the diseases present. It has been suggested that gastric ulcer and duodenal ulcer both arose or became more frequent in Europe in the 19th century. Here, we show that gastric cancer and gastric ulcer were present throughout the 17th to 19th centuries consistent with atrophic gastritis being the predominant pattern, as it proved to be when it could be examined directly in the late 19th century. The environment before the 20th century favored acquisition of H. pylori infection and atrophic gastritis (e.g., poor sanitation and standards of living, seasonal diets poor in fresh fruits and vegetables, especially in winter, vitamin deficiencies, and frequent febrile infections in childhood). The latter part of the 19th century saw improvements in standards of living, sanitation, and diets with a corresponding decrease in rate of development of atrophic gastritis allowing duodenal ulcers to become more prominent. In the early 20th century physician's believed they could diagnose ulcers clinically and that the diagnosis required hospitalization for "surgical disease" or for "Sippy" diets. We show that while H. pylori remained common and virulent in Europe and the United States, environmental changes resulted in changes of the pattern of gastritis producing a change in the manifestations of H. pylori infections and subsequently to a rapid decline in transmission and a rapid decline in all H. pylori-related diseases.

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.

Helicobacter pylori colonization critically depends on postprandial gastric conditions

Science.gov (United States)

Bücker, Roland; Azevedo-Vethacke, Marina; Groll, Claudia; Garten, Désirée; Josenhans, Christine; Suerbaum, Sebastian; Schreiber, Sören

2012-01-01

The risk of Helicobacter pylori infection is highest in childhood, but the colonization process of the stomach mucosa is poorly understood. We used anesthetized Mongolian gerbils to study the initial stages of H. pylori colonization. Prandial and postprandial gastric conditions characteristic of humans of different ages were simulated. The fraction of bacteria that reached the deep mucus layer varied strongly with the modelled postprandial conditions. Colonization success was weak with fast gastric reacidification typical of adults. The efficiency of deep mucus entry was also low with a slow pH decrease as seen in pH profiles simulating the situation in babies. Initial colonization was most efficient under conditions simulating the postprandial reacidification and pepsin activation profiles in young children. In conclusion, initial H. pylori colonization depends on age-related gastric physiology, providing evidence from an in vivo infection model that suggests an explanation why the bacterium is predominantly acquired in early childhood. PMID:23251780

Accumulation of 8-nitroguanine in human gastric epithelium induced by Helicobacter pylori infection

International Nuclear Information System (INIS)

Ma, Ning; Adachi, Yukihiko; Hiraku, Yusuke; Horiki, Noriyuki; Horiike, Shinichirou; Imoto, Ichiro; Pinlaor, Somchai; Murata, Mariko; Semba, Reiji; Kawanishi, Shosuke

2004-01-01

Helicobacter pylori infection causes chronic inflammation, which can lead to gastric carcinoma. A double immunofluorescence labeling study demonstrated that the level of 8-nitroguanine and 8-oxo-7,8-dihydro-2 ' -deoxyguanosine (8-oxodG) apparent in gastric gland epithelium was significantly higher in gastritis patients with H. pylori infection than in those without infection. A significant accumulation of proliferating cell nuclear antigen, a prognostic factor for gastric cancer, was observed in gastric gland epithelial cells in patients with H. pylori infection as compared to those without infection, and its accumulation was closely correlated with the formation of 8-nitroguanine and 8-oxodG. These results suggest that nitrosative and oxidative DNA damage in gastric epithelial cells and their proliferation by H. pylori infection may lead to gastric carcinoma. 8-Nitroguanine could be not only a promising biomarker for inflammation but also a useful indicator of the risk of gastric cancer development in response to chronic H. pylori infection

Molecular Mechanism of Gastric Carcinogenesis in Helicobacter pylori-Infected Rodent Models

Directory of Open Access Journals (Sweden)

Takeshi Toyoda

2014-06-01

Full Text Available Since the discovery of Helicobacter pylori (H. pylori, many efforts have been made to establish animal models for the investigation of the pathological features and molecular mechanisms of gastric carcinogenesis. Among the animal models, Mongolian gerbils and mice are particularly useful for the analysis of H. pylori-associated inflammatory reactions and gastric cancer development. Inhibitors of oxidative stress, cyclooxygenase-2 (COX-2 and nuclear factor-κB, exert preventive effects on chronic gastritis and the development of adenocarcinomas in H. pylori-infected gerbils. Genetically-modified mouse models, including transgenic and knockout mice, have also revealed the importance of p53, COX-2/prostaglandin, Wnt/β-catenin, proinflammatory cytokines, gastrin and type III mucin in the molecular mechanisms of gastric carcinogenesis. Microarray technology is available for comprehensive gene analysis in the gastric mucosa of mouse models, and epigenetics, such as DNA methylation, could be an alternative approach to correlate the observations in animal models with the etiology in humans.

The Importance of Urease in Acid Protection for the Gastric-colonising Bacteria Helicobacter pylori and Helicobacter felis sp. nov.

OpenAIRE

Ferrero, R. L.; Lee, A.

2011-01-01

The urease of the gastric pathogen Helicobacter pylori shares numerous characteristics with the urease of a bacterium isolated from cat gastric mucosa, Helicobacter felis sp. nov. The native enzymes have similar apparent molecular weights and, when subjected to SDS-PAGE, disassociate into active subunits of comparable relative mobilities. In contrast, a bacterium (St1) that colonises rodent ileal mucosa, and is related to Helicobacter spp., expresses a distinct urease from those of the gastri...

Serum and gastric fluid levels of cytokines and nitrates in gastric diseases infected with Helicobacter pylori.

Science.gov (United States)

Mehmet, N; Refik, M; Harputluoglu, M; Ersoy, Y; Aydin, N Engin; Yildirim, B

2004-04-01

This case control study presents data on the concentrations of nitrite and nitrate and a variety of pro-inflammatory cytokines such as interleukin-1 beta (IL-1 beta), interleukin-2R (IL-2R), interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor TNF-alpha in gastric fluid and serum. Patients with gastritis, gastric ulcer and gastric cancer are studied and grouped according to infection by Helicobacter pylori. The 208 patients who underwent upper gastrointestinal endoscopic examination were classified as follows; H. pylori-positive gastritis (n = 32), H. pylori-negative gastritis (n = 32), H. pylori-positive ulcers (n = 34), H. pylori-negative ulcers (n = 34), 43 patients with H. pylori-positive gastric cancer in addition to 33 H. pylori-negative healthy control individuals. Gastric fluids and blood samples were taken concomitantly. Cytokines and nitrite and nitrate determinations were attempted as soon as possible after collection of the samples. Nitrite and nitrate levels of serum and gastric fluids of H. pylori-positive gastritis and ulcers were higher than H. pylori-negative gastritis and ulcers. The concentrations of total nitrite and nitrate and cytokines (TNF-alpha, IL-2R, IL-6, and IL-8) in gastric fluids and sera of H. pylori-positive gastric cancer patients were higher than H. pylori-negative control groups. IL-1 beta level was significantly elevated in gastric fluid of infected cancer patients but not in serum. Taken together, the results suggest that an increase in cytokine-NO combination in gastric mucosa previously reported by many studies is not restricted to local infected gastric tissue but also detected in gastric fluid and sera of H. pylori-positive subjects and may have an important role in the pathogenesis and development of common gastric diseases.

Eradication of Helicobacter pylori infection favourably affects altered gastric mucosal MMP-9 levels

NARCIS (Netherlands)

Kubben, F.J.G.M.; Sier, C.F.M.; Schram, M.; Witte, T.A.M.C.; Veenendaal, R.A.; Duijn, W. van; Verheijen, J.H.; Hanemaaijer, R.; Lamers, C.B.H.W.; Verspaget, H.W.

2007-01-01

Background: Helicobacter pylori gastritis is recognized as an important pathogenetic factor in peptic ulcer disease and gastric carcinogenesis, and is accompanied by strongly enhanced gastric mucosal matrix metalloproteinase-9 (MMP-9) levels. Aim: This study was performed to investigate whether H.

Inhibitory effect of piperine on Helicobacter pylori growth and adhesion to gastric adenocarcinoma cells

OpenAIRE

Tharmalingam, Nagendran; Kim, Sa-Hyun; Park, Min; Woo, Hyun Jun; Kim, Hyun Woo; Yang, Ji Yeong; Rhee, Ki-Jong; Kim, Jong Bae

2014-01-01

Background Piperine is a compound comprising 5-9% of black pepper (Piper nigrum), which has a variety of biological roles related to anticancer activities. Helicobacter pylori has been classified as a gastric carcinogen, because it causes gastritis and gastric cancer by injecting the virulent toxin CagA and translocating VacA. The present study investigated the inhibitory action of piperine on H. pylori growth and adhesion. Methods Inhibition of H. pylori growth was determined by the broth ma...

Gastric mucosa in Mongolian and Japanese patients with gastric cancer and Helicobacter pylori infection

Science.gov (United States)

Matsuhisa, Takeshi; Yamaoka, Yoshio; Uchida, Tomohisa; Duger, Davaadorj; Adiyasuren, Battulga; Khasag, Oyuntsetseg; Tegshee, Tserentogtokh; Tsogt-Ochir, Byambajav

2015-01-01

AIM: To investigate the characteristics of gastric cancer and gastric mucosa in a Mongolian population by comparison with a Japanese population. METHODS: A total of 484 Mongolian patients with gastric cancer were enrolled to study gastric cancer characteristics in Mongolians. In addition, a total of 208 Mongolian and 3205 Japanese consecutive outpatients who underwent endoscopy, had abdominal complaints, no history of gastric operation or Helicobacter pylori eradication treatment, and no use of gastric secretion inhibitors such as histamine H2-receptor antagonists or proton pump inhibitors were enrolled. This study was conducted with the approval of the ethics committees of all hospitals. The triple-site biopsy method was used for the histologic diagnosis of gastritis and H. pylori infection in all Mongolian and Japanese cases. The infection rate of H. pylori and the status of gastric mucosa in H. pylori-infected patients were compared between Mongolian and Japanese subjects. Age (± 5 years), sex, and endoscopic diagnosis were matched between the two countries. RESULTS: Approximately 70% of Mongolian patients with gastric cancer were 50-79 years of age, and approximately half of the cancers were located in the upper part of the stomach. Histologically, 65.7% of early cancers exhibited differentiated adenocarcinoma, whereas 73.9% of advanced cancers displayed undifferentiated adenocarcinoma. The infection rate of H. pylori was higher in Mongolian than Japanese patients (75.9% vs 48.3%, P gastritis changed from antrum-predominant gastritis to corpus-predominant gastritis with age in both populations. CONCLUSION: Gastric cancer was located in the upper part of the stomach in half of the Mongolian patients; Mongolian patients were infected with non-East-Asian-type H. pylori. PMID:26217093

Effects of EGFR Inhibitor on Helicobacter pylori Induced Gastric Epithelial Pathology in Vivo

Directory of Open Access Journals (Sweden)

Philip A. Robinson

2013-10-01

Full Text Available Helicobacter pylori transactivates the Epidermal Growth Factor Receptor (EGFR and predisposes to gastric cancer development in humans and animal models. To examine the importance of EGFR signalling to gastric pathology, this study investigated whether treatment of Mongolian gerbils with a selective EGFR tyrosine kinase inhibitor, EKB-569, altered gastric pathology in chronic H. pylori infection. Gerbils were infected with H. pylori and six weeks later received either EKB-569-supplemented, or control diet, for 32 weeks prior to sacrifice. EKB-569-treated H. pylori-infected gerbils had no difference in H. pylori colonisation or inflammation scores compared to infected animals on control diet, but showed significantly less corpus atrophy, mucous metaplasia and submucosal glandular herniations along with markedly reduced antral and corpus epithelial proliferation to apoptosis ratios. EKB-569-treated infected gerbils had significantly decreased abundance of Cox-2, Adam17 and Egfr gastric transcripts relative to infected animals on control diet. EGFR inhibition by EKB-569 therefore reduced the severity of pre-neoplastic gastric pathology in chronically H. pylori-infected gerbils. EKB-569 increased gastric epithelial apoptosis in H. pylori-infected gerbils which counteracted some of the consequences of increased gastric epithelial cell proliferation. Similar chemopreventative strategies may be useful in humans who are at high risk of developing H.pylori-induced gastric adenocarcinoma.

Management of Helicobacter Pylori Infection

African Journals Online (AJOL)

Dr Olaleye

90%, the sequential therapy seems to have a potential of becoming the standard first-line treatment for H pylori infection in the interim, while search is being made for the ideal antimicrobial monotherapy. . Keywords: Helicobacter pylori, Dyspepsia, Gastric cancer, Gastric Ulcer, Duodenal ulcer. INTRODUCTION. 1. Since the ...

The overmethylated genes in Helicobacter pylori-infected gastric mucosa are demethylated in gastric cancers

Directory of Open Access Journals (Sweden)

Choi Sang-Wook

2010-11-01

Full Text Available Abstract Background The transitional-CpG sites between weakly methylated genes and densely methylated retroelements are overmethylated in the gastric mucosa infected with Helicobacter pylori (H. pylori and they are undermethylated in the gastric cancers depending on the level of loss of heterozygosity (LOH events. This study delineated the transitional-CpG methylation patterns of CpG-island-containing and -lacking genes in view of the retroelements. Methods The transitional-CpG sites of eight CpG-island-containing genes and six CpG-island-lacking genes were semi-quantitatively examined by performing radioisotope-labelling methylation-specific PCR under stringent conditions. The level of LOH in the gastric cancers was estimated using the 40 microsatellite markers on eight cancer-associated chromosomes. Each gene was scored as overmethylated or undermethylated based on an intermediate level of transitional-CpG methylation common in the H. pylori-negative gastric mucosa. Results The eight CpG-island genes examined were overmethylated depending on the proximity to the nearest retroelement in the H. pylori-positive gastric mucosa. The six CpG-island-lacking genes were similarly methylated in the H. pylori-positive and -negative gastric mucosa. In the gastric cancers, long transitional-CpG segments of the CpG-island genes distant from the retroelements remained overmethylated, whereas the overmethylation of short transitional-CpG segments close to the retroelements was not significant. Both the CpG-island-containing and -lacking genes tended to be decreasingly methylated in a LOH-level-dependent manner. Conclusions The overmethylated genes under the influence of retroelement methylation in the H. pylori-infected stomach are demethylated in the gastric cancers influenced by LOH.

Helicobacter pylori as a crucial factor in intestinal metaplasia development of gastric mucosa

Directory of Open Access Journals (Sweden)

Sergii Vernygorodskyi

2016-06-01

Full Text Available Helicobacter pylori (H. pylori is detected on the surface of gastric epithelium and in goblet cells, predominantly in patients with chronic atrophic gastritis and incomplete intestinal metaplasia (IM. H. pylori infection persistence leads to the formation of gastrointestinal phenotype of IM. H. pylori can be considered as an etiological factor of IM. It inhibits the expression of SOX2 in gastric epithelial cells, hence activating transcription factor CDX2 as a counterpart to MUC5AC gene inhibition and MUC2 gene induction. Thus, in metaplastic cells, programming differentiation after intestinal phenotype will develop. The role of H. pylori in the origin of intestinal metaplasia of gastric mucosa was defined in this study to elucidate the probable mechanism of cell reprogramming. The activation of CDX2, with simultaneous inactivation and decreased number of genes (e.g., SHH, SOX2, and RUNX3 responsible for gastric differentiation, was identified to cause the appearance of IM.

CagA+ Helicobacter pylori infection and gastric cancer risk in the EPIC-EURGAST study.

NARCIS (Netherlands)

Palli, D.; Masala, G.; Giudice, G. Del; Plebani, M.; Basso, D.; Berti, D.; Numans, M.E.; Ceroti, M.; Peeters, P.H.; Bueno de Mesquita, H.B.; Buchner, F.L.; Clavel-Chapelon, F.; Boutron-Ruault, M.C.; Krogh, V.; Saieva, C.; Vineis, P.; Panico, S.; Tumino, R.; Nyren, O.; Siman, H.; Berglund, G.; Hallmans, G.; Sanchez, M.J.; Larrañaga, N.; Barricarte, A.; Navarro, C; Quiros, J.R.; Key, T.; Allen, N.; Bingham, S.; Khaw, K.T.; Boeing, H.; Weikert, C.; Linseisen, J.; Nagel, G.; Overvad, K.; Thomsen, R.W.; Tjonneland, A.; Olsen, A.; Trichoupoulou, A.; Trichopoulos, D.; Arvaniti, A.; Pera, G.; Kaaks, R.; Jenab, M.; Ferrari, P.; Nesi, G.; Carneiro, F.; Riboli, E.; Gonzalez, C.A.

2007-01-01

Helicobacter pylori (H. pylori), atrophic gastritis, dietary and life-style factors have been associated with gastric cancer (GC). These factors have been evaluated in a large case-control study nested in the European Prospective Investigation into Cancer and Nutrition carried out in 9 countries,

Effect of Native Gastric Mucus on in vivo Hybridization Therapies Directed at Helicobacter pylori

DEFF Research Database (Denmark)

Santos, Rita S; Dakwar, George R; Xiong, Ranhua

2015-01-01

Helicobacter pylori infects more than 50% of the worldwide population. It is mostly found deep in the gastric mucus lining of the stomach, being a major cause of peptic ulcers and gastric adenocarcinoma. To face the increasing resistance of H. pylori to antibiotics, antimicrobial nucleic acid...... barriers-the highly viscoelastic gastric mucus and the bacterial cell envelope. We found that LNA/2'OMe is capable of diffusing rapidly through native, undiluted, gastric mucus isolated from porcine stomachs, without degradation. Moreover, although LNA/2'OMe hybridization was still successful without...

Review article: the prevalence of Helicobacter pylori and the incidence of gastric cancer across Europe.

Science.gov (United States)

Roberts, S E; Morrison-Rees, S; Samuel, D G; Thorne, K; Akbari, A; Williams, J G

2016-02-01

There is little up-to-date review evidence on the prevalence of Helicobacter pylori across Europe. To establish regional and national patterns in H. pylori prevalence across Europe. Secondly, to establish trends over time in H. pylori prevalence and gastric cancer incidence and, thirdly, to report on the relationship between H. pylori prevalence and age group across Europe. A review of H. pylori prevalence from unselected surveys of adult or general populations across 35 European countries and four European regions since 1990. Secondly, an analysis of trends over time in H. pylori prevalence and in gastric cancer incidence from cancer registry data. Helicobacter pylori prevalence was lower in northern and western Europe than in eastern and southern Europe (P Europe from 1993 to 2007 was 2.1% with little variation regionally across Europe (north 2.2%, west 2.3%, east 1.9% and south 2.0%). Sharp increases in age-related prevalence of H. pylori often levelled off for middle age groups of about 50 years onwards, especially in areas with high prevalence. This review shows that H. pylori prevalence is much higher in less affluent regions of Europe and that age-related increases in prevalence are confined to younger age groups in some areas. There were sharp reductions in both H. pylori prevalence and gastric cancer incidence throughout Europe. © 2015 John Wiley & Sons Ltd.

CagA and VacA Helicobacter Pylori Antibodies in Gastric Cancer

Directory of Open Access Journals (Sweden)

Renzo Suriani

2008-01-01

Full Text Available BACKGROUND: Infection with different genotypes of virulent Helicobacter pylori strains (cytotoxin-associated gene A [CagA]-and/or vacuolating cytotoxin A [VacA]-positive can play a role in the development of atrophic gastritis, duodenal ulcer (DU and gastric cancer (GC.

Detection of Helicobacter pylori urease antigen in saliva in patients with different gastric H. pylori status.

Science.gov (United States)

El Khadir, Mounia; Alaoui Boukhris, Samia; Benajah, Dafr-Allah; El Rhazi, Karima; Ibrahimi, Sidi Adil; El Abkari, Mohamed; Harmouch, Taoufiq; Nejjari, Chakib; Mahmoud, Mustapha; Benlemlih, Mohamed; Bennani, Bahia

2016-07-01

Finding a simple, accurate, and noninvasive diagnosis method is a substantial challenge for the detection of Helicobacter pylori. The aim of the present study was to compare the presence of H. pylori urease antigen in saliva with the presence of this bacterium in gastric mucosa. Saliva samples and gastric biopsies were taken from 153 consenting Moroccan patients. Saliva samples were analyzed using an immunochromatographic test for urease antigen H. pylori detection. Thereafter, the gastric biopsies were analyzed by histology and polymerase chain reaction (PCR) to detect this bacterium. From a total of 153 recruited Moroccan patients, H. pylori was detected in 28 (18.30%), 87 (57.24%), and 69 (45.10%) cases by saliva test, histology, and PCR, respectively. A significant association was observed between the presence of H. pylori antigen in saliva and age. However, no association was found with sex, H. pylori virulence factors, gastric disease outcome, and density of the bacterium on the gastric mucosa. Considering that only 90 patients presented concordant results on H. pylori diagnosis (positive or negative) by both histology and PCR, the immunochromatographic test showed very low sensitivity (29.79%) and high specificity (90.70%). Of these two tests, the positive and negative predictive values were 77.78% and 54.17%, respectively. The accuracy of the test for salivary detection of urease antigen H. pylori was 58.89%. This study demonstrated a low detection rate of H. pylori antigens in saliva compared with the presence of this bacterium in gastric mucosa, suggesting that saliva cannot be used as a suitable sample for the diagnosis of H. pylori in our study population. Copyright © 2016. Published by Elsevier Taiwan LLC.

The influence of duodeno-gastric reflux on frequency of Helicobacter pylori infection at patients with ulcer gastric

International Nuclear Information System (INIS)

Kopanski, Z.; Niziol, J.; Micherdzinski, J.; Wasilewska-Radwanska, M.; Cienciala, A.; Lasa, J.

1996-01-01

To estimate the correlation between frequency of Helicobacter pylori (H. pylori) infection and intensity of duodeno-gastric reflux it was analysed 61 species with ulcer gastric. Bacterial infection was diagnosed by the breath test with 14 C-labelled urea, whereas presence and intensity of the reflux was found with dynamic scintigraphy with 99 Tm MBrIDA support. The H. pylori infection was present at 42 (68.9%) patients. The presence of throwing back the duodenal liquid was found at 32 (52.5%) diagnosed patients. At 19 (31.2%) of them the reflux has intensity of 1%, at 11 (18%)-2 o and 2 (3.3%)-3 o .The investigations which were carried out, showed that at patients with ulcer gastric disease, duodeno-gastric reflux is an agent which slows down H. pylori infection, however it is easily seen not earlier than at 2 o of its intensity. (author)

Geographic pathology of Helicobacter pylori gastritis

NARCIS (Netherlands)

Liu, Yi; Ponsioen, Cyriel I. J.; Xiao, Shu-Dong; Tytgat, Guido N. J.; ten Kate, Fiebo J. W.

2005-01-01

Background and aim. Helicobacter pylori is etiologically associated with gastritis and gastric cancer. There are significant geographical differences between the clinical manifestation of H. pylori infections. The aim of this study was to compare gastric mucosal histology in relation to age among H.

Detouring the Undesired Route of Helicobacter pylori-Induced Gastric Carcinogenesis

Directory of Open Access Journals (Sweden)

Ki Baik Hahm

2011-07-01

Full Text Available Epidemiological and experimental evidence has emerged that a dysregulated inflammation is associated with most of the tumors, and many studies have begun to unravel the molecular pathways linking inflammation and cancer. As a typical example linking these associations, Helicobacter pylori (H. pylori infection-associated atrophic gastritis has been recognized as precursor lesion of gastric cancer. The identification of transcription factors such as NF-κB and STAT3, and their gene products such as IL-8, COX-2, iNOS, cytokines, chemokines and their receptors, etc have laid the molecular foundation for our understanding of the decisive role of inflammation in carcinogenesis. In addition to the role as the initiator of cancer, inflammation contributes to survival and proliferation of malignant cells, tumor angiogenesis, and even metastasis. In this review, the fundamental mechanisms of H. pylori-induced carcinogenesis as well as the possibility of cancer prevention through suppressing H. pylori-induced inflammation are introduced. We infer that targeting inflammatory pathways have a potential role to detour the unpleasant journey to H. pylori-associated gastric carcinogenesis.

Detouring the Undesired Route of Helicobacter pylori-Induced Gastric Carcinogenesis

Energy Technology Data Exchange (ETDEWEB)

Kim, Eun-Hee; Hong, Kyung-Sook; Hong, Hua [Lab of Translational Medicine, Lee Gil Ya Cancer and Diabetes Institute, Gachon University of Medicine and Science, 7-45 Songdo-dong, Yeonsu-gu, Incheon 406-840 (Korea, Republic of); Hahm, Ki Baik, E-mail: hahmkb@gachon.ac.kr [Lab of Translational Medicine, Lee Gil Ya Cancer and Diabetes Institute, Gachon University of Medicine and Science, 7-45 Songdo-dong, Yeonsu-gu, Incheon 406-840 (Korea, Republic of); Department of Gastroenterology, Gachon Graduate School of Medicine, Gil Hospital, Incheon 406-840 (Korea, Republic of)

2011-07-25

Epidemiological and experimental evidence has emerged that a dysregulated inflammation is associated with most of the tumors, and many studies have begun to unravel the molecular pathways linking inflammation and cancer. As a typical example linking these associations, Helicobacter pylori (H. pylori) infection-associated atrophic gastritis has been recognized as precursor lesion of gastric cancer. The identification of transcription factors such as NF-κB and STAT3, and their gene products such as IL-8, COX-2, iNOS, cytokines, chemokines and their receptors, etc have laid the molecular foundation for our understanding of the decisive role of inflammation in carcinogenesis. In addition to the role as the initiator of cancer, inflammation contributes to survival and proliferation of malignant cells, tumor angiogenesis, and even metastasis. In this review, the fundamental mechanisms of H. pylori-induced carcinogenesis as well as the possibility of cancer prevention through suppressing H. pylori-induced inflammation are introduced. We infer that targeting inflammatory pathways have a potential role to detour the unpleasant journey to H. pylori-associated gastric carcinogenesis.

Detouring the Undesired Route of Helicobacter pylori-Induced Gastric Carcinogenesis

International Nuclear Information System (INIS)

Kim, Eun-Hee; Hong, Kyung-Sook; Hong, Hua; Hahm, Ki Baik

2011-01-01

Epidemiological and experimental evidence has emerged that a dysregulated inflammation is associated with most of the tumors, and many studies have begun to unravel the molecular pathways linking inflammation and cancer. As a typical example linking these associations, Helicobacter pylori (H. pylori) infection-associated atrophic gastritis has been recognized as precursor lesion of gastric cancer. The identification of transcription factors such as NF-κB and STAT3, and their gene products such as IL-8, COX-2, iNOS, cytokines, chemokines and their receptors, etc have laid the molecular foundation for our understanding of the decisive role of inflammation in carcinogenesis. In addition to the role as the initiator of cancer, inflammation contributes to survival and proliferation of malignant cells, tumor angiogenesis, and even metastasis. In this review, the fundamental mechanisms of H. pylori-induced carcinogenesis as well as the possibility of cancer prevention through suppressing H. pylori-induced inflammation are introduced. We infer that targeting inflammatory pathways have a potential role to detour the unpleasant journey to H. pylori-associated gastric carcinogenesis

Helicobacter pylori and primary gastric lymphoma. A histopathologic and immunohistochemical analysis of 237 patients.

Science.gov (United States)

Nakamura, S; Yao, T; Aoyagi, K; Iida, M; Fujishima, M; Tsuneyoshi, M

1997-01-01

Few previous articles have analyzed the relation between infection with Helicobacter pylori (H. pylori) and primary gastric lymphoma in a large number of patients. Resected and biopsied specimens from 237 patients with primary gastric lymphoma were investigated for H. pylori using hematoxylin and eosin stain, modified Giemsa stain, and immunohistochemistry. These specimens were compared with specimens from 29 patients with chronic active gastritis, 33 with peptic ulcers, and 41 with gastric carcinoma. H. pylori was detected in 145 of 237 patients (61%) with gastric lymphoma. The frequency of H. pylori positivity was higher in patients with lymphoma restricted to the mucosa and submucosa (76%) than in those with lymphoma invading beyond the submucosa (48%) (P gastritis (100%) (P gastritis and peptic ulcer. The H. pylori grading score for patients with lymphoma (0.9 +/- 1.0) was lower than for those with chronic active gastritis (1.9 +/- 0.8) (P < 0.001), peptic ulcers (2.2 +/- 1.0) (P < 0.001), or gastric carcinoma (1.2 +/- 1.1) (P < 0.05). These results suggest that H. pylori is more likely to be associated with early states of primary gastric lymphoma than with advanced states. Thus, H. pylori may disappear during the progression of primary gastric lymphoma.

Alterations in Helicobacter pylori triggered by contact with gastric epithelial cells

Directory of Open Access Journals (Sweden)

Elizabeth M. Johnson

2012-02-01

Full Text Available Helicobacter pylori lives within the mucus layer of the human stomach, in close proximity to gastric epithelial cells. While a great deal is known about the effects of H. pylori on human cells and the specific bacterial products that mediate these effects, relatively little work has been done to investigate alterations in H. pylori that may be triggered by bacterial contact with human cells. In this review, we discuss the spectrum of changes in bacterial physiology and morphology that occur when H. pylori is in contact with gastric epithelial cells. Several studies have reported that cell contact causes alterations in H. pylori gene transcription. In addition, H. pylori contact with gastric epithelial cells promotes the formation of pilus-like structures at the bacteria-host cell interface. The formation of these structures requires multiple genes in the cag pathogenicity island, and these structures are proposed to have an important role in the type IV secretion system-dependent process through which CagA enters host cells. Finally, H. pylori contact with epithelial cells can promote bacterial replication and the formation of microcolonies, phenomena that are facilitated by the acquisition of iron and other nutrients from infected cells. In summary, the gastric epithelial cell surface represents an important niche for H. pylori, and upon entry into this niche, the bacteria alter their behavior in a manner that optimizes bacterial proliferation and persistent colonization of the host.

Helicobacter pylori in the gastric mucosa of dead children Helicobacter pylori en la mucosa gástrica de cadáveres de niños

Directory of Open Access Journals (Sweden)

John Jairo Duque Alzate

1999-03-01

Full Text Available 23 children under the age of 12 years who died violently without receiving any treatment, had their gastric mucosa studied by means of he Warthin-Starry stain and immunohistochemistry in search for Helicobacter pylori. It was found that 60.9% (14 cases were positive; of them 64,3% belonged to a low social class and 35,7% to the middle one. Of the positive cases, 9 had acute gastritis, 1 had chronic gastritis and only 4 had normal gastric mucosa. A clear association between Helicobacter pylory and changes in gastritis was observed. En 23 niños menores de 12 años que murieron en forma violenta sin haber recibido tratamiento, se estudiaron para Helicobacter pylori las mucosas gástricas con las coloraciones de hematoxilina eosina, Warthin Starry e inmunohistoquímica. Se encontró que 14 casos (60,9% fueron positivos para esta bacteria, de los cuales 9 (64,3% pertenecían a un estrato social bajo y 5 (35,7% a uno medio. De los casos positivos para H. pylori, 9 tenían gastritis aguda, 1 gastritis crónica y sólo en 4 la mucosa gástrica era normal. Se observó una clara asociación entre H. pylori y cambios de gastritis.

EKSPRESI ANTI-HELICOBACTER PYLORI PADA GASTRITIS KRONIS, LESI PRAKANKER, DAN KARSINOMA GASTER

Directory of Open Access Journals (Sweden)

Lina Damayanti

2015-08-01

Full Text Available Prevalence of Helicobacter pylori infection in Indonesia was 36-46%. In Jakarta and Surabaya, the prevalence were 85,7%-93,9%. Helicobacter pylori infection play role in pathogenesis of pectic ulcers, chronic gastritis, carcinoma of gaster and gastric lymphoma. Epidemiologic study showed 80% of carcinoma of gaster related with H pylori infection.This study analyzed expression of anti-Helicobacter pylori in chronic gastritis, precancer lesion , and carcinoma of gaster. This study was a observational descriptive study with case control design. Thirty (30 samples from paraffin bloc that were diagnosed with chronic gastritis, precancer lesion, and carcinoma of gaster at Dokter Kariadi hospital in 2013 was stained by hematoxylin eosin, giemsa and immunohistochemistry of anti-helicobacter pylori. Data was analyzed by descriptive analysis. Thirty (30 samples were diagnosed as gastritis chronis 13 (43,3% , pra cancer lesion(36.6%, and carcinoma(20.1%. Chronic gastritis can be occurred at all age and no distinct difference on sex, while gastric carcinoma predominant in male older than 40 years. Expresion of Helicobacter pylori on chronic gastritis was 84.6%, precancer lesion was 54.5%, and gastric carcinoma was 83.3%. The Giemsa stain gave 23.3% false positive and 20% false negative. Helicobacter pylori expression can be showed in chronic gastritis, precancer lesion, and gastric carcinoma. Keywords: Chronic gastritis, gastric carcinoma, Helicobacter pylori

Detection of Helicobacter pylori in gastric cancer Detecção do Helicobacter pylori no câncer gástrico

Directory of Open Access Journals (Sweden)

Luana Paredes Leite de Barros PEREIRA

2001-10-01

Full Text Available Background and Objectives — Considering the high prevalence of stomach cancer in the northern region of Brazil and the recognized relationship between chronic gastric inflammation caused by Helicobacter pylori, and its carcinogenic potential, the objective we had with this study was to investigate the presence of the microorganism in macro and microscopic presentations of neoplasm in different regions of the stomach, and in non-malignant lesions concomitant to the adenocarcinoma in patients originating from the metropolitan area of Belém (State of Pará, Brazil. Methods - Examinations were made on 172 patients divided into two groups: group I, formed by 75 patients with gastric carcinoma, and group II, formed by 97 patients with mild enanthematic gastritis, considered control group. The diagnosis was obtained during endoscopic examination and the respective biopsy. Gastric neoplasms were classified macroscopically in accordance with Borrmann's classification, and microscopically in accordance with Laurén's classification. In group I, 54 patients were male and 21 female while in group II, 22 patients were male and 75 female. The average age in group I was 61.2 years (range 27 to 86 years, while in group II it was 37.5 years (range 16 to 69 years. Thin sections were prepared and stained using the hematoxylin-eosin method. In the Helicobacter pylori research, the modified Gram stain was utilized. Statistical analysis was done by utilizing the chi-squared (chi ² test, Mann-Whitney test (U, and Fisher's exact test. Results - The results showed the detection of Helicobacter pylori were significantly greater in patients with mild enanthematic gastritis than in patients with gastric carcinoma. The presence of Helicobacter pylori in patients with gastric carcinoma and mild enanthematic gastritis was significantly greater in the antral region than in other gastric regions. Helicobacter pylori detection in patients with gastric carcinoma did not

Gastric Cancer Screening by Combined Determination of Serum Helicobacter pylori Antibody and Pepsinogen Concentrations: ABC Method for Gastric Cancer Screening.

Science.gov (United States)

Chen, Xian-Zhe; Huang, Cheng-Zhi; Hu, Wei-Xian; Liu, Ying; Yao, Xue-Qing

2018-05-20

Gastroscopy combined with gastric mucosa biopsies is currently regarded as a gold standard for diagnosis of gastric cancer. However, its application is restricted in clinical practice due to its invasive property. A new noninvasive population screening process combining the assay of anti-Helicobacter pylori antibody and serum pepsinogen (PG) (ABC method) is adopted to recognize the high-risk patients for further endoscopy examination, avoiding the unnecessary gastroscopy for most population and saving the cost consumption for mass screening annually. Nevertheless, controversies exist for the grouping of ABC method and the intervals of gastroscopy surveillance for each group. In this review, we summarized these popular concerned topics for providing useful references to the healthcare practitioner in clinical practice. The PubMed databases were systematically searched from the inception dates to November 22, 2017, using the keywords "Helicobacter pylori," "Pepsinogens," and "Stomach Neoplasms." Original articles and reviews on the topics were selected. Anti-H. pylori antibody and serum PG concentration showed significant changes under the different status of H. pylori infection and the progression of atrophic gastritis, which can be used for risk stratification of gastric cancer in clinic. In addition, anti-H. pylori antibody titer can be used for further risk stratification of gastric cancer contributing to determine better endoscopy surveillance interval. The early detection and diagnosis of gastric cancer benefit from the risk stratification, but the cutoff values for H. pylori antibody and serum PG concentration require further modification.

Effect of depression on Helicobacter pylori infection in patients with gastric cancer and its correlation with oncogene expression

Institute of Scientific and Technical Information of China (English)

Chun-Rong Xiao

2017-01-01

Objective: To study the effect of depression on Helicobacter pylori (H. pylori) infection in patients with gastric cancer and its correlation with oncogene expression. Methods: A total of 82 patients who accepted radical operation for gastric cancer in Zigong Third People's Hospital between March 2015 and February 2017 were selected as the research subjects and divided into depression group and non-depression group according to the preoperative HAMD scores, and helicobacter pylori infection as well as the mRNA expression of proliferation genes and invasion genes in gastric cancer lesions was detected. Results: The positive rate of H. pylori in gastric cancer lesions of depression group was significantly higher than that of non-depression group; LOXL2, RAB1A, UHRF1, Slug and ADAM8 mRNA expression in gastric cancer lesions of depression group were significantly higher than those of non-depression group while MTS1, NOX, E-cadherin and TIMP1 mRNA expression were significantly lower than those of non-depression group; LOXL2, RAB1A, UHRF1, Slug and ADAM8 mRNA expression in H. pylori-positive gastric cancer lesions of depression group were significantly higher than those in H. pylori-negative gastric cancer lesions of depression group while MTS1, NOX, E-cadherin and TIMP1 mRNA expression were significantly lower than those in H. pylori-negative gastric cancer lesions of depression group. Conclusion: Depression can increase the H. pylori infection rate and promote the proliferation and invasion of cancer cells in gastric cancer lesions.

Helicobacter pylori detection in gastric biopsies, saliva and dental plaque of Brazilian dyspeptic patients

Directory of Open Access Journals (Sweden)

Lucas Trevizani Rasmussen

2010-05-01

Full Text Available Helicobacter pylori is an important human pathogen that causes chronic gastritis and is associated with the development of peptic ulcer disease and gastric malignancies. The oral cavity has been implicated as a potential H. pylori reservoir and may therefore be involved in the reinfection of the stomach, which can sometimes occur following treatment of an H. pylori infection. The objectives of this paper were (i to determine the presence of H. pylori in the oral cavity and (ii to examine the relationship between oral H. pylori and subsequent gastritis. Gastric biopsies, saliva samples and dental plaques were obtained from 78 dyspeptic adults. DNA was extracted and evaluated for the presence of H. pylori using polymerase chain reaction and Southern blotting methods. Persons with gastritis were frequently positive for H. pylori in their stomachs (p < 0.0001 and there was a statistically significant correlation between the presence of H. pylori in gastric biopsies and the oral cavity (p < 0.0001. Our results suggest a relationship between gastric infection and the presence of this bacterium in the oral cavity. Despite this, H. pylori were present in the oral cavity with variable distribution between saliva and dental plaques, suggesting the existence of a reservoir for the species and a potential association with gastric reinfection.

Prevalence of Helicobacter pylori infection in advanced gastric carcinoma

Directory of Open Access Journals (Sweden)

Irami Araújo-Filho

2006-12-01

Full Text Available BACKGROUD: There is substantial evidence that infection with Helicobacter pylori plays a role in the development of gastric cancer and that it is rarely found in gastric biopsy of atrophic gastritis and gastric cancer. On advanced gastric tumors, the bacteria can be lost from the stomach. AIMS: To analyze the hypothesis that the prevalence of H.pylori in operated advanced gastric carcinomas and adjacent non-tumor tissues is high, comparing intestinal and diffuse tumors according to Lauren's classification METHODS: A prospective controlled study enrolled 56 patients from "Hospital Universitário", Federal University of Rio Grande do Norte, Natal, RN, Brazil, with advanced gastric cancer, treated from February 2000 to March 2003. Immediately after partial gastrectomy, the resected stomach was opened and several mucosal biopsy samples were taken from the gastric tumor and from the adjacent mucosa within 4 cm distance from the tumor margin. Tissue sections were stained with hematoxylin and eosin. Lauren's classification for gastric cancer was used, to analyse the prevalence of H. pylori in intestinal or diffuse carcinomas assessed by the urease rapid test, IgG by ELISA and Giemsa staining. H. pylori infected patients were treated with omeprazole, clarithromycin and amoxicillin for 7 days. Follow-up endoscopy and serology were performed 6 months after treatment to determine successful eradication of H. pylori in non-tumor tissue. Thereafter, follow-up endoscopies were scheduled annually. Chi-square and MacNemar tests with 0.05 significance were used. RESULTS: Thirty-four tumors (60.7% were intestinal-type and 22 (39.3% diffuse type carcinomas. In adjacent non-tumor gastric mucosa, chronic gastritis were found in 53 cases (94.6% and atrophic mucosa in 36 patients (64.3%. All the patients with atrophic mucosa were H. pylori positive. When examined by Giemsa and urease test, H. pylori positive rate in tumor tissue of intestinal type carcinomas was

Will Treatment of Helicobacter Pylori Infection in Childhood Alter the Risk of Developing Gastric Cancer?

Directory of Open Access Journals (Sweden)

Billy Bourke

2005-01-01

Full Text Available Helicobacter pylori has been classified as a group 1 carcinogen for gastric cancer. It is estimated that there is between a two- and sixfold increase in the risk of developing gastric cancer among infected patients. Among different populations, the risk of H pylori-infected individuals developing gastric cancer varies greatly. However, on a worldwide scale, gastric cancer is the second most common cause of cancer-related death. Therefore, H pylori eradication could help prevent up to three to four million gastric cancer deaths per year. H pylori is usually acquired in childhood. Because infected children have not harboured the organism for long enough to have developed precancerous lesions, childhood is theoretically an attractive time for H pylori eradication and, thus, could help prevent gastric cancer later in life. However, as H pylori prevalence and the incidence of gastric cancer are falling rapidly in developed nations, widespread population screening programs aimed at the eradication of H pylori in these countries would be enormously expensive. Therefore, except in groups with a high risk for development of gastric cancer (eg, Japanese or those with a strong positive family history of gastric cancer, a population-based test-and-treat policy is not justified.

DETECTION OF Helicobacter pylori IN GASTRIC MUCOSA OF SHEEP: PRELIMINARY RESULTS

Directory of Open Access Journals (Sweden)

A. Rella

2013-02-01

Full Text Available Helicobacter pylori is an organism widespread in humans and sometimes responsible for serious illnesses. It has been hypothesized the existence of animal reservoirs, and that the infection route by H. pylori involves multiple pathways including food-borne transmission as the microorganism has been detected from sheep, goat and cow milk. This work reports the preliminary results of a survey conducted in order to investigate the presence of H. pylori in gastric mucosa of sheep slaughtered in Apulia region (Italy employing a Nested Polymerase Chain Reaction (Nested-PCR assay for the detection of the phosphoglucosamine mutase gene (glmM, as screening method followed by conventional bacteriological isolation. Out of the 50 gastric mucosa samples examined, 3 (6% resulted positive for the presence of glmMgene, but at this time no strains were isolated. The results deserve further investigations to asses the role of ruminants as possible reservoirs of H. pylori.

Helicobacter and Gastric Malignancies

OpenAIRE

Ferreira, António Carlos; Isomoto, Hajime; Moriyama, Masatsugu; Fujioka, Toshio; Machado, José Carlos; Yamaoka, Yoshio

2008-01-01

Individuals infected with Helicobacter pylori, a stomach colonizing bacteria, have an increased risk of developing gastric malignancies. The risk for developing cancer relates to the physiologic and histologic changes that H. pylori infection induces in the stomach. In the last year numerous studies have been conducted in order to characterize the association between H. pylori infection and gastric cancer. These studies range from epidemiologic approaches aiming at the identification of envir...

The influence of duodeno-gastric reflux on frequency of Helicobacter pylori infection at patients with ulcer gastric; Wplyw refluksu dwunastniczo-zoladkowego na czestosc wystepowania zakazenia Helicobacter pylori u chorych z wrzodem zoladka

Energy Technology Data Exchange (ETDEWEB)

Kopanski, Z.; Niziol, J.; Micherdzinski, J.; Wasilewska-Radwanska, M.; Cienciala, A.; Lasa, J. [Kliniczny Oddzial Chirurgii Ogolnej, Pracownia Medycyny Nuklearnej, Szpital Wojskowy, Cracow (Poland)]|[Wydzial Fizyki i Techniki Jadrowej AGH, Cracow (Poland)]|[Pracownia Chromatografii Gazowej, Instytut Fizyki Jadrowej, Cracow (Poland)

1996-12-31

To estimate the correlation between frequency of Helicobacter pylori (H. pylori) infection and intensity of duodeno-gastric reflux it was analysed 61 species with ulcer gastric. Bacterial infection was diagnosed by the breath test with {sup 14}C-labelled urea, whereas presence and intensity of the reflux was found with dynamic scintigraphy with {sup 99}Tm MBrIDA support. The H. pylori infection was present at 42 (68.9%) patients. The presence of throwing back the duodenal liquid was found at 32 (52.5%) diagnosed patients. At 19 (31.2%) of them the reflux has intensity of 1%, at 11 (18%)-2{sup o} and 2 (3.3%)-3{sup o}.The investigations which were carried out, showed that at patients with ulcer gastric disease, duodeno-gastric reflux is an agent which slows down H. pylori infection, however it is easily seen not earlier than at 2{sup o} of its intensity. (author) 33 refs, 1 tab

Helicobacter pylori dupA and gastric acid secretion are negatively associated with gastric cancer development.

Science.gov (United States)

Imagawa, Shinobu; Ito, Masanori; Yoshihara, Masaharu; Eguchi, Hidetaka; Tanaka, Shinji; Chayama, Kazuaki

2010-12-01

Few reports have described the cancer prevalence of peptic ulcer patients with long-term follow-up studies. We have conducted a long-term retrospective cohort study of Japanese peptic ulcer patients and evaluated the risk factors for the occurrence of gastric cancer (GCa). A total of 136 patients diagnosed with peptic ulcers from 1975 to 1983 were enrolled. These 136 cases [102 males and 34 females; 69 gastric ulcer (GU) and 67 duodenal ulcer (DU) patients at the time of enrollment; mean follow-up period of 14.4 years (range 1-30 years)] after being matched with a tumour registry database in Hiroshima prefecture were surveyed for GCa. We investigated Helicobacter pylori duodenal ulcer promoter gene A (dupA) using paraffin-embedded gastric biopsy specimens in 56 cases. Gastric acid secretion and basal acid output (BAO) in 40 cases, and maximal acid output in 68 cases, had been measured at first diagnosis of peptic ulcers. GCa was detected in 24 patients (17 with GU, 7 with DU) during the follow-up. The prevalence of GCa was significantly higher in GU patients than in DU patients (log-rank test PdupA-positive H. pylori was detected not only in DU patients (9/20) but also in GU patients (9/36). Gastric acid output was significantly larger in quantity in patients with dupA-positive H. pylori than in those with dupA-negative H. pylori (PdupA-positive H. pylori and a high BAO level (log-rank test PdupA-positive H. pylori were negatively associated with GCa.

Role of Helicobacter pylori infection in gastric carcinogenesis: Current knowledge and future directions

Science.gov (United States)

Sokic-Milutinovic, Aleksandra; Alempijevic, Tamara; Milosavljevic, Tomica

2015-01-01

Helicobacter pylori (H. pylori) plays a role in the pathogenesis of gastric cancer. The outcome of the infection depends on environmental factors and bacterial and host characteristics. Gastric carcinogenesis is a multistep process that is reversible in the early phase of mucosal damage, but the exact point of no return has not been identified. Therefore, two main therapeutic strategies could reduce gastric cancer incidence: (1) eradication of the already present infection; and (2) immunization (prior to or during the course of the infection). The success of a gastric cancer prevention strategy depends on timing because the prevention strategy must be introduced before the point of no return in gastric carcinogenesis. Although the exact point of no return has not been identified, infection should be eradicated before severe atrophy of the gastric mucosa develops. Eradication therapy rates remain suboptimal due to increasing H. pylori resistance to antibiotics and patient noncompliance. Vaccination against H. pylori would reduce the cost of eradication therapies and lower gastric cancer incidence. A vaccine against H. pylori is still a research challenge. An effective vaccine should have an adequate route of delivery, appropriate bacterial antigens and effective and safe adjuvants. Future research should focus on the development of rescue eradication therapy protocols until an efficacious vaccine against the bacterium becomes available. PMID:26556993

Evaluation of gastric histology in children and adolescents with Helicobacter pylori gastritis using the Update Sydney System.

Science.gov (United States)

Langner, Marini; Machado, Rodrigo Strehl; Patrício, Francy R S; Kawakami, Elisabete

2009-01-01

Although Helicobacter pylori infection is prevalent in our country, there are few studies evaluating the associated histological abnormalities in children. To evaluate the histological features of the gastric mucosa in children and adolescents with Helicobacter pylori gastritis. One hundred and thirty two gastric biopsies from 22 symptomatic patients infected with H. pylori (14F/8M, median age 10 y 5 mo, age range 2 y 11 mo to 16 y 9 mo) were evaluated. Evaluated gastric regions included: antrum (lesser and greater curvature), corpus (lesser and greater curvature), incisura angularis and fundus. Histological examination was performed according to the Updated Sydney System, and regional scores for polymorphonuclear and mononuclear cell infiltrate as well as bacterial density were generated. Fifteen (68.2%) patients presented H. pylori-chronic active gastritis, six (27.3%) presented antrum-predominant H. pylori-chronic active gastritis, and one (4.5%) presented corpus-predominant H. pylori-chronic active gastritis. Polymorphonuclear cell infiltrate and mononuclear cell infiltrate were observed in 93.9% and 98.5% of the biopsy specimens, respectively. Higher histological scores for polymorphonuclear infiltrate, mononuclear infiltrate, and bacterial density were observed in the gastric antrum. Intestinal metaplasia and gastric atrophy were not identified in any patient. Lymphoid aggregates and lymphoid follicles were observed in the gastric antrum of three (13.6%) and seven (31.8%) patients, respectively, but they were not related to antral nodularity. Chronic active gastritis was observed in all patients with H. pylori infection. However, antral or corporeal predominance was not observed in most patients.

Association of mast cells with helicobacter pylori infection in the antral mucosa

Directory of Open Access Journals (Sweden)

SR KC

2011-03-01

Full Text Available Background: Helicobacter pylori infection is associated with mixed inflammatory cell infiltrate consisting of neutrophils, eosinophils, lymphocytes and plasma cells. Helicobacter pylori lead to mast cell degranulation and release of active chemical compounds in in-vitro conditions. The objective of this study was to find out the association of mast cell density and Helicobacter pylori in the antral mucosa of the stomach. Materials and Methods: A total of 150 endoscopic biopsies were included in the study. In addition to routine Hematoxylin and Eosin stained slides, Giemsa stain was done in each case for the evaluation of Helicobacter pylori and mast cell density in the gastric mucosa. Results: Out of 150 gastric biopsies with histopathological diagnosis of chronic gastritis, 36 cases (24% were positive for Helicobacter pylori. In the antral mucosa, mast cell density was significantly higher in the Helicobacter pylori-positive group than in the Helicobacter pylori-negative group (P<0.01. Conclusion: Mast cells may play a role in the development of Helicobacter pylori gastritis. Keywords: Gastritis; Mast Cell; Helicobacter pylori DOI: 10.3126/jpn.v1i1.4448 Journal of Pathology of Nepal (2011 Vol.1, 34-36

Presence of Helicobacter pylori in supragingival dental plaque of individuals with periodontal disease and upper gastric diseases

NARCIS (Netherlands)

Silva, D.G.; Stevens, R.H.; Macedo, J.M.B.; Albano, R.M.; Falabella, M.E.V.; Fisher, R.G.; Veerman, E.C.; Tinoco, E.M.B.

2010-01-01

Background Helicobacter pylori is a Gram-negative microorganism which is able to colonize the gastric mucosa and is associated with peptic ulcer, gastric carcinoma, and gastric mucosa-associated lymphoid tissue lymphoma. Several studies have detected this bacterium in the oral cavity, suggesting it

Effect of helicobacter pylori L-form infection on proliferation, apoptosis and invasion molecule expression in gastric cancer tissue

Directory of Open Access Journals (Sweden)

Hua Xin

2017-05-01

Full Text Available Objective: To study the effect of Helicobacter pylori L-form infection on proliferation, apoptosis and invasion molecule expression in gastric cancer tissue. Methods: The gastric cancer tissues surgically removed in our hospital between May 2013 and October 2016 were collected and divided into Hp negative, Hp-L negative and Hp-L positive according to the condition of helicobacter pylori infection. The proliferation, apoptosis and invasion gene expression were detected. Results: LOXL2, PCNA, CyclinD1, Rab1A, Bcl-2, Snail, N-cadherin, UHRF1 and AnnexinII mRNA expression in Hp-L-positive gastric cancer tissues were significantly higher than those in Hp-L-negative and Hp-negative gastric cancer tissues while ING5, PTPN13, Beclin1 and Mst1 mRNA expression were significantly lower than those in Hp-L-negative and Hp-negative gastric cancer tissues; LOXL2, PCNA, CyclinD1, Rab1A, Bcl-2, ING5, PTPN13, Beclin1, Mst1, Snail, N-cadherin, UHRF1 and AnnexinII mRNA expression in Hp-L-negative gastric cancer tissues were not different from those in Hpnegative gastric cancer tissues. Conclusion: Helicobacter pylori L-form infection can influence the proliferation, apoptosis and invasion gene expression to promote cell proliferation and invasion, and inhibit cell apoptosis.

Comparative analysis of gastric bacterial microbiota in Mongolian gerbils after long-term infection with Helicobacter pylori.

Science.gov (United States)

Osaki, Takako; Matsuki, Takahiro; Asahara, Takashi; Zaman, Cynthia; Hanawa, Tomoko; Yonezawa, Hideo; Kurata, Satoshi; Woo, Timothy Derg-hoong; Nomoto, Koji; Kamiya, Shigeru

2012-07-01

Quantitative (qt) real time PCR using 16SrDNA primers is useful for determination of the bacterial composition of the gastric microbiota in Mongolian gerbils. The aim of this study was to determine the change in the gastric microbiota after long-term infection with Helicobacter pylori. One year after inoculation with H. pylori, five gerbils were determined as H. pylori-positive and 6 gerbils H. pylori-negative by culture and real time qt PCR methods. The gastric microbiota of each group of gerbils was also compared with that of 6 gerbils uninfected with H. pylori. DNA from the Atopobium cluster, Bifidobacterium spp., Clostridium coccoides group, Clostridium leptum subgroup, Enterococcus spp. and Lactobacillus spp. were detected in the gastric mucus of both infected and uninfected gerbils. In contrast, Eubacterium cylindroides group and Prevotella spp. were detected only in H. pylori-negative gerbils. The numbers of C. leptum subgroup, C. coccoides group and Bifidobacterium spp. in gastric mucus of H. pylori-negative Mongolian gerbils were significantly lower than those in non-infected gerbils. The results obtained suggest that the composition of gastric indigenous microbiota in Mongolian gerbils may be disturbed by long-term infection with H. pylori, and that these changes may in fact inhibit H. pylori infection.

Epidemiology of Helicobacter pylori and CagA-Positive Infections and Global Variations in Gastric Cancer

Science.gov (United States)

Forman, David; Crabtree, Jean E.

2018-01-01

Gastric cancer is a major health burden and is the fifth most common malignancy and the third most common cause of death from cancer worldwide. Development of gastric cancer involves several aspects, including host genetics, environmental factors, and Helicobacter pylori infection. There is increasing evidence from epidemiological studies of the association of H. pylori infection and specific virulence factors with gastric cancer. Studies in animal models indicate H. pylori is a primary factor in the development of gastric cancer. One major virulence factor in H. pylori is the cytotoxin-associated gene A (cagA), which encodes the CagA protein in the cag pathogenicity island (cag PAI). Meta-analysis of studies investigating CagA seropositivity irrespective of H. pylori status identified that CagA seropositivity increases the risk of gastric cancer (OR = 2.87, 95% CI: 1.95–4.22) relative to the risk of H. pylori infection alone (OR = 2.31, 95% CI: 1.58–3.39). Eradicating H. pylori is a strategy for reducing gastric cancer incidence. A meta-analysis of six randomised controlled trials (RCTs) suggests that searching for and eradicating H. pylori infection reduces the subsequent incidence of gastric cancer with a pooled relative risk of 0.66 (95% CI: 0.46–0.95). The introduction in regions of high gastric cancer incidence of population-based H. pylori screening and treatment programmes, with a scientifically valid assessment of programme processes, feasibility, effectiveness and possible adverse consequences, would impact the incidence of H. pylori-induced gastric cancer. Given the recent molecular understanding of the oncogenic role of CagA, targeting H. pylori screening and treatment programmes in populations with a high prevalence of H. pylori CagA-positive strains, particularly the more oncogenic East Asian H. pylori CagA strains, may be worth further investigation to optimise the benefits of such strategies. PMID:29671784

Epidemiology of Helicobacter pylori and CagA-Positive Infections and Global Variations in Gastric Cancer

Directory of Open Access Journals (Sweden)

Jin Young Park

2018-04-01

Full Text Available Gastric cancer is a major health burden and is the fifth most common malignancy and the third most common cause of death from cancer worldwide. Development of gastric cancer involves several aspects, including host genetics, environmental factors, and Helicobacter pylori infection. There is increasing evidence from epidemiological studies of the association of H. pylori infection and specific virulence factors with gastric cancer. Studies in animal models indicate H. pylori is a primary factor in the development of gastric cancer. One major virulence factor in H. pylori is the cytotoxin-associated gene A (cagA, which encodes the CagA protein in the cag pathogenicity island (cag PAI. Meta-analysis of studies investigating CagA seropositivity irrespective of H. pylori status identified that CagA seropositivity increases the risk of gastric cancer (OR = 2.87, 95% CI: 1.95–4.22 relative to the risk of H. pylori infection alone (OR = 2.31, 95% CI: 1.58–3.39. Eradicating H. pylori is a strategy for reducing gastric cancer incidence. A meta-analysis of six randomised controlled trials (RCTs suggests that searching for and eradicating H. pylori infection reduces the subsequent incidence of gastric cancer with a pooled relative risk of 0.66 (95% CI: 0.46–0.95. The introduction in regions of high gastric cancer incidence of population-based H. pylori screening and treatment programmes, with a scientifically valid assessment of programme processes, feasibility, effectiveness and possible adverse consequences, would impact the incidence of H. pylori-induced gastric cancer. Given the recent molecular understanding of the oncogenic role of CagA, targeting H. pylori screening and treatment programmes in populations with a high prevalence of H. pylori CagA-positive strains, particularly the more oncogenic East Asian H. pylori CagA strains, may be worth further investigation to optimise the benefits of such strategies.

Dietary Composition Influences Incidence of Helicobacter pylori-Induced Iron Deficiency Anemia and Gastric Ulceration

Science.gov (United States)

Beckett, Amber C.; Piazuelo, M. Blanca; Noto, Jennifer M.; Peek, Richard M.; Washington, M. Kay; Algood, Holly M. Scott

2016-01-01

Epidemiologic studies have provided conflicting data regarding an association between Helicobacter pylori infection and iron deficiency anemia (IDA) in humans. Here, a Mongolian gerbil model was used to investigate a potential role of H. pylori infection, as well as a possible role of diet, in H. pylori-associated IDA. Mongolian gerbils (either H. pylori infected or uninfected) received a normal diet or one of three diets associated with increased H. pylori virulence: high-salt, low-iron, or a combination of a high-salt and low-iron diet. In an analysis of all infected animals compared to uninfected animals (independent of diet), H. pylori-infected gerbils had significantly lower hemoglobin values than their uninfected counterparts at 16 weeks postinfection (P Anemia was associated with the presence of gastric ulceration but not gastric cancer. Infected gerbils consuming diets with a high salt content developed gastric ulcers significantly more frequently than gerbils consuming a normal-salt diet, and the lowest hemoglobin levels were in infected gerbils consuming a high-salt/low-iron diet. These data indicate that H. pylori infection can cause IDA and that the composition of the diet influences the incidence and severity of H. pylori-induced IDA. PMID:27620719

Helicobacter pylori infection affects mitochondrial function and DNA repair, thus, mediating genetic instability in gastric cells

DEFF Research Database (Denmark)

Machado, Ana Manuel Dantas; Desler, Claus; Boggild, Sisse

2013-01-01

Helicobacter pylori infection is an important factor for the development of atrophic gastritis and gastric carcinogenesis. However, the mechanisms explaining the effects of H. pylori infection are not fully elucidated. H. pylori infection is known to induce genetic instability in both nuclear and....... pylori infection, furthermore, the results demonstrate that multiple DNA repair activities are involved in protecting mtDNA during infection. (C) 2013 Elsevier Ireland Ltd. All rights reserved....

Roadmap to eliminate gastric cancer with Helicobacter pylori eradication and consecutive surveillance in Japan.

Science.gov (United States)

Asaka, Masahiro; Kato, Mototsugu; Sakamoto, Naoya

2014-01-01

In Japan, the annual number of deaths from gastric cancer is approximately 50,000 and there has been no change over the last 50 years. So far, all efforts have been directed toward improving the detection of early gastric cancer by barium X-ray and endoscopy, since early cancer has a good prognosis, resulting in Japan having the best diagnostic capability for early gastric cancer worldwide. The 5-year survival rate of gastric cancer patients exceeds 60 % in Japan and is much higher than that in Europe and the US (20 %) because of this superior diagnosis of early gastric cancer. In February 2013, national health insurance coverage for Helicobacter pylori eradication therapy to treat H. pylori-associated chronic gastritis became available in Japan. H. pylori-associated gastritis leads to development of gastric and duodenal ulcers and gastric polyps. Therefore, providing treatment for gastritis is likely to substantially decrease the prevalence of both gastric and duodenal ulcers and polyps. Because treatment for H. pylori-associated gastritis, which leads to atrophic gastritis and gastric cancer, is now covered by health insurance in Japan, a strategy to eliminate gastric cancer-related deaths by taking advantage of this innovation was planned. According to this strategy, patients with gastritis will be investigated for H. pylori infection and those who are positive will receive eradication therapy followed by periodic surveillance. If this strategy is implemented, deaths from gastric cancer in Japan will decrease dramatically after 10-20 years.

Characterization in Helicobacter pylori of a Nickel Transporter Essential for Colonization That Was Acquired during Evolution by Gastric Helicobacter Species

Science.gov (United States)

Turlin, Evelyne; Mancuso, Francesco; Michel, Valérie; Richaud, Pierre; Veyrier, Frédéric J.; De Reuse, Hilde; Vinella, Daniel

2016-01-01

Metal acquisition is crucial for all cells and for the virulence of many bacterial pathogens. In particular, nickel is a virulence determinant for the human gastric pathogen Helicobacter pylori as it is the cofactor of two enzymes essential for in vivo colonization, urease and a [NiFe] hydrogenase. To import nickel despite its scarcity in the human body, H. pylori requires efficient uptake mechanisms that are only partially defined. Indeed, alternative ways of nickel entry were predicted to exist in addition to the well-described NixA permease. Using a genetic screen, we identified an ABC transporter, that we designated NiuBDE, as a novel H. pylori nickel transport system. Unmarked mutants carrying deletions of nixA, niuD and/or niuB, were constructed and used to measure (i) tolerance to toxic nickel exposure, (ii) intracellular nickel content by ICP-OES, (iii) transport of radioactive nickel and (iv) expression of a reporter gene controlled by nickel concentration. We demonstrated that NiuBDE and NixA function separately and are the sole nickel transporters in H. pylori. NiuBDE, but not NixA, also transports cobalt and bismuth, a metal currently used in H. pylori eradication therapy. Both NiuBDE and NixA participate in nickel-dependent urease activation at pH 5 and survival under acidic conditions mimicking those encountered in the stomach. However, only NiuBDE is able to carry out this activity at neutral pH and is essential for colonization of the mouse stomach. Phylogenomic analyses indicated that both nixA and niuBDE genes have been acquired via horizontal gene transfer by the last common ancestor of the gastric Helicobacter species. Our work highlights the importance of this evolutionary event for the emergence of Helicobacter gastric species that are adapted to the hostile environment of the stomach where the capacity of Helicobacter to import nickel and thereby activate urease needs to be optimized. PMID:27923069

Helicobacter pylori Therapy for the Prevention of Metachronous Gastric Cancer.

Science.gov (United States)

Choi, Il Ju; Kook, Myeong-Cherl; Kim, Young-Il; Cho, Soo-Jeong; Lee, Jong Yeul; Kim, Chan Gyoo; Park, Boram; Nam, Byung-Ho

2018-03-22

Patients with early gastric cancers that are limited to gastric mucosa or submucosa usually have an advanced loss of mucosal glandular tissue (glandular atrophy) and are at high risk for subsequent (metachronous) development of new gastric cancer. The long-term effects of treatment to eradicate Helicobacter pylori on histologic improvement and the prevention of metachronous gastric cancer remain unclear. In this prospective, double-blind, placebo-controlled, randomized trial, we assigned 470 patients who had undergone endoscopic resection of early gastric cancer or high-grade adenoma to receive either H. pylori eradication therapy with antibiotics or placebo. Two primary outcomes were the incidence of metachronous gastric cancer detected on endoscopy performed at the 1-year follow-up or later and improvement from baseline in the grade of glandular atrophy in the gastric corpus lesser curvature at the 3-year follow-up. A total of 396 patients were included in the modified intention-to-treat analysis population (194 in the treatment group and 202 in placebo group). During a median follow-up of 5.9 years, metachronous gastric cancer developed in 14 patients (7.2%) in the treatment group and in 27 patients (13.4%) in the placebo group (hazard ratio in the treatment group, 0.50; 95% confidence interval, 0.26 to 0.94; P=0.03). Among the 327 patients in the subgroup that underwent histologic analysis, improvement from baseline in the atrophy grade at the gastric corpus lesser curvature was observed in 48.4% of the patients in the treatment group and in 15.0% of those in the placebo group (Pgastric cancer who received H. pylori treatment had lower rates of metachronous gastric cancer and more improvement from baseline in the grade of gastric corpus atrophy than patients who received placebo. (Funded by the National Cancer Center, South Korea; ClinicalTrials.gov number, NCT02407119 .).

Intracellular delivery of oligonucleotides in Helicobacter pylori by fusogenic liposomes in the presence of gastric mucus.

Science.gov (United States)

Santos, Rita S; Dakwar, George R; Zagato, Elisa; Brans, Toon; Figueiredo, Céu; Raemdonck, Koen; Azevedo, Nuno F; De Smedt, Stefaan C; Braeckmans, Kevin

2017-09-01

The rising antimicrobial resistance contributes to 25000 annual deaths in Europe. This threat to the public health can only be tackled if novel antimicrobials are developed, combined with a more precise use of the currently available antibiotics through the implementation of fast, specific, diagnostic methods. Nucleic acid mimics (NAMs) that are able to hybridize intracellular bacterial RNA have the potential to become such a new class of antimicrobials and additionally could serve as specific detection probes. However, an essential requirement is that these NAMs should be delivered into the bacterial cytoplasm, which is a particular challenge given the fact that they are charged macromolecules. We consider these delivery challenges in relation to the gastric pathogen Helicobacter pylori, the most frequent chronic infection worldwide. In particular, we evaluate if cationic fusogenic liposomes are suitable carriers to deliver NAMs across the gastric mucus barrier and the bacterial envelope. Our study shows that DOTAP-DOPE liposomes post-PEGylated with DSPE-PEG (DSPE Lpx) can indeed successfully deliver NAMs into Helicobacter pylori, while offering protection to the NAMs from binding and inactivation in gastric mucus isolated from pigs. DSPE Lpx thus offer exciting new possibilities for in vivo diagnosis and treatment of Helicobacter pylori infections. Copyright © 2017 Elsevier Ltd. All rights reserved.

A Novel Assay for Easy and Rapid Quantification of Helicobacter pylori Adhesion

DEFF Research Database (Denmark)

Skindersoe, Mette E; Rasmussen, Lone; Andersen, Leif P

2015-01-01

BACKGROUND: Reducing adhesion of Helicobacter pylori to gastric epithelial cells could be a new way to counteract infections with this organism. We here present a novel method for quantification of Helicobacter pylori adhesion to cells. METHODS: Helicobacter pylori is allowed to adhere to AGS...

Oxidative Stress Resulting From Helicobacter pylori Infection Contributes to Gastric CarcinogenesisSummary

Directory of Open Access Journals (Sweden)

Lindsay D. Butcher

2017-05-01

Full Text Available Helicobacter pylori is a gram-negative, microaerophilic bacterium that infects the stomach and can lead to, among other disorders, the development of gastric cancer. The inability of the host to clear the infection results in a chronic inflammatory state with continued oxidative stress within the tissue. Reactive oxygen species and reactive nitrogen species produced by the immune and epithelial cells damage the host cells and can result in DNA damage. H pylori has evolved to evoke this damaging response while blunting the host’s efforts to kill the bacteria. This long-lasting state with inflammation and oxidative stress can result in gastric carcinogenesis. Continued efforts to better understand the bacterium and the host response will serve to prevent or provide improved early diagnosis and treatment of gastric cancer. Keywords: AP Endonuclease, DNA Damage, H pylori, Gastric Cancer, Oxidative Stress

Gastric ulcer treatment: cure of Helicobacter pylori infection without subsequent acid-suppressive therapy: is it effective?

Science.gov (United States)

van Zanten, Sander Veldhuyzen; van der Knoop, Bloeme

2008-06-01

Whether it is a requirement to continue with anti-secretory therapy following anti-Helicobacter therapy in H. pylori positive gastric ulcers is an important question. As gastric ulcers tend to heal more slowly than duodenal ulcers, may be asymptomatic or only causing mild symptoms and success at curing H. pylori with current fist line therapies is 80% at best, clinicians will likely err on the side of caution and continue acid suppressive therapy to ensure healing of gastric ulcers. This is certainly recommended when dealing with bleeding ulcers.

Treatment of low-grade gastric malt lymphoma using Helicobacter pylori eradication

Directory of Open Access Journals (Sweden)

Grgov Saša

2015-01-01

Full Text Available Background/Aim. Lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma of the stomach usually occurs as a consequence of Helicobacter pylori (H. pylori infection. The aim of this study was to investigate the long-term effect of treatment of low-grade gastric MALT lymphoma with the H. pylori eradication method. Methods. In the period 2002-2012 in 20 patients with dyspepsia, mean age 55.1 years, the endoscopic and histologic diagnosis of gastric MALT lymphoma in the early stages were made. Histological preparations of endoscopic biopsy specimens were stained with hematoxyllineosin (HE, histochemical and immunohistochemical methods. Results. Endoscopic findings of gastritis were documented in 25% of the patients, and 75% of the patients had hypertrophic folds, severe mucosal hyperemia, fragility, nodularity, exulcerations and rigidity. Histopathologically, pathognomonic diagnostic criterion were infiltration and destruction of glandular epithelium with neoplastic lymphoid cells, the so-called lymphoepithelial lesions. In all 20 patients H. pylori was verified by rapid urease test and Giemsa stain. After the triple eradication therapy complete remission of MALT lymphoma was achieved in 85% of the patients, with no recurrence of lymphoma and H. pylori infection in the average follow-up period of 48 months. In 3 (15% of the patients, there was no remission of MALT lymphoma 12 months after the eradication therapy. Of these 3 patients 2 had progression of MALT lymphoma to diffuse large-cell lymphoma. Conclusion. Durable complete re-mission of low-grade gastric MALT lymphoma is achieved in a high percentage after eradication of H. pylori infection, thus preventing the formation of diffuse large-cell lymphoma and gastric adenocarcinoma.

The number of Foxp3-positive regulatory T cells is increased in Helicobacter pylori gastritis and gastric cancer.

Science.gov (United States)

Jang, Tae Jung

2010-01-15

Helicobacter pylori (H. pylori) colonization induces vigorous innate and specific immune responses; however, the infection is not removed, a state of chronic active gastritis persists for life if untreated. Recent studies have shown that CD4(+) CD25(+) Foxp3-positive regulatory T cells (Tregs) suppress the immune response to H. pylori. Persistent H. pylori-associated gastritis is closely associated with gastric carcinogenesis. We investigated the number of Tregs in the context of H. pylori colonization in chronic gastritis, examined the relationship between it and histopathological findings and compared it with that of gastric dysplasia and adenocarcinoma. This study was based on the analysis of gastric biopsy specimens from 126 cases of H. pylori-associated gastritis, 16 cases of H. pylori-negative gastritis, 17 cases of gastric dysplasia, and 25 cases of gastric adenocarcinoma. The number of Tregs was elevated in H. pylori-associated gastritis, where it was positively correlated with the grade of chronic inflammation and the number of lymphoid follicles. It was significantly elevated in adenocarcinomas compared to chronic gastritis and gastric dysplasia. In summary, the number of Tregs is increased in H. pylori-associated gastritis and gastric cancer. Copyright 2009 Elsevier GmbH. All rights reserved.

"Targeted disruption of the epithelial-barrier by Helicobacter pylori"

Directory of Open Access Journals (Sweden)

Wroblewski Lydia E

2011-11-01

Full Text Available Abstract Helicobacter pylori colonizes the human gastric epithelium and induces chronic gastritis, which can lead to gastric cancer. Through cell-cell contacts the gastric epithelium forms a barrier to protect underlying tissue from pathogenic bacteria; however, H. pylori have evolved numerous strategies to perturb the integrity of the gastric barrier. In this review, we summarize recent research into the mechanisms through which H. pylori disrupts intercellular junctions and disrupts the gastric epithelial barrier.

Detection of Helicobacter pylori in the Gastric Mucosa by Fluorescence In Vivo Hybridization

DEFF Research Database (Denmark)

Fontenete, Silvia; Leite, Marina; Figueiredo, Céu

2017-01-01

In this chapter, we describe a fluorescence in vivo hybridization (FIVH) protocol, using nucleic acid probes, for the detection of the bacterium Helicobacter pylori in the gastric mucosa of an infected C57BL/6 mouse model. This protocol should be easily extended to other microorganisms not only...

Curcumin Inhibits Gastric Inflammation Induced by Helicobacter Pylori Infection in a Mouse Model

Directory of Open Access Journals (Sweden)

António M. Santos

2015-01-01

Full Text Available Helicobacter pylori (H. pylori infection triggers a sequence of gastric alterations starting with an inflammation of the gastric mucosa that, in some cases, evolves to gastric cancer. Efficient vaccination has not been achieved, thus it is essential to find alternative therapies, particularly in the nutritional field. The current study evaluated whether curcumin could attenuate inflammation of the gastric mucosa due to H. pylori infection. Twenty-eight C57BL/6 mice, were inoculated with the H. pylori SS1 strain; ten non-infected mice were used as controls. H. pylori infection in live mice was followed-up using a modified 13C-Urea Breath Test (13C-UBT and quantitative real-time polymerase chain reaction (PCR. Histologically confirmed, gastritis was observed in 42% of infected non-treated mice at both 6 and 18 weeks post-infection. These mice showed an up-regulation of the expression of inflammatory cytokines and chemokines, as well as of toll-like receptors (TLRs and MyD88, at both time points. Treatment with curcumin decreased the expression of all these mediators. No inflammation was observed by histology in this group. Curcumin treatment exerted a significant anti-inflammatory effect in H. pylori-infected mucosa, pointing to the promising role of a nutritional approach in the prevention of H. pylori induced deleterious inflammation while the eradication or prevention of colonization by effective vaccine is not available.

Helicobacter pylori and oral pathology: relationship with the gastric infection.

Science.gov (United States)

Adler, Isabel; Muiño, Andrea; Aguas, Silvia; Harada, Laura; Diaz, Mariana; Lence, Adriana; Labbrozzi, Mario; Muiño, Juan Manuel; Elsner, Boris; Avagnina, Alejandra; Denninghoff, Valeria

2014-08-07

Helicobacter pylori (H. pylori) has been found in the oral cavity and stomach, and its infection is one of the most frequent worldwide. We reviewed the literature and conducted a Topic Highlight, which identified studies reporting an association between H. pylori-infection in the oral cavity and H. pylori-positive stomach bacterium. This work was designed to determine whether H. pylori is the etiologic agent in periodontal disease, recurrent aphthous stomatitis (RAS), squamous cell carcinoma, burning and halitosis. Record selection focused on the highest quality studies and meta-analyses. We selected 48 articles reporting on the association between saliva and plaque and H. pylori-infection. In order to assess periodontal disease data, we included 12 clinical trials and 1 meta-analysis. We evaluated 13 published articles that addressed the potential association with RAS, and 6 with squamous cell carcinoma. Fourteen publications focused on our questions on burning and halitosis. There is a close relation between H. pylori infection in the oral cavity and the stomach. The mouth is the first extra-gastric reservoir. Regarding the role of H. pylori in the etiology of squamous cell carcinoma, no evidence is still available.

Helicobacter pylori infection as a cause of gastritis, duodenal ulcer, gastric cancer and nonulcer dyspepsia: a systematic overview.

Science.gov (United States)

Veldhuyzen van Zanten, S J; Sherman, P M

1994-01-15

To evaluate current evidence for a causal relation between Helicobacter pylori infection and gastritis, duodenal ulcer, gastric cancer and nonulcer dyspepsia. A MEDLINE search for articles published in English between January 1983 and December 1992 with the use of MeSH terms Helicobacter pylori, gastritis, duodenal ulcer, gastric cancer, dyspepsia and clinical trial; abstracts were excluded. Six journals and Current Contents were searched manually for pertinent articles published in that time frame. Original studies with at least 25 patients, case reports and reviews that examined the relation between H. pylori and the four gastrointestinal disorders; 350 articles were on gastritis, 122 on duodenal ulcer, 44 on gastric cancer and 96 on nonulcer dyspepsia. The quality of the studies was rated independently on a four-point scale. The strength of the evidence was assessed using a six-point scale for each of the eight established guidelines for determining a causal relation. There was conclusive evidence of a causal relation between H. pylori infection and histologic gastritis. Koch's postulates for the identification of a microorganism as the causative agent of a disease were fulfilled for H. pylori as a causative agent of gastritis. There was strong evidence that H. pylori is the main cause of duodenal ulcers not induced by nonsteroidal anti-inflammatory drugs, but all of Koch's postulates were not fulfilled. There was moderate epidemiologic evidence of an association between chronic H. pylori infection and gastric cancer. There was a lack of convincing evidence of a causal association between H. pylori and nonulcer dyspepsia. The evidence supports a strong causal relation between H. pylori infection and gastritis and duodenal ulcer and a moderate relation between such infection and gastric cancer. Further studies are needed to clarify the role of H. pylori in these disorders. Thus far, there is no evidence of a causal relation between H. pylori and nonulcer

Impact of Helicobacter pylori on the healing process of the gastric barrier

Science.gov (United States)

Mnich, Eliza; Kowalewicz-Kulbat, Magdalena; Sicińska, Paulina; Hinc, Krzysztof; Obuchowski, Michał; Gajewski, Adrian; Moran, Anthony P; Chmiela, Magdalena

2016-01-01

AIM To determine the impact of selected well defined Helicobacter pylori (H. pylori) antigens on gastric barrier cell turnover. METHODS In this study, using two cellular models of gastric epithelial cells and fibroblasts, we have focused on exploring the effects of well defined H. pylori soluble components such as glycine acid extract antigenic complex (GE), subunit A of urease (UreA), cytotoxin associated gene A protein (CagA) and lipopolysaccharide (LPS) on cell turnover by comparing the wound healing capacity of the cells in terms of their proliferative and metabolic activity as well as cell cycle distribution. Toxic effects of H. pylori components have been assessed in an association with damage to cell nuclei and inhibition of signal transducer and activator of transcription 3 (STAT3) phosphorylation. RESULTS We showed that H. pylori GE, CagA and UreA promoted regeneration of epithelial cells and fibroblasts, which is necessary for effective tissue healing. However, in vivo increased proliferative activity of these cells may constitute an increased risk of gastric neoplasia. In contrast, H. pylori LPS showed a dose-dependent influence on the process of wound healing. At a low concentration (1 ng/mL) H. pylori LPS accelerated of healing epithelial cells, which was linked to significantly enhanced cell proliferation and MTT reduction as well as lack of alterations in cell cycle and downregulation of epidermal growth factor (EGF) production as well as cell nuclei destruction. By comparison, H. pylori LPS at a high concentration (25 ng/mL) inhibited the process of wound repair, which was related to diminished proliferative activity of the cells, cell cycle arrest, destruction of cell nuclei and downregulation of the EGF/STAT3 signalling pathway. CONCLUSION In vivo H. pylori LPS driven effects might lead to the maintenance of chronic inflammatory response and pathological disorders on the level of the gastric mucosal barrier. PMID:27672275

Helicobacter Pylori –Infected Patients | Eltayeb | Sudan Journal of ...

African Journals Online (AJOL)

Background: The role of Helicobacter pylori on gastric carcinogenesis is still unclear but it is considered to predispose carriers to gastric cancer. Objective: The aim of this study is to investigate the relationship between the extent of DNA damage of normal gastric epithelial cells and H. Pylori positive & negative gastritis ...

[Presence of Helicobacter pylori in gastric biopsies and feces of pediatric patients with celiac disease].

Science.gov (United States)

Medina, M G; Medina, M L; Martín, G T; Dikstein, B C; Picón, S O; Gorodner, J O; Merino, L A

2009-01-01

Helicobacter pylori (H. pylori) is the main etiologic agent of chronic gastritis and it is an important cause of gastric damage. The celiac disease can affect the morphology and the function of the gastrointestinal tract from the stomach to the colon and it is frequently associated with chronic gastritis. to assess the presence of H. pylori in gastric biopsies and in feces of pediatric patients with celiac disease and to relate it with the symptoms. Pediatric patients with celiac disease attending the Gastroenterology Service at the "Avelino Castelán" Hospital in Resistencia (Argentina) were included in the study. Gastric biopsies samples were obtained by endoscopy for histological studies, the symptoms and socio-epidemiological characteristics were recorded and the polimerase chain reaction(PCR) was applied in feces in order to detect the presence of H. pylori. Thirty one patients with celiac disease were studied (16 female and 15 male; age range:1-14 years; median 6.7 years); 14 (45.2%) were positive for H. pylori in gastric biopsy and among them, only 2 (14.2%) were positive for H. pylori in stool samples. There were not significant differences between symptoms between H. pylori positive and negative patients. 45.2% of the patients with celiac disease were infected by H. pylori. There was no correlation between the frequencies of bacterial detection in feces and in gastric biopsies. The clinical manifestations of celiac disease did not increase in children infected with H. pylori.

New monoclonal antibody-based test for Helicobacter pylori urease in gastric tissue.

Science.gov (United States)

Kim, Do Hyun; Kim, Ho Dong; Park, Hyeuk; Choi, Seung; Beom, Jae Won; Kim, Woo Jong; Park, Chang Kook; Lee, Young Jik; Park, Ju Young; Kim, Hyung Rag; Park, Chul; Joo, Young Eun; Jung, Young Do

2016-01-01

To evaluate a new monoclonal antibody for Helicobacter pylori urease in gastric tissue. A total of 107 volunteers were enrolled. All subjects underwent a (13)C-urea breath test and esophagogastroduodenoscopy. Gastric aspirates were analyzed for pH and ammonia. Six biopsy specimens in the gastric antrum and body were obtained for a rapid urease test and histology. The new monoclonal antibody-based H. pylori urease test (HPU) was performed to rapidly and qualitatively detect urease in two biopsy specimens. H. pylori infection was diagnosed in 73 subjects. The sensitivity and specificity of the HPU was 89% and 74%, respectively. The subjects were divided into two groups: one with true-positive and true-negative HPU results (n = 90) and the other with false-positive and false-negative HPU results (n = 17). Across all subjects, ammonia levels were 900.5 ± 646.7 and 604.3 ± 594.3 μmol/L (p > 0.05), and pH was 3.37 ± 1.64 and 2.82 ± 1.51 (p > 0.05). Sensitivity was higher in the presence of atrophic gastritis or intestinal metaplasia. HPU detected H. pylori in approximately 10 min. Gastric aspirate ammonia and pH levels did not affect the test results. Sensitivity was good in the presence of atrophic gastritis or intestinal metaplasia.

Motility and chemotaxis mediate the preferential colonization of gastric injury sites by Helicobacter pylori.

Directory of Open Access Journals (Sweden)

Eitaro Aihara

2014-07-01

Full Text Available Helicobacter pylori (H. pylori is a pathogen contributing to peptic inflammation, ulceration, and cancer. A crucial step in the pathogenic sequence is when the bacterium first interacts with gastric tissue, an event that is poorly understood in vivo. We have shown that the luminal space adjacent to gastric epithelial damage is a microenvironment, and we hypothesized that this microenvironment might enhance H. pylori colonization. Inoculation with 106 H. pylori (wild-type Sydney Strain 1, SS1 significantly delayed healing of acetic-acid induced ulcers at Day 1, 7 and 30 post-inoculation, and wild-type SS1 preferentially colonized the ulcerated area compared to uninjured gastric tissue in the same animal at all time points. Gastric resident Lactobacillus spp. did not preferentially colonize ulcerated tissue. To determine whether bacterial motility and chemotaxis are important to ulcer healing and colonization, we analyzed isogenic H. pylori mutants defective in motility (ΔmotB or chemotaxis (ΔcheY. ΔmotB (10(6 failed to colonize ulcerated or healthy stomach tissue. ΔcheY (10(6 colonized both tissues, but without preferential colonization of ulcerated tissue. However, ΔcheY did modestly delay ulcer healing, suggesting that chemotaxis is not required for this process. We used two-photon microscopy to induce microscopic epithelial lesions in vivo, and evaluated accumulation of fluorescently labeled H. pylori at gastric damage sites in the time frame of minutes instead of days. By 5 min after inducing damage, H. pylori SS1 preferentially accumulated at the site of damage and inhibited gastric epithelial restitution. H. pylori ΔcheY modestly accumulated at the gastric surface and inhibited restitution, but did not preferentially accumulate at the injury site. H. pylori ΔmotB neither accumulated at the surface nor inhibited restitution. We conclude that bacterial chemosensing and motility rapidly promote H. pylori colonization of injury sites

Motility and Chemotaxis Mediate the Preferential Colonization of Gastric Injury Sites by Helicobacter pylori

Science.gov (United States)

Aihara, Eitaro; Closson, Chet; Matthis, Andrea L.; Schumacher, Michael A.; Engevik, Amy C.; Zavros, Yana; Ottemann, Karen M.; Montrose, Marshall H.

2014-01-01

Helicobacter pylori (H. pylori) is a pathogen contributing to peptic inflammation, ulceration, and cancer. A crucial step in the pathogenic sequence is when the bacterium first interacts with gastric tissue, an event that is poorly understood in vivo. We have shown that the luminal space adjacent to gastric epithelial damage is a microenvironment, and we hypothesized that this microenvironment might enhance H. pylori colonization. Inoculation with 106 H. pylori (wild-type Sydney Strain 1, SS1) significantly delayed healing of acetic-acid induced ulcers at Day 1, 7 and 30 post-inoculation, and wild-type SS1 preferentially colonized the ulcerated area compared to uninjured gastric tissue in the same animal at all time points. Gastric resident Lactobacillus spp. did not preferentially colonize ulcerated tissue. To determine whether bacterial motility and chemotaxis are important to ulcer healing and colonization, we analyzed isogenic H. pylori mutants defective in motility (ΔmotB) or chemotaxis (ΔcheY). ΔmotB (106) failed to colonize ulcerated or healthy stomach tissue. ΔcheY (106) colonized both tissues, but without preferential colonization of ulcerated tissue. However, ΔcheY did modestly delay ulcer healing, suggesting that chemotaxis is not required for this process. We used two-photon microscopy to induce microscopic epithelial lesions in vivo, and evaluated accumulation of fluorescently labeled H. pylori at gastric damage sites in the time frame of minutes instead of days. By 5 min after inducing damage, H. pylori SS1 preferentially accumulated at the site of damage and inhibited gastric epithelial restitution. H. pylori ΔcheY modestly accumulated at the gastric surface and inhibited restitution, but did not preferentially accumulate at the injury site. H. pylori ΔmotB neither accumulated at the surface nor inhibited restitution. We conclude that bacterial chemosensing and motility rapidly promote H. pylori colonization of injury sites, and thereby biases

Ursodeoxycholic acid does not interfere with in vivo Helicobacter pylori colonization

Directory of Open Access Journals (Sweden)

Silva José Guilherme Nogueira da

2000-01-01

Full Text Available A low frequency of Helicobacter pylori in the gastric mucosa of patients with alkaline gastritis has been reported. At the same time, it can be noted that the growth of bacteria can be inhibited by bile acids. We studied 40 patients with chronic gastritis related to Helicobacter pylori in order to determine the effect of ursodeoxycholic acid on this infection. Diagnoses of the infection and the inflammatory process were obtained by histologic study of gastric biopsies collected during endoscopy. Two groups were studied: group I received ursodeoxycholic acid - 300 mg/day, and group II received the placebo, twice a day, both for 28 days. The colonization by Helicobacter pylori and the intensity of the mononuclear and polymorphonuclear inflammatory infiltrate were determined before (time 1 and after (time 2 treatment. Ursodeoxycholic acid had no effect on the Helicobacter pylori infection. A significant reduction in the intensity of the mononuclear inflammatory infiltrate of the gastric antrum mucosa was observed in patients from group I, when we compared not only times 1 and 2 but also groups I and II. However, this was not the case with the body mucosa. We concluded that ursodeoxycholic acid had no action on the colonization by Helicobacter pylori or on the polymorphonuclear inflammatory infiltrate, but it caused a significant reduction in the intensity of the mononuclear inflammatory infiltrate of the gastric antrum.

HELICOBACTER PYLORI: THE CAUSATIVE AGENT OF PEPTIC ...

African Journals Online (AJOL)

DR. AMINU

Helicobacter pylori by treatment with antibiotics in peptic ulcer patients resulted in the healing of the ulcer. ... and gastric cancers. .... H. pyloris cause chronic active gastritis in humans and ... of the night when the stomach is empty and is.

Systematic review: Helicobacter pylori infection and impaired drug absorption.

Science.gov (United States)

Lahner, E; Annibale, B; Delle Fave, G

2009-02-15

Impaired acid secretion may affect drug absorption and may be consequent to corporal Helicobacter pylori-gastritis, which may affect the absorption of orally administered drugs. To focus on the evidence of impaired drug absorption associated with H. pylori infection. Data sources were the systematic search of MEDLINE/EMBASE/SCOPUS databases (1980-April 2008) for English articles using the keywords: drug malabsorption/absorption, stomach, Helicobacter pylori, gastritis, gastric acid, gastric pH, hypochlorhydria, gastric hypoacidity. Study selection was made from 2099 retrieved articles, five studies were identified. Data were extracted from selected papers, investigated drugs, study type, main features of subjects, study design, intervention type and results were extracted. In all, five studies investigated impaired absorption of l-dopa, thyroxine and delavirdine in H. pylori infection. Eradication treatment led to 21-54% increase in l-dopa in Parkinson's disease. Thyroxine requirement was higher in hypochlorhydric goitre with H. pylori-gastritis and thyrotropin levels decreased by 94% after treatment. In H. pylori- and HIV-positive hypochlorhydric subjects, delavirdine absorption increased by 57% with orange juice administration and by 150% after eradication. A plausible mechanism of impaired drug absorption is decreased acid secretion in H. pylori-gastritis patients. Helicobacter pylori infection and hypochlorhydria should be considered in prescribing drugs the absorption of which is potentially affected by intragastric pH.

Helicobacter pylori eradication and reflux disease onset: did gastric acid get "crazy"?

Science.gov (United States)

Zullo, Angelo; Hassan, Cesare; Repici, Alessandro; Bruzzese, Vincenzo

2013-02-14

Gastroesophageal reflux disease (GORD) is highly prevalent in the general population. In the last decade, a potential relationship between Helicobacter pylori (H. pylori) eradication and GORD onset has been claimed. The main putative mechanism is the gastric acid hypersecretion that develops after bacterial cure in those patients with corpus-predominant gastritis. We performed a critical reappraisal of the intricate pathogenesis and clinical data available in this field. Oesophagitis onset after H. pylori eradication in duodenal ulcer patients has been ascribed to a gastric acid hypersecretion, which could develop following body gastritis healing. However, the absence of an acid hypersecretive status in these patients is documented by both pathophysiology and clinical studies. Indeed, duodenal ulcer recurrence is virtually abolished following H. pylori eradication. In addition, intra-oesophageal pH recording studies failed to demonstrated increased acid reflux following bacterial eradication. Moreover, oesophageal manometric studies suggest that H. pylori eradication would reduce--rather than favor--acid reflux into the oesophagus. Finally, data of clinical studies would suggest that H. pylori eradication is not significantly associated with either reflux symptoms or erosive oesophagitis onset, some data suggesting also an advantage in curing the infection when oesophagitis is already present. Therefore, the legend of "crazy acid" remains--as all the others--a fascinating, but imaginary tale.

Low concentrations of zinc in gastric mucosa are associated with increased severity of Helicobacter pylori-induced inflammation.

Science.gov (United States)

Sempértegui, Fernando; Díaz, Myriam; Mejía, Ricardo; Rodríguez-Mora, Oswaldo G; Rentería, Edgar; Guarderas, Carlos; Estrella, Bertha; Recalde, Ramiro; Hamer, Davidson H; Reeves, Philip G

2007-02-01

Chronic Helicobacter pylori infection is the most common cause of gastric cancer. H. pylori induces oxidative stress while zinc deficiency results in increased sensitivity to it. In Ecuador, the prevalence of gastric cancer and zinc deficiency are high. We hypothesized that zinc deficiency in Ecuadorian people would cause increased H. pylori-induced inflammation in the gastric mucosa associated with lower tissue zinc concentrations. Three hundred and fifty-two patients with dyspepsia underwent endoscopy to obtain gastric mucosa biopsies. Diagnosis of H. pylori infection and its severity, histopathology, mucosal zinc concentration, and inflammation intensity were determined. H. pylori-infected patients with non-atrophic chronic gastritis had lower concentrations of zinc in gastric mucosa than uninfected patients with the same type of gastritis (251.3 +/- 225.3 vs. 426.2 +/- 279.9 ng/mg of protein; p = .016). Considering all patients, the more severe the H. pylori infection, the higher the percentage of subjects with infiltration by polymorphonuclear (PMN) cells (p = .0001). Patients with high PMN infiltration had lower mucosal zinc concentrations than patients with low PMN infiltration (35.2 +/- 20.7 vs. 242.9 +/- 191.8 ng/mg of protein; p = .021). The degree of inflammation in H. pylori-induced gastritis appears to be modulated by gastric tissue zinc concentrations.

Helicobacter pylori Outer Membrane Protein-Related Pathogenesis

Directory of Open Access Journals (Sweden)

Yuichi Matsuo

2017-03-01

Full Text Available Helicobacter pylori colonizes the human stomach and induces inflammation, and in some cases persistent infection can result in gastric cancer. Attachment to the gastric mucosa is the first step in establishing bacterial colonization, and outer membrane proteins (OMPs play a pivotal role in binding to human cells. Some OMP interaction molecules are known in H. pylori, and their associated host cell responses have been gradually clarified. Many studies have demonstrated that OMPs are essential to CagA translocation into gastric cells via the Type IV secretion system of H. pylori. This review summarizes the mechanisms through which H. pylori utilizes OMPs to colonize the human stomach and how OMPs cooperate with the Type IV secretion system.

Helicobacter pylori induces cell migration and invasion through casein kinase 2 in gastric epithelial cells.

Science.gov (United States)

Lee, Yeo Song; Lee, Do Yeon; Yu, Da Yeon; Kim, Shin; Lee, Yong Chan

2014-12-01

Chronic infection with Helicobacter pylori (H. pylori) is causally linked with gastric carcinogenesis. Virulent H. pylori strains deliver bacterial CagA into gastric epithelial cells. Induction of high motility and an elongated phenotype is considered to be CagA-dependent process. Casein kinase 2 plays a critical role in carcinogenesis through signaling pathways related to the epithelial mesenchymal transition. This study was aimed to investigate the effect of H. pylori infection on the casein kinase 2-mediated migration and invasion in gastric epithelial cells. AGS or MKN28 cells as human gastric epithelial cells and H. pylori strains Hp60190 (ATCC 49503, CagA(+)) and Hp8822 (CagA(-)) were used. Cells were infected with H. pylori at multiplicity of infection of 100 : 1 for various times. We measured in vitro kinase assay to examine casein kinase 2 activity and performed immunofluorescent staining to observe E-cadherin complex. We also examined β-catenin transactivation through promoter assay and MMP7 expression by real-time PCR and ELISA. H. pylori upregulates casein kinase 2 activity and inhibition of casein kinase 2 in H. pylori-infected cells profoundly suppressed cell invasiveness and motility. We confirmed that casein kinase 2 mediates membranous α-catenin depletion through dissociation of the α-/β-catenin complex in H. pylori-infected cells. We also found that H. pylori induces β-catenin nuclear translocation and increases MMP7 expressions mediated through casein kinase 2. We show for the first time that CagA(+) H. pylori upregulates cellular invasiveness and motility through casein kinase 2. The demonstration of a mechanistic interplay between H. pylori and casein kinase 2 provides important insights into the role of CagA(+) H. pylori in the gastric cancer invasion and metastasis. © 2014 John Wiley & Sons Ltd.

Regulation of the actin cytoskeleton in Helicobacter pylori-induced migration and invasive growth of gastric epithelial cells

Directory of Open Access Journals (Sweden)

Rieder Gabriele

2011-11-01

Full Text Available Abstract Dynamic rearrangement of the actin cytoskeleton is a significant hallmark of Helicobacter pylori (H. pylori infected gastric epithelial cells leading to cell migration and invasive growth. Considering the cellular mechanisms, the type IV secretion system (T4SS and the effector protein cytotoxin-associated gene A (CagA of H. pylori are well-studied initiators of distinct signal transduction pathways in host cells targeting kinases, adaptor proteins, GTPases, actin binding and other proteins involved in the regulation of the actin lattice. In this review, we summarize recent findings of how H. pylori functionally interacts with the complex signaling network that controls the actin cytoskeleton of motile and invasive gastric epithelial cells.

Growth cycle of Helicobacter pylori in gastric mucous layer.

Science.gov (United States)

Nakazawa, Teruko

2002-12-01

Helicobacter pylori bacterium is characterized by its strong urease activity. Our studies on the role of H. pylori urease revealed; (i) it is essential for colonization, (ii) exogenous urea is required for acid resistance, (iii) the bacteria have the ability to move toward urea and sodium bicarbonate, (iv) urea hydrolysis accelerates chemotactic locomotion, and (v) decay of urease mRNA to accomplish the active center is pH-regulated; i.e., the mRNA is stabilized and destabilized under acidic and neutral conditions, respectively. Based on the above results, I propose the growth cycle of H. pylori in gastric mucous layer. H. pylori bacteria proliferate on the epithelial cell surface by utilizing nutrients derived from degraded cells. Proliferated bacteria leave the cell surface to pH-variable region where they encounter strong acid. Urease is activated with simultaneous opening of UreI channel so that urea is hydrolyzed to neutralize acid. Chemotaxis of H. pylori toward urea and sodium bicarbonate that are abundant on the cell surface is accelerated by urea hydrolysis so that the bacteria go back to the cell surface for the next round of proliferation. This growth cycle may allow the bacteria to infect persistently in the stomach.

HELICOBACTER PYLORI AND t(11;18(q21;q21 TRANSLOCATION IN GASTRIC MALT LYMPHOMA

Directory of Open Access Journals (Sweden)

Karine Sampaio LIMA

2014-04-01

Full Text Available Context Gastric mucosa-associated lymphoid tissue (MALT lymphoma is clearly associated with Helicobacter pylori gastritis and can be cured with anti- H pylori therapy alone. The presence of t(11;18(q21;q21 translocation is thought to predict a lower response rate to anti- H pylori treatment. Objectives To study the presence of t(11;18(q21;q21 genetic translocation and its clinical impact in low-grade gastric MALT lymphoma Brazilian patients. Methods A consecutive series of eight patients with gastric MALT lymphoma were submitted to gastroscopy, endoscopic ultrasound, histopathological examination, H pylori search and RT-PCR-based methodology. All patients received anti-H pylori treatment. Eradicated patients were followed-up every 3-6 months for 2 years. Results Eight patients were studied. All patients had tumor involvement restricted to the mucosa or submucosa and seven patients had low-grade gastric MALT lymphoma. All infected patients achieved H pylori eradication. Histological tumor regression was observed in 5/7 (71% of the low-grade gastric MALT lymphoma patients. The presence of t(11;18(q21;q21 translocation was found in 4 (57% of these patients; among them only two had histological tumor regression following H pylori eradication. Conclusions RT-PCR is a feasible and efficient method to detect t(11;18(q21;q21 translocation, being carried out in routine molecular biology laboratories. The early detection of such translocation can be very helpful for better targeting the therapy to be applied to gastric MALT lymphoma patients.

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

Directory of Open Access Journals (Sweden)

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.

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.

Human gastric mucins differently regulate Helicobacter pylori proliferation, gene expression and interactions with host cells.

Directory of Open Access Journals (Sweden)

Emma C Skoog

Full Text Available Helicobacter pylori colonizes the mucus niche of the gastric mucosa and is a risk factor for gastritis, ulcers and cancer. The main components of the mucus layer are heavily glycosylated mucins, to which H. pylori can adhere. Mucin glycosylation differs between individuals and changes during disease. Here we have examined the H. pylori response to purified mucins from a range of tumor and normal human gastric tissue samples. Our results demonstrate that mucins from different individuals differ in how they modulate both proliferation and gene expression of H. pylori. The mucin effect on proliferation varied significantly between samples, and ranged from stimulatory to inhibitory, depending on the type of mucins and the ability of the mucins to bind to H. pylori. Tumor-derived mucins and mucins from the surface mucosa had potential to stimulate proliferation, while gland-derived mucins tended to inhibit proliferation and mucins from healthy uninfected individuals showed little effect. Artificial glycoconjugates containing H. pylori ligands also modulated H. pylori proliferation, albeit to a lesser degree than human mucins. Expression of genes important for the pathogenicity of H. pylori (babA, sabA, cagA, flaA and ureA appeared co-regulated in response to mucins. The addition of mucins to co-cultures of H. pylori and gastric epithelial cells protected the viability of the cells and modulated the cytokine production in a manner that differed between individuals, was partially dependent of adhesion of H. pylori to the gastric cells, but also revealed that other mucin factors in addition to adhesion are important for H. pylori-induced host signaling. The combined data reveal host-specific effects on proliferation, gene expression and virulence of H. pylori due to the gastric mucin environment, demonstrating a dynamic interplay between the bacterium and its host.

[Unpleasant Journey from Helicobacter pylori-associated Gastritis to Gastric Cancer: Cancer Prevention by Taking a Detour].

Science.gov (United States)

Lee, Sang Hwan; Park, Jong Min; Han, Young Min; Ko, Weon Jin; Hahm, Ki Baik

2015-12-01

As a commensal or a pathogen, Helicobacter pylori can change the balance of a complex interaction that exists among gastric epithelial cells, microbes, and their environment. Therefore, unraveling this complex relationship of these mixtures can be expected to help prevent cancer as well as troublesome unmet medical needs of H. pylori infection. Though gastric carcinogenesis is a multi-step process, precancerous lesion can be reversible in the early phase of mucosal damage before reaching the stage of no return. However, biomarkers to predict rejuvenation of precancerous atrophic gastritis have not been identified yet and gastric cancer prevention is still regarded as an impregnable fortress. However, when we take the journey from H. pylori-associated gastritis to gastric cancer, it provides us with the clue for prevention since there are two main preventive strategies: eradication and anti-inflammation. The evidence supporting the former strategy is now ongoing in Japan through a nation-wide effort to eradicate H. pylori in patients with chronic gastritis, but suboptimal apprehension to increasing H. pylori resistance to antibiotics and patient non-compliance still exists. The latter strategy has been continued in the author'sresearch center under siTRP (short-term intervention to revert premalignant lesion) strategy. By focusing on the role of inflammation in the development of H. pylori-associated gastric carcinogenesis, this review is intended to explain the connection between inflammation and gastric cancer. Strategies on H. pylori eradication, removal of inflammation, and reverting preneoplastic lesion will also be introduced. In the end, we expect to be able to prevent gastric cancer by take a detour from the unpleasant journey, i.e. from H. pylori-associated gastritis to gastric cancer.

Helicobacter pylori infection in patients with dyspeptic symptoms having normal endoscopy

International Nuclear Information System (INIS)

Malik, M.F.; Hussain, T.; Khan, M.N.; Mirza, S.A.

2010-01-01

To find out the frequency of Helicobacter pylori infection in the local population presenting with dyspeptic symptoms but having normal upper gastrointestinal endoscopic findings. Hundred cases of dyspepsia having normal upper gastrointestinal endoscopy were taken as study population. Although the gold standard for presence or absence of Helicobacter pylori infection is culture but in this study the diagnostic method used was histopathology of gastric antrum. The male and female ratio was 2:1. Majority of the patients were either 40 years of age or less, mean age being 40.52 (sd+-13.22). The chief symptoms were pain epigastrium (46%) and upper abdominal discomfort (27%). Helicobacter pylori gastritis was found in 51% of cases. We conclude that Helicobacter pylori infection is quite common in dyspeptic patients apparently having normal endoscopic gastric mucosal findings. Eradication therapy should be instituted in positive cases to avoid its long-term complications. (author)

Associations among Gastric Juice pH, Atrophic Gastritis, Intestinal Metaplasia and Helicobacter pylori Infection

Science.gov (United States)

Sung, Jihee; Lee, Jongchan; Hwang, Young-Jae; Kim, Hyoung Woo; Chung, Jung Wha; Kim, Jin-Wook; Lee, Dong Ho

2018-01-01

Background/Aims Gastric juice plays a crucial role in the physiology of the stomach. The aim of this study is to evaluate associations among the pH of gastric juice, atrophic gastritis (AG), intestinal metaplasia (IM), pepsinogen, and Helicobacter pylori infection. Methods Gastric biopsies and juice were collected from 46 subjects who underwent endoscopies at Seoul National University Bundang Hospital between November 2011 and March 2013. H. pylori, AG and IM were evaluated, and pepsinogen I or II, I/II ratio, and interleukin (IL)-1β levels were measured. Results The mean pH of gastric juice was higher in the H. pylori-positive group (n=17) than that in the H. pylori-negative group (n=29) (4.54 vs 2.46, p=0.002). When patients were divided into pH <3 (n=28) and pH ≥3 (n=18) groups, H. pylori was lower in the pH <3 group (21.4%) than in the pH ≥3 group (61.1%) (p=0.007). The pH ≥3 group demonstrated AG and IM more frequently than the pH <3 group in the body (p=0.047 and p=0.051, respectively) but not in the antrum. There were no differences in pepsinogen I or II, I/II ratio, and IL-1β levels between the two groups. Conclusions There is a relationship between chronic H. pylori infection and gastric juice pH ≥3, which may originate from AG and IM in the body. PMID:28918609

Associations among Gastric Juice pH, Atrophic Gastritis, Intestinal Metaplasia and Helicobacter pylori Infection.

Science.gov (United States)

Sung, Jihee; Kim, Nayoung; Lee, Jongchan; Hwang, Young-Jae; Kim, Hyoung Woo; Chung, Jung Wha; Kim, Jin-Wook; Lee, Dong Ho

2018-03-15

Gastric juice plays a crucial role in the physiology of the stomach. The aim of this study is to evaluate associations among the pH of gastric juice, atrophic gastritis (AG), intestinal metaplasia (IM), pepsinogen, and Helicobacter pylori infection. Gastric biopsies and juice were collected from 46 subjects who underwent endoscopies at Seoul National University Bundang Hospital between November 2011 and March 2013. H. pylori , AG and IM were evaluated, and pepsinogen I or II, I/II ratio, and interleukin (IL)-1β levels were measured. The mean pH of gastric juice was higher in the H. pylori -positive group (n=17) than that in the H. pylori -negative group (n=29) (4.54 vs 2.46, p=0.002). When patients were divided into pH ＜3 (n=28) and pH ≥3 (n=18) groups, H. pylori was lower in the pH ＜3 group (21.4%) than in the pH ≥3 group (61.1%) (p=0.007). The pH ≥3 group demonstrated AG and IM more frequently than the pH ＜3 group in the body (p=0.047 and p=0.051, respectively) but not in the antrum. There were no differences in pepsinogen I or II, I/II ratio, and IL-1β levels between the two groups. There is a relationship between chronic H. pylori infection and gastric juice pH ≥3, which may originate from AG and IM in the body.

Magnitude of Helicobacter pylori among Dyspeptic patients ...

African Journals Online (AJOL)

Background: Helicobacter pylori (H.pylori) infection is predominantly acquired in childhood from family members. The infection can cause dypepepsia, chronic and acute gastritis and gastric cancer. Dyspepsia is the most common illness in the Ethiopian population visiting outpatient department of health facilities, and it has ...

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. A...

Helicobacter-negative gastritis: a distinct entity unrelated to Helicobacter pylori infection.

Science.gov (United States)

Genta, R M; Sonnenberg, A

2015-01-01

Helicobacter-negative gastritis is diagnosed when no organisms are detected in a gastric mucosa with typical features of Helicobacter gastritis (Hp-gastritis). If Helicobacter-negative gastritis consisted mostly of 'missed' Helicobacter infections, its prevalence should represent a constant percentage of these infections in a population, and their clinico-epidemiological features would overlap. To compare the epidemiologic patterns of Hp-positive and Hp-negative gastritis. From a pathology database, we extracted demographic, clinical and histopathological data from patients with gastric biopsies (1.2008-12.2013). We allocated patients to high (≥12%) and low (≤6%) H. pylori prevalence regions defined by ZIP code-based data. The prevalence of H. pylori-positive and -negative gastritis by sex, age and state were expressed as a per cent of the total study population stratified accordingly. Of 895 323 patients, 10.6% had Hp-gastritis and 1.5% Helicobacter-negative gastritis. Hp-gastritis, but not Helicobacter-negative gastritis, was more common in males than females (OR 1.17, 95% CI: 1.16-1.19). While Hp-gastritis was more prevalent in high than in low-prevalence areas (OR 3.65, 95% CI: 3.57-3.74), Helicobacter-negative gastritis was only minimally affected by the underlying H. pylori prevalence (1.7% vs. 1.5%). The age-specific prevalence of Hp-gastritis peaked in the 4th to 5th decades; Helicobacter-negative gastritis exhibited a low and relatively flat pattern. The geographic distribution of H. pylori-positive and -negative gastritis showed no significant correlation. Intestinal metaplasia was found in 13.0% of patients with Hp-gastritis and in 6.1% of those with Helicobacter-negative gastritis (OR 0.43, 95% CI: 0.40-0.47). These data suggest that Helicobacter-negative gastritis is, in the vast majority of cases, a nosologically and epidemiologically distinct entity that deserves further investigation. © 2014 John Wiley & Sons Ltd.

Anti Helicobacter pylori IgG and IgA response in patients with gastric cancer and chronic gastritis.

Science.gov (United States)

Manojlovic, Nebojsa; Babic, Dragana; Filipovic-Ljeshovic, Ivana; Pilcevic, Dijana

2008-01-01

Immune response against Helicobacter pylori is important for the course and outcome of infection. We conducted study looking for the difference in anti H. pylori IgG and IgA between patients with intestinal type of gastric cancer, superficial and atrophic gastritis. For this study, 133 patients infected with H. pylori were enrolled: 50 with superficial gastritis, 42 with atrophic gastritis and 41 with gastric cancer. Anti H. pylori IgG and IgA ELISA tests were performed. The difference in antibody titers of IgG and IgA, frequency of IgA > IgG ratio and combination of low IgG and IgA > IgG ratio were analyzed. The patients with gastritis had higher titer of IgG that the patients with gastric cancer (p gastritis had higher titer of IgA than the patients with gastric cancer (p IgG ratio is more frequent in patients with gastric cancer than in the patients with superficial gastritis (p IgG is more frequent in the patients with gastric cancer than in the patients with gastritis (p cancer elicit different anti H. pylori IgG and IgA response than the patients with superficial and atrophic gastritis. Low IgG and IgA predominance seems characteristic for gastric cancer.

Exploiting the Gastric Epithelial Barrier: Helicobacter pylori's Attack on Tight and Adherens Junctions.

Science.gov (United States)

Backert, Steffen; Schmidt, Thomas P; Harrer, Aileen; Wessler, Silja

2017-01-01

Highly organized intercellular tight and adherens junctions are crucial structural components for establishing and maintenance of epithelial barrier functions, which control the microbiota and protect against intruding pathogens in humans. Alterations in these complexes represent key events in the development and progression of multiple infectious diseases as well as various cancers. The gastric pathogen Helicobacter pylori exerts an amazing set of strategies to manipulate these epithelial cell-to-cell junctions, which are implicated in changing cell polarity, migration and invasive growth as well as pro-inflammatory and proliferative responses. This chapter focuses on the H. pylori pathogenicity factors VacA, CagA, HtrA and urease, and how they can induce host cell signaling involved in altering cell-to-cell permeability. We propose a stepwise model for how H. pylori targets components of tight and adherens junctions in order to disrupt the gastric epithelial cell layer, giving fresh insights into the pathogenesis of this important bacterium.

[The effect of Helicobacter pylori eradication on chronic gastritis].

Science.gov (United States)

Kodama, Masaaki; Murakami, Kazunari; Okimoto, Tadayoshi; Fujioka, Toshio

2013-08-01

Helicobacter pylori (H. pylori) is a major pathogen of chronic atrophic gastritis, intestinal metaplasia, and gastric cancer. Atrophic gastritis and intestinal metaplasia are recognized as precancerous lesion of gastric cancer. Many studies reported that H. pylori eradication had the preventive effect of gastric cancer. Moreover many studies mentioned the improvement of gastric atrophy and/or intestinal metaplasia. Two meta-analysis indicated the improvement of atrophic gastritis but not of intestinal metaplasia. In our study, intestinal metaplasia improved at lesser curvature of the corpus six years after eradication. H. pylori eradication has benefit for gastric cancer prevention provably due to improvement of the precancerous lesion such as atrophic gastritis and intestinal metaplasia. Especially, H. pylori eradication before the appearance of atrophy and intestinal metaplasia has been considered to be effective in inhibiting the development of gastric cancer. Therefore, improvement or elimination of chronic gastritis with H. pylori eradication might have possibility of gastric cancer inhibition.

A potential role for Helicobacter pylori heat shock protein 60 in gastric tumorigenesis

Energy Technology Data Exchange (ETDEWEB)

Lin, Chen-Si [Department of Biological Science and Technology, National Chiao-Tung University, Hsin-Chu, Taiwan (China); School of Veterinary Medicine, National Taiwan University, Taipei, Taiwan (China); He, Pei-Juin [Department of Biological Science and Technology, National Chiao-Tung University, Hsin-Chu, Taiwan (China); Tsai, Nu-Man [School of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan (China); Li, Chi-Han; Yang, Shang-Chih; Hsu, Wei-Tung [Department of Biological Science and Technology, National Chiao-Tung University, Hsin-Chu, Taiwan (China); Wu, Ming-Shiang [Department of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan (China); Wu, Chang-Jer [Department of Food Science, National Taiwan Ocean University, Keelung, Taiwan (China); Cheng, Tain-Lu [Department of Biotechnology, Kaohsiung Medical University, Kaohsiung, Taiwan (China); Liao, Kuang-Wen, E-mail: kitchhen@yahoo.com.tw [Department of Biological Science and Technology, National Chiao-Tung University, Hsin-Chu, Taiwan (China)

2010-02-05

Helicobacter pylori has been found to promote the malignant process leading to gastric cancer. Heat shock protein 60 of H. pylori (HpHSP60) was previously been identified as a potent immunogene. This study investigates the role of HpHSP60 in gastric cancer carcinogenesis. The effect of HpHSP60 on cell proliferation, anti-death activity, angiogenesis and cell migration were explored. The results showed that HpHSP60 enhanced migration by gastric cancer cells and promoted tube formation by umbilical vein endothelial cells (HUVECs); however, HpHSP60 did not increase cell proliferation nor was this protein able to rescue gastric cancer cells from death. Moreover, the results also indicated HpHSP60 had different effects on AGS gastric cancer cells or THP-1 monocytic cells in terms of their expression of pro-inflammatory cytokines, which are known to be important to cancer development. We propose that HpHSP60 may trigger the initiation of carcinogenesis by inducing pro-inflammatory cytokine release and by promoting angiogenesis and metastasis. Thus, this extracellular pathogen-derived HSP60 is potentially a vigorous virulence factor that can act as a carcinogen during gastric tumorigenesis.

Correlation between virulence markers of Helicobacter pylori in the oral cavity and gastric biopsies

Directory of Open Access Journals (Sweden)

Myriam Lucrecia MEDINA

2017-07-01

Full Text Available ABSTRACT BACKGROUND: The clinical outcome of Helicobacter pylori infection has been associated with virulence factors. The presence of these factors is useful as molecular markers in the identification of the high risk for developing severe gastric pathologies. OBJECTIVE: To correlate the presence of virulence markers cagA and bab2A of H. pylori in oral and gastric biopsy samples. METHODS: An observational, prospective, descriptive, and cross-sectional study was carried out between September 2011 and September 2012. Patients suffering dyspepsia with indication for upper gastrointestinal video endoscopy who attended the Gastroenterology Service of the Hospital Dr. Julio C. Perrando were included. Epidemiological investigation was completed. To detect the bacteria and their virulence genes, samples of saliva, dental plaque and gastric biopsy were taken and processed by PCR. RESULTS: Sixty-one patients were selected for this study (30 women and 31 men. H. pylori was detected in 31 gastric biopsies and 31 oral samples. Significant difference between oral and gastric samples was found in cagA genotype. Agreement between oral and gastric genotypes was found in 38.7% of samples from the same patient. CONCLUSION: This study is the first in provide information about the genotypes of the Argentinean Northeast H. pylori strains. Despite the high prevalence of H. pylori infection, the most of patients had less virulent genotypes in oral cavity and gastric tissue. The cagA / babA2 combination was not frequent in the samples studied. There was not a statistical correlation between the virulence genes and gastroduodenal or oral diseases. Although in some patients the same genotype was found both in oral and gastric samples, it cannot be ensure that they corresponding to the same strain because a DNA sequencing was not performed.

Braf, Kras and Helicobacter pylori epigenetic changes-associated chronic gastritis in Egyptian patients with and without gastric cancer.

Science.gov (United States)

Sabry, Dina; Ahmed, Rasha; Abdalla, Sayed; Fathy, Wael; Eldemery, Ahmed; Elamir, Azza

2016-06-01

We aimed to study MLH1 and MGMT methylation status in Helicobacter pylori-associated chronic gastritis in Egyptian patients with and without gastric cancer. 39 patients were included in our study. They were divided into 2 groups; patients without (group I) and with gastric adenocarcinoma (group II). Patients were subjected to clinical examination, abdominal ultrasound and upper endoscopy for gastric biopsy. Biopsies were subjected to urease test, histological examination, and DNA purification. H. pylori, Braf, Kras, MLH1 and MGMT methylation were assessed by quantitative PCR. DNA sequencing was performed to assess Braf and Kras genes mutation. qPCR of H. pylori was significantly higher in patients with adenocarcinoma (group II) than those without adenocarcinoma (group I); with a p gastritis patients. DNA sequence analysis of Braf (codon 12) and Kras (codon 600) had genes mutation in gastric adenocarcinoma versus chronic gastritis. H. pylori may cause epigenetic changes predisposing the patients to cancer stomach. Estimation of H. pylori by qPCR can be a good predictor to adenocarcinoma. Braf and Kras genes mutation were reveled in gastritis and adenocarcinoma patients.

Helicobacter pylori y dispepsia, un problema de salud comunitario

Directory of Open Access Journals (Sweden)

Miguel González-Carbajal Pascual

2002-06-01

Full Text Available Mientras la relación causal entre el Helicobacter pylori y la gastritis crónica, así como la importante conexión entre esta infección, la úlcera gastroduodenal y el cáncer gástrico han sido bien establecidas, la asociación entre la infección por Helicobacter pylori y la dispepsia "no ulcerosa" es un problema que dista mucho de estar esclarecido. Hay autores que no dudan en utilizar tratamiento de erradicación en la dispepsia "no ulcerosa" con Helicobacter pylori, pero existen enfoques alternativos a este problema. La realización de tratamiento de erradicación en los pacientes con dispepsia "no ulcerosa" pudiera beneficiar o no a los enfermos y a la comunidad, pero seguramente no puede dejar de beneficiar a las transnacionales productoras de medicamentos que cosechan cuantiosas ganancias con la comercialización de los bloqueadores de la bomba de protones y los antibióticos que se incluyen en cualquier esquema de terapia erradicadora de la infección por Helicobacter pylori. El alivio de los síntomas dispépticos como consecuencia del tratamiento de erradicación del Helicobacter pylori no ha sido comprobado. El problema de realizar tratamiento de erradicación de la infección a los pacientes con dispepsia "no ulcerosa" continúa siendo un dilema y, por tanto, no debe indicarse sistemáticamente.Although the causative relationship between Helicobacter pylori and chronic gastritis as well as the important connection of this infection with gastric-duodenal ulcer and gastric cancer are well established, the association of Helicobacter pylori infection and non-ulcer dispepsia is a problem that is still unclear. Some authors do not hesitate in using Helicobacter pylori eradication treatment in cases of non-ulcer dispepsia but there are other alternative approaches to this problem. The eradication treatment in patients with non-ulcer dispepsia may or may not benefit patients and the community, but will benefit for sure the big drug

How host regulation of Helicobacter pylori-induced gastritis protects against peptic ulcer disease and gastric cancer.

Science.gov (United States)

Dhar, Poshmaal; Ng, Garrett Z; Sutton, Philip

2016-09-01

The bacterial pathogen Helicobacter pylori is the etiological agent of a range of gastrointestinal pathologies including peptic ulcer disease and the major killer, gastric adenocarcinoma. Infection with this bacterium induces a chronic inflammatory response in the gastric mucosa (gastritis). It is this gastritis that, over decades, eventually drives the development of H. pylori-associated disease in some individuals. The majority of studies investigating H. pylori pathogenesis have focused on factors that promote disease development in infected individuals. However, an estimated 85% of those infected with H. pylori remain completely asymptomatic, despite the presence of pathogenic bacteria that drive a chronic gastritis that lasts many decades. This indicates the presence of highly effective regulatory processes in the host that, in most cases, keeps a check on inflammation and protect against disease. In this minireview we discuss such known host factors and how they prevent the development of H. pylori-associated pathologies. Copyright © 2016 the American Physiological Society.

Helicobacter pylori moves through mucus by reducing mucin viscoelasticity

OpenAIRE

Celli, Jonathan P.; Turner, Bradley S.; Afdhal, Nezam H.; Keates, Sarah; Ghiran, Ionita; Kelly, Ciaran P.; Ewoldt, Randy H.; McKinley, Gareth H.; So, Peter; Erramilli, Shyamsunder; Bansil, Rama

2009-01-01

The ulcer-causing gastric pathogen Helicobacter pylori is the only bacterium known to colonize the harsh acidic environment of the human stomach. H. pylori survives in acidic conditions by producing urease, which catalyzes hydrolysis of urea to yield ammonia thus elevating the pH of its environment. However, the manner in which H. pylori is able to swim through the viscoelastic mucus gel that coats the stomach wall remains poorly understood. Previous rheology studies on gastric mucin, the key...

Prevalence of Helicobacter Pylori in gastric cancer in a south-east Asian population by 14C-urea breath test

International Nuclear Information System (INIS)

Chung, A.Y-F; Chow, P.K.H.; Yu, W-K.; Ho, J.M.S.; Chan, H-S.; Wong, W-K.; Soo, K-C.

2001-01-01

Helicobacter pylori is believed to play an important role in the aetiology of gastric cancer. There is a great variability in seropositivity and histological frequency of H. pylori in gastric cancer. The present prospective study investigates the prevalence of H. pylori infection in gastric cancer patients using 14C-urea breath testing. Patients with endoscopic biopsy-proven gastric cancer were fasted for 6 h prior to ingesting 18.5 x 104 Bq of 14C-urea cocktail orally. Breath samples were collected after 20 min by AS/King them to blow into a hyamine solution and measurements were read in a scintillation counter. Fifty out of 51 patients (98%) with gastric cancer were positive on the 14C-urea breath test compared to 29 patients (61%) who were positive on histology. There was no association between sex, age or tumour site, stage, differentiation, Lauren type and H. pylori status. The test was negative in one patient with cardiac tumour in which histology of the resected specimen was also negative for the bacteria. Active H. pylori infection is highly prevalent in gastric cancer in a South-East Asian population. The 14C-urea breath test is a highly sensitive method for detecting the presence of H. pylori even in gastric adenocarcinoma irrespective of the stage

VacA and CagA Status as Biomarker of Two Opposite End Outcomes of Helicobacter pylori Infection (Gastric Cancer and Duodenal Ulcer) in a Moroccan Population

OpenAIRE

El Khadir, Mounia; Alaoui Boukhris, Samia; Benajah, Dafr-Allah; El Rhazi, Karima; Ibrahimi, Sidi Adil; El Abkari, Mohamed; Harmouch, Taoufiq; Nejjari, Chakib; Mahmoud, Mustapha; Benlemlih, Mohamed; Bennani, Bahia

2017-01-01

Helicobacter pylori (H. pylori) infection induces inflammation of the gastric mucosa, which may progress to precancerous lesions leading to gastric cancer. Pathological determinism is associated to some virulence genes of the bacterium, notably the vacA and cagA genes. The present study aimed to determine the H. pylori genotypes distribution and their association with sex, age and gastric diseases in a Moroccan population. Gastric biopsy was taken from 1079 consenting patients. The specimens ...

EGFR and Bcl-2 in gastric mucosa of children infected with Helicobacter pylori

Directory of Open Access Journals (Sweden)

Ewa Ryszczuk

2016-03-01

Full Text Available Aim: The aim of the study was to evaluate the expression of EGFR and Bcl-2 proteins as inhibitory markers of apoptosis in surface epithelial cells and gland cells of antral gastric mucosa in children infected with Helicobacter pylori according to the severity and activity of antral gastritis and to assess the correlation between the number of cells expressing EGFR and the number of cells expressing Bcl-2 in H. pylori infected children.Materials and methods: The study included 44 children: 68.2% with chronic gastritis and positive IgG against H. pylori, and 31.8% with functional disorders of the gastrointestinal tract and with normal IgG against H. pylori. The evaluation of EGFR expression in gastric mucosa was performed immunohistochemically using monoclonal mouse anti-EGFR antibody. The polyclonal antibody was used to determine the expression of anti-Bcl-2.Results: A significant increase in the number of cells expressing EGFR and Bcl-2 protein was found in the epithelial cells in severe as well as mild and moderate gastritis in the group of children infected with H. pylori. An increase in the number of cells expressing EGFR and Bcl-2 protein was also found in the epithelial cells in group I according to the activity of gastritis. There was a statistically significant positive correlation between the numbers of cells expressing EGFR and Bcl-2 in H. pylori infected children.Conclusion: Increased expression of EGFR and Bcl-2 proteins in the epithelial cells and a statistically significant positive correlation between the numbers of cells expressing EGFR and Bcl-2 in H. pylori infected children could suggest increased regeneration abilities of gastric mucosa.

3rd Brazilian consensus on Helicobacter pylori 3º Consenso Brasileiro para Estudo do Helicobacter pylori

Directory of Open Access Journals (Sweden)

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 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.Os avanços significativos ocorridos desde o Segundo Consenso Brasileiro sobre H. pylori realizado em 2004, em São Paulo, justificam este terceiro consenso. O evento foi organizado pelo Núcleo Brasileiro para Estudo do Helicobacter, departamento da Federação Brasileira de Gastroenterologia, tendo sido realizado em Bento Gonçalves, RS, nos dias 12 a 15 de abril de 2011. Contou com a participação de 30 delegados provenientes das cinco regiões brasileiras e um convidado internacional, incluindo gastroenterologistas

SURVIVAL OF HELICOBACTER PYLORI IN A NATURAL FRESHWATER ENVIRONMENT

Science.gov (United States)

The mode by which Helicobacter pylori, the causative agent of most gastric ulcers, is transmitted remains undetermined. Epidemiological evidence suggests these organisms are waterborne; however, H. pylori has rarely been grown from potential water sources. This may be due to th...

Is the presence of Helicobacter pylori in the Dental Plaque of Patients with Chronic Periodontitis a Risk Factor for Gastric Infection?

Directory of Open Access Journals (Sweden)

Mohammed Al Asqah

2009-01-01

Full Text Available BACKGROUND: Helicobacter pylori is considered to be a pathogen responsible for gastritis and peptic ulcers, and a risk factor for gastric cancer. A periodontal pocket in the teeth of individuals with chronic periodontitis may function as a reservoir for H pylori.

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.

Virulence genes of Helicobacter pylori in gastritis, peptic ulcer and gastric cancer in Laos.

Science.gov (United States)

Vannarath, Sengdao; Vilaichone, Ratha-korn; Rasachak, Bouachanh; Mairiang, Pisaln; Yamaoka, Yoshio; Shiota, Seiji; Binh, Tran Thanh; Mahachai, Varocha

2014-01-01

Helicobacter pylori (H. pylori) infection is an established cause of peptic ulcers and gastric cancer. The aim of this study was to identify H. pylori genotypes and to examine their associations with geographical regions and gastritis, peptic ulcers and gastric cancer in Laos. A total of 329 Lao dyspeptic patients who underwent gastroscopy at Mahosot Hospital, Vientiane, Laos during December 2010--March 2012 were enrolled. Two biopsy specimens (one each from the antrum and corpus) were obtained for CLO testing and only CLO test-positive gastric tissue were used to extract DNA. PCR and sequencing were identified for variants of the cagA and vacA genotypes. Some 119 Laos patients (36.2%) were found to be infected with H. pylori including 83 with gastritis, 13 with gastric ulcers (GU), 20 with duodenal ulcers (DU) and 3 with gastric cancer. cagA was detected in 99.2%. East-Asian-type cagA (62%) and vacA s1c (64.7%) were predominant genotypes in Laos. vacA s1c-m1b was significantly higher in GU than gastritis (53.8% vs. 24.1%; P-value=0.04) whereas vacA s1a-m2 was significantly higher in DU than gastritis (40.0% vs. 16.9%; P-value=0.03). East-Asian-type cagA and vacA s1c were significantly higher in highland than lowland Lao (100% vs. 55.8%; P-value=0.001 and 88.2% vs. 61.5%, P-value=0.03 respectively). H. pylori is a common infection in Laos, as in other countries in Southeast Asia. The cagA gene was demonstrated in nearly all Laos patients, cagA and vacA genotypes being possible important factors in explaining H. pylori infection and disease outcomes in Laos.

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.

A changing gastric environment leads to adaptation of lipopolysaccharide variants in Helicobacter pylori populations during colonization.

Directory of Open Access Journals (Sweden)

Anna Skoglund

2009-06-01

Full Text Available The human gastric pathogen Helicobacter pylori colonizes the stomachs of half of the human population, and causes development of peptic ulcer disease and gastric adenocarcinoma. H. pylori-associated chronic atrophic gastritis (ChAG with loss of the acid-producing parietal cells, is correlated with an increased risk for development of gastric adenocarcinoma. The majority of H. pylori isolates produce lipopolysaccharides (LPS decorated with human-related Lewis epitopes, which have been shown to phase-vary in response to different environmental conditions. We have characterized the adaptations of H. pylori LPS and Lewis antigen expression to varying gastric conditions; in H. pylori isolates from mice with low or high gastric pH, respectively; in 482 clinical isolates from healthy individuals and from individuals with ChAG obtained at two time points with a four-year interval between endoscopies; and finally in isolates grown at different pH in vitro. Here we show that the gastric environment can contribute to a switch in Lewis phenotype in the two experimental mouse models. The clinical isolates from different human individuals showed that intra-individual isolates varied in Lewis antigen expression although the LPS diversity was relatively stable within each individual over time. Moreover, the isolates demonstrated considerable diversity in the levels of glycosylation and in the sizes of fucosylated O-antigen chains both within and between individuals. Thus our data suggest that different LPS variants exist in the colonizing H. pylori population, which can adapt to changes in the gastric environment and provide a means to regulate the inflammatory response of the host during disease progression.

Oxyntic gastric atrophy in Helicobacter pylori gastritis is distinct from autoimmune gastritis.

Science.gov (United States)

Venerito, Marino; Varbanova, Mariya; Röhl, Friedrich-Wilhelm; Reinhold, Dirk; Frauenschläger, Katrin; Jechorek, Doerthe; Weigt, Jochen; Link, Alexander; Malfertheiner, Peter

2016-08-01

To assess characteristics of oxyntic gastric atrophy (OGA) in autoimmune gastritis (AIG) compared with OGA as a consequence of Helicobacter pylori infection. Patients undergoing oesophagogastroduodenoscopy from July 2011 to October 2014 were prospectively included (N=452). Gastric biopsies were obtained for histology and H. pylori testing. Serum gastrin-17 (G17), pepsinogen (PG) I, PGII and antibodies against H. pylori and cytotoxin-associated gene A protein were determined in all patients. Antibodies against parietal cells and intrinsic factor were determined in patients with advanced (moderate to severe) OGA. Areas under the receiver operating characteristic curves (AUCs) were calculated for serum biomarkers and compared with histology. Overall, 34 patients (8.9%) had advanced OGA by histology (22 women, age 61±15 years). Current or past H. pylori infection and AIG were present in 14/34 and 22/34 patients, respectively. H. pylori-negative AIG patients (N=18) were more likely to have another autoimmune disease (OR 6.3; 95% CI 1.3 to 29.8), severe corpus atrophy (OR 10.1; 95% CI 1.9 to 54.1) and corpus intestinal metaplasia (OR 26.9; 95% CI 5.3 to 136.5) compared with H. pylori-positive patients with advanced OGA. Antrum atrophy was present in 39% of H. pylori-negative AIG patients. The diagnostic performance of G17, PG I and PGI/II was excellent for AIG patients (AUC=0.83, 0.95 and 0.97, respectively), but limited for H. pylori-positive patients with advanced OGA (AUC=0.62, 0.75 and 0.67, respectively). H. pylori-negative AIG has a distinct clinical, morphological and serological phenotype compared with advanced OGA in H. pylori gastritis. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/

Empiric treatment based on Helicobacter Pylori serology cannont ...

African Journals Online (AJOL)

Background: Evidence that chronic gastric Helicobacter pylori (HP) infection is an aetiological factor in dyspepsia, peptic ulcer disease, gastric carcinoma and lymphoma has led to the suggestion that all serologically positive dyspeptic patients should be treated empirically with antibiotics to eradicate the infection, without ...

Critical pathogenic steps to high risk Helicobacter pylori gastritis and gastric carcinogenesis.

Science.gov (United States)

Lee, Inchul

2014-06-07

Helicobacter pylori (H. pylori) gastritis may progress to high risk gastropathy and cancer. However, the pathological progression has not been characterized in detail. H. pylori induce persistent inflammatory infiltration. Neutrophils are unique in that they directly infiltrate into foveolar epithelium aiming the proliferative zone specifically. Neutrophilic proliferative zone foveolitis is a critical pathogenic step in H. pylori gastritis inducing intensive epithelial damage. Epithelial cells carrying accumulated genomic damage and mutations show the Malgun (clear) cell change, characterized by large clear nucleus and prominent nucleolus. Malgun cells further undergo atypical changes, showing nuclear folding, coarse chromatin, and multiple nucleoli. The atypical Malgun cell (AMC) change is a novel premalignant condition in high risk gastropathy, which may progress and undergo malignant transformation directly. The pathobiological significance of AMC in gastric carcinogenesis is reviewed. A new diagnosis system of gastritis is proposed based on the critical pathologic steps classifying low and high risk gastritis for separate treatment modality. It is suggested that the regulation of H. pylori-induced neutrophilic foveolitis might be a future therapeutic goal replacing bactericidal antibiotics approach.

Helicobacter pylori associated chronic gastritis, clinical syndromes, precancerous lesions, and pathogenesis of gastric cancer development

Science.gov (United States)

Watari, Jiro; Chen, Nancy; Amenta, Peter S; Fukui, Hirokazu; Oshima, Tadayuki; Tomita, Toshihiko; Miwa, Hiroto; Lim, Kheng-Jim; Das, Kiron M

2014-01-01

Helicobacter pylori (H. pylori) infection is well known to be associated with the development of precancerous lesions such as chronic atrophic gastritis (AG), or gastric intestinal metaplasia (GIM), and cancer. Various molecular alterations are identified not only in gastric cancer (GC) but also in precancerous lesions. H. pylori treatment seems to improve AG and GIM, but still remains controversial. In contrast, many studies, including meta-analysis, show that H. pylori eradication reduces GC. Molecular markers detected by genetic and epigenetic alterations related to carcinogenesis reverse following H. pylori eradication. This indicates that these changes may be an important factor in the identification of high risk patients for cancer development. Patients who underwent endoscopic treatment of GC are at high risk for development of metachronous GC. A randomized controlled trial from Japan concluded that prophylactic eradication of H. pylori after endoscopic resection should be used to prevent the development of metachronous GC, but recent retrospective studies did not show the tendency. Patients with precancerous lesions (molecular alterations) that do not reverse after H. pylori treatment, represent the “point of no return” and may be at high risk for the development of GC. Therefore, earlier H. pylori eradication should be considered for preventing GC development prior to the appearance of precancerous lesions. PMID:24833876

Helicobacter pylori associated chronic gastritis, clinical syndromes, precancerous lesions, and pathogenesis of gastric cancer development.

Science.gov (United States)

Watari, Jiro; Chen, Nancy; Amenta, Peter S; Fukui, Hirokazu; Oshima, Tadayuki; Tomita, Toshihiko; Miwa, Hiroto; Lim, Kheng-Jim; Das, Kiron M

2014-05-14

Helicobacter pylori (H. pylori) infection is well known to be associated with the development of precancerous lesions such as chronic atrophic gastritis (AG), or gastric intestinal metaplasia (GIM), and cancer. Various molecular alterations are identified not only in gastric cancer (GC) but also in precancerous lesions. H. pylori treatment seems to improve AG and GIM, but still remains controversial. In contrast, many studies, including meta-analysis, show that H. pylori eradication reduces GC. Molecular markers detected by genetic and epigenetic alterations related to carcinogenesis reverse following H. pylori eradication. This indicates that these changes may be an important factor in the identification of high risk patients for cancer development. Patients who underwent endoscopic treatment of GC are at high risk for development of metachronous GC. A randomized controlled trial from Japan concluded that prophylactic eradication of H. pylori after endoscopic resection should be used to prevent the development of metachronous GC, but recent retrospective studies did not show the tendency. Patients with precancerous lesions (molecular alterations) that do not reverse after H. pylori treatment, represent the "point of no return" and may be at high risk for the development of GC. Therefore, earlier H. pylori eradication should be considered for preventing GC development prior to the appearance of precancerous lesions.

Helicobacter pylori infection and typhoid fever in Jakarta, Indonesia.

NARCIS (Netherlands)

Vollaard, A.M.; Verspaget, H.W.; Ali, S.; Visser, L.G.; Veenendaal, R.A.; Asten, H.A.G.H. van; Widjaja, S.; Surjadi, C.; Dissel, J.T. van

2006-01-01

We evaluated the association between typhoid fever and Helicobacter pylori infection, as the latter microorganism may influence gastric acid secretion and consequently increase susceptibility to Salmonella typhi infection. Anti-H. pylori IgG and IgA antibody titres (ELISA) and gastrin concentration

Review article: Medical decision models of Helicobacter pylori therapy to prevent gastric cancer.

Science.gov (United States)

Sonnenberg, A; Inadomi, J M

1998-02-01

The aim of the present article is to study the utility of Helicobacter pylori eradication programmes in decreasing the incidence of gastric cancer. Three types of decision models are employed to pursue this aim, i.e. decision tree, present value, and declining exponential approximation of life expectancy (DEALE). 1) A decision tree allows one to model the interaction of multiple variables in great detail and to calculate the marginal cost, as well as the marginal cost-benefit ratio, of a preventive strategy. The cost of gastric cancer, the efficacy of H. pylori therapy in preventing cancer, and the cumulative probability of developing gastric cancer exert the largest influence on the marginal cost of cancer prevention. The high cost of future gastric cancer and a high efficacy of therapy make screening for H. pylori and its eradication the preferred strategy. 2) The present value is an economic method to adjust future costs or benefits to their current value using a discount rate and the length of time between now and a given time point in the future. It accounts for the depreciation of money and all material values over time. During childhood, the present value of future gastric cancer is very low. Vaccination of children to prevent gastric cancer would need to be very inexpensive to be practicable. Cancer prevention becomes a feasible option, only if the time period between the preventive measures and the occurrence of gastric cancer can be made relatively short. 3) The DEALE provides a means to calculate the increase in life expectancy that would occur, if death from a particular disease became preventable. Life expectancy of the general population is hardly affected by gastric cancer. For life expectancy to increase appreciably by vaccination or antibiotic therapy directed against H. pylori infection, these interventions would need to be focused towards a sub-population with an a priori high risk for gastric cancer.

Helicobacter pylori as a potential target for the treatment of central serous chorioretinopathy

Directory of Open Access Journals (Sweden)

Antonio Marcelo Barbante Casella

2012-09-01

Full Text Available OBJECTIVES: The objective of this study was to evaluate the relationship between the treatment of Helicobacter pylori gastric infection and changes in best-corrected visual acuity and macular detachment in patients with chronic central serous chorioretinopathy. METHODS: Seventeen patients diagnosed with central serous chorioretinopathy were examined for gastric infection with Helicobacter pylori using the urease test and gastric biopsy. Helicobacter pylory-positive patients were treated with the appropriate medication. The response to therapy was monitored by evaluating the best-corrected visual acuity and optical coherence tomography. The data were analyzed using Student's t-test before and after treatment. RESULTS: Fourteen patients (15 eyes aged 30-56 years (mean 43.4 ± 8.3 years were positive for Helicobacter pylori. Most of the positive patients had gastric symptoms (78.5%; one had bilateral central serous chorioretinopathy. The mean baseline best-corrected visual acuity was 20/98 (logMAR = 0.53 ± 0.28. Three months after starting treatment with antibiotics, the serous detachment had resolved in 14 of 15 eyes, but two cases required laser treatment. The follow-up period ranged from 6 to 27 months. The mean final best-corrected visual acuity differed significantly from baseline. CONCLUSION: Our findings suggest that Helicobacter pylori infection may be present in many chronic central serous chorioretinopathy patients and that treatment for the infection may have a favorable effect on the outcome of chronic central serous chorioretinopathy. Due to the possibility of the spontaneous regression of chronic central serous chorioretinopathy and the high prevalence of the infection in the general population, prospective and masked clinical trials are necessary to confirm that treatment for Helicobacter pylori infection may benefit patients with chronic central serous chorioretinopathy.

Helicobacter pylori and gastric cancer: correlation with gastritis, intestinal metaplasia, and tumour histology.

OpenAIRE

Wee, A; Kang, J Y; Teh, M

1992-01-01

This study aimed to examine the association between Helicobacter pylori, histological gastritis, and intestinal metaplasia in gastric cancers of different histological types. A total of 169 gastrectomy specimens received in one pathology department were studied. Altogether 156 were adenocarcinomas (intestinal type 87, diffuse type 50, mixed type 19). Gastritis occurred in 137 of 163 body specimens (84%) and in 126 of 131 antral specimens (96%). Its presence was unrelated to tumour histology. ...

Secondary prevention of epidemic gastric cancer in the model of Helicobacter pylori-associated gastritis.

Science.gov (United States)

Pizzi, Marco; Saraggi, Deborah; Fassan, Matteo; Megraud, Francis; Di Mario, Francesco; Rugge, Massimo

2014-01-01

Irrespective of its etiology, long-standing, non-self-limiting gastric inflammation (mostly in Helicobacter pylori-associated cases) is the cancerization ground on which epidemic (intestinal-type) gastric carcinoma (GC) can develop. The natural history of invasive gastric adenocarcinoma encompasses gastritis, atrophic mucosal changes, and intraepithelial neoplasia (IEN). The topography, the extent and the severity of the atrophic changes significantly correlate with the risk of developing both IEN and GC. In recent years, both noninvasive (serological) tests and invasive (endoscopy/biopsy) procedures have been proposed to stratify patients according to different classes of GC risk. As a consequence, different patient-tailored GC secondary prevention strategies have been put forward. This review summarizes the histological features of H. pylori-related gastritis and the natural history of the disease. Histological and serological strategies to assess GC risk as well as the clinical management of atrophic gastritis patients are also discussed. © 2014 S. Karger AG, Basel.

Macrophage migration inhibitory factor stimulated by Helicobacter pylori increases proliferation of gastric epithelial cells

Science.gov (United States)

Xia, Harry Hua-Xiang; Lam, Shiu Kum; Chan, Annie O.O.; Lin, Marie Chia Mi; Kung, Hsiang Fu; Ogura, Keiji; Berg, Douglas E.; Wong, Benjamin C. Y.

2005-01-01

AIM: Helicobacter pylori (H pylori) is associated with increased gastric inflammatory and epithelial expression of macrophage migration inhibitory factor (MIF) and gastric epithelial cell proliferation. This study aimed at determining whether H pylori directly stimulates release of MIF in monocytes, whether the cag pathogenicity island (PAI) is involved for this function, and whether MIF stimulated by H pylori increases gastric epithelial cell proliferation in vitro. METHODS: A cytotoxic wild-type H pylori strain (TN2)and its three isogenic mutants (TN2△cag, TN2△cagA and TN2△cagE) were co-cultured with cells of a human monocyte cell line, THP-1, for 24 h at different organism/cell ratios. MIF in the supernatants was measured by an ELISA. Cells of a human gastric cancer cell line, MKN45, were then co-cultured with the supernatants, with and without monoclonal anti-MIF antibody for 24 h. The cells were further incubated for 12 h after addition of 3H-thymidine, and the levels of incorporation of 3H-thymidine were measured with a liquid scintillation counter. RESULTS: The wild-type strain and the isogenic mutants, TN2△cagA and TN2△cagE, increased MIF release at organism/cell ratios of 200/1 and 400/1, but not at the ratios of 50/1 and 100/1. However, the mutant TN2△cag did not increase the release of MIF at any of the four ratios. 3H-thymidine readings for MKN-45 cells were significantly increased with supernatants derived from the wild-type strain and the mutants TN2△cagA and TN2△cagE, but not from the mutant TN2△cag. Moreover, in the presence of monoclonal anti-MIF antibody, the stimulatory effects of the wild-type strain on cell proliferation disappeared. CONCLUSION: H pylori stimulates MIF release in monocytes, likely through its cag PAI, but not related to cagA or cagE. H pylori-stimulated monocyte culture supernatant increases gastric cell proliferation, which is blocked by anti-MIF antibody, suggesting that MIF plays an important role in H

DNA Fingerprinting of Single Colonies of Helicobacter pylori from Gastric Cancer Patients Suggests Infection with a Single Predominant Strain

OpenAIRE

Miehlke, Stephan; Thomas, Rachel; Guiterrez, Oscar; Graham, David Y.; Go, Mae F.

1999-01-01

In each of six gastric cancer patients, repetitive extragenic palindromic PCR DNA fingerprints of 18 single colonies of Helicobacter pylori from the gastric antrum, corpus, and cardia were identical and matched that of the parental isolate. In three additional gastric cancer patients, 17 of 18 single-colony DNA fingerprints were identical to each other and to the DNA fingerprint of the corresponding parental isolate.

Helicobacter pylori infection in apparently healthy South Indian children

International Nuclear Information System (INIS)

Kurpad, A.V.; Caszo, B.; Raj, T.; Vaz, M.

2000-01-01

Helicobacter pylori infection has been established as a major cause of chronic gastritis in adults, and it has been implicated in the genesis of gastric carcinomas and the development of gastric and duodenal ulcers. It is now postulated that neatly 90% of the adult population in developing countries may be affected with the infection since childhood. Earlier studies on Indians using serology and endoscopic biopsy have shown a high incidence of H. pylori infection in small numbers of patients. The 13 C-urea breath test, which is simple, specific and non-invasive, is also increasingly being used to determine the presence of Helicobacter pylori infection. Preliminary data from India has shown a high prevalence in the urban Indian environment, and there is an urgent need to quantify the prevalence of H. pylori infections on an epidemiological basis in both urban and rural settings. It is also important to study the possible impact of this infection on growth in children, particularly in environments with low sanitation and high crowding. In this paper, we outline a proposal to study the prevalence of Helicobacter pylori infections in children from the following different environments: urban middle socio-economic class, urban slum, rural middle socio-economic class and rural village. (author)

Mechanisms of disease: Helicobacter pylori virulence factors.

Science.gov (United States)

Yamaoka, Yoshio

2010-11-01

Helicobacter pylori plays an essential role in the development of various gastroduodenal diseases; however, only a small proportion of people infected with H. pylori develop these diseases. Some populations that have a high prevalence of H. pylori infection also have a high incidence of gastric cancer (for example, in East Asia), whereas others do not (for example, in Africa and South Asia). Even within East Asia, the incidence of gastric cancer varies (decreasing in the south). H. pylori is a highly heterogeneous bacterium and its virulence varies geographically. Geographic differences in the incidence of gastric cancer can be explained, at least in part, by the presence of different types of H. pylori virulence factor, especially CagA, VacA and OipA. However, it is still unclear why the pathogenicity of H. pylori increased as it migrated from Africa to East Asia during the course of evolution. H. pylori infection is also thought to be involved in the development of duodenal ulcer, which is at the opposite end of the disease spectrum to gastric cancer. This discrepancy can be explained in part by the presence of H. pylori virulence factor DupA. Despite advances in our understanding of the development of H. pylori-related diseases, further work is required to clarify the roles of H. pylori virulence factors.

Helicobacter pylori infection

Science.gov (United States)

... this page: //medlineplus.gov/ency/article/007715.htm Helicobacter pylori infection To use the sharing features on this page, please enable JavaScript. Helicobacter pylori ( H pylori ) is a type of bacteria that ...

Helicobacter pylori HP1034 (ylxH) is required for motility

NARCIS (Netherlands)

van Amsterdam, Karin; van der Ende, Arie

2004-01-01

Background. Helicobacter pylori motility is essential for the colonization and persistence in the human gastric mucosa. So far, more than 50 genes have been described to play a role in flagellar biosynthesis. H. pylori YlxH (HP1034) is annotated as an ATP-binding protein. However, H. pylori YlxH

Helicobacter pylori infection and atrophic gastritis | Ebule | African ...

African Journals Online (AJOL)

Background: Helicobacter pylori-infection associated gastritis is known to be a significant risk factor of gastric cancer. Serum levels of Gastrin-17 and Pepsinogen1which are respectively biomarkers of gastric antral and corpus mucosal activity are well known parameters of atrophic gastritis. Objectives: To determine the ...

Consensus on the clinical management, screening-to-treat, and surveillance of Helicobacter pylori infection to improve gastric cancer control on a nationwide scale.

Science.gov (United States)

Sheu, Bor-Shyang; Wu, Ming-Shiang; Chiu, Cheng-Tang; Lo, Jing-Chuan; Wu, Deng-Chyang; Liou, Jyh-Ming; Wu, Chun-Ying; Cheng, Hsiu-Chi; Lee, Yi-Chia; Hsu, Ping-I; Chang, Chun-Chao; Chang, Wei-Lun; Lin, Jaw-Town

2017-06-01

Previous international consensus statements provided general policies for the management of Helicobacter pylori infection. However, there are geographic differences in the prevalence and antimicrobial resistance of H. pylori, and in the availability of medications and endoscopy. Thus, nationwide or regional consensus statements are needed to improve control of H. pylori infection and gastric cancer. This consensus statement for management of H. pylori in Taiwan has three major sections: (1) optimal diagnosis and indications; (2) current treatment strategies; and (3) screening-to-treat and surveillance for control of gastric cancer. The literature review emphasized recent data for development of draft statements and determination of levels of evidence. Twenty-five Taiwan experts conducted a consensus conference, by a modified Delphi process, to modify the draft statements. Consensus, defined as an agreement of least 80% of the experts, and recommendation grade were determined by anonymous voting. There were 24 consensus statements. Section 1 has seven statements on recommendations for the diagnosis and indications for treatment of H. pylori infection. Section 2 has 10 statements that provide an updated treatment algorithm for first-line, second-line, and third-line regimens. Section 3 has seven statements regarding H. pylori eradication for reducing the risk of gastric cancer, with a cost-benefit analysis. After H. pylori eradication, the consensus highlights the use of endoscopic surveillance and/or chemoprevention to further reduce the burden of gastric cancer. This consensus statement has updated recommendations for improving the clinical management of H. pylori infection in areas such as Taiwan, which have high prevalence of H. pylori infection and gastric cancer. © 2017 The Authors. Helicobacter Published by John Wiley & Sons Ltd.

Gastric mucosa-associated lymphoid tissue lymphomas and Helicobacter pylori infection: A Colombian perspective

Institute of Scientific and Technical Information of China (English)

Sally Yepes; Maria Mercedes Torres; Carlos Saavedra; Rafael Andrade

2012-01-01

AIM:To assess the significance of chromosome translocation t(11;18)(q21;q21),B-cell lymphoma 10 (BCL-10)protein and Helicobacter pylori (H.pylori) infection in gastric mucosa-associated lymphoid tissue (MALT) lymphoma in Colombia.METHODS:Fifty cases of gastric MALT lymphoma and their respective post-treatment follow-up biopsies were examined to assess the presence of the translocation t(11;18)(q21;q21) as identified by fluorescence in situ hybridization; to detect protein expression patterns of BCL10 using immunohistochemistry; and for evaluation of tumor histology to determine the correlation of these factors and resistance to H.pylori eradication.RESULTS:Infection with H.pylori was confirmed in all cases of gastric MALT lymphoma in association with chronic gastritis.Bacterial eradication led to tumor regression in 66％ of cases.The translocation t(11;18)(q21;q21) was not present in any of these cases,nor was there evidence of tumor transformation to diffuse large B-cell lymphoma.Thirty-four percent of the patients showed resistance to tumor regression,and within this group,7 cases,representing 14％ of all those analyzed,were considered to be t(11;18)(q21;q21)-positive gastric MALT lymphomas.Protein expression of BCL10 in the nucleus was associated with the presence of translocation and treatment resistance.Cases that were considered unresponsive to therapy were histologically characterized by the presence of homogeneous tumor cells and a lack of plasmacytic differentiation.Responder cases exhibited higher cellular heterogeneity and a greater frequency of plasma cells.CONCLUSION:Both t(11;18)(q21;q21)-positive MALT lymphoma cases and those with nuclear BCL10 expression are considered resistant to H,pylori eradication.It is suggested that chronic antigenic stimulation is not a dominant event in resistant cases.

Helicobacter pylori eradication therapy: A review of current trends ...

African Journals Online (AJOL)

Helicobacter pylori has been implicated in the formation of chronic gastritis, peptic ulcer disease, mucosa‑associated lymphoid tissue lymphoma and gastric cancer. Eradication of H. Pylori has been recommended as treatment and prevention for these complications. This review is based on a search of Medline, the ...

Alteration in Methylation Pattern of Retinoblastoma 1 Gene Promotor Region in Intestinal Metaplasia with or without Helicobacter pylori and Gastric Cancer Patients.

Science.gov (United States)

Boyacioglu, Seda Orenay; Kasap, Elmas; Yuceyar, Hakan; Korkmaz, Mehmet

2016-01-01

Helicobacter pylori, intestinal metaplasia (IM), and gene methylation play important roles in gastric carcinogenesis. However, the association among H. pylori infection, IM, gastric cancer (GC), and gene methylation is not fully understood. Cell cycle control involving retinoblastoma 1 (RB1) gene is one of the main regulatory pathways reported to be altered in gastric carcinogenesis. The purpose of this research is to assess the methylation status of RB1 gene in GC and IM with or without H. pylori infection, and to discuss the possible role of H. pylori-induced RB1 gene methylation in the mechanism of gastric carcinogenesis. The methylation profile of RB1 gene was analyzed by sodium bisulfite modification and methylation-specific PCR in GC (n = 24), IM patients with H. pylori positive (n = 20) and negative (n = 20), and control subjects (n = 20). According to methylation levels in RB1 gene; the high correlation values were detected between H. pylori positive-IM group and GC group, and between H. pylori positive-IM and H. pylori negative-IM groups (p gene. High methylation levels in RB1 gene in H. pylori positive individuals may suggest an elevated risk of gastric cancer occurrence.

Phylogeographic origin of Helicobacter pylori determines host-adaptive responses upon coculture with gastric epithelial cells.

Science.gov (United States)

Sheh, Alexander; Chaturvedi, Rupesh; Merrell, D Scott; Correa, Pelayo; Wilson, Keith T; Fox, James G

2013-07-01

While Helicobacter pylori infects over 50% of the world's population, the mechanisms involved in the development of gastric disease are not fully understood. Bacterial, host, and environmental factors play a role in disease outcome. To investigate the role of bacterial factors in H. pylori pathogenesis, global gene expression of six H. pylori isolates was analyzed during coculture with gastric epithelial cells. Clustering analysis of six Colombian clinical isolates from a region with low gastric cancer risk and a region with high gastric cancer risk segregated strains based on their phylogeographic origin. One hundred forty-six genes had increased expression in European strains, while 350 genes had increased expression in African strains. Differential expression was observed in genes associated with motility, pathogenicity, and other adaptations to the host environment. European strains had greater expression of the virulence factors cagA, vacA, and babB and were associated with increased gastric histologic lesions in patients. In AGS cells, European strains promoted significantly higher interleukin-8 (IL-8) expression than did African strains. African strains significantly induced apoptosis, whereas only one European strain significantly induced apoptosis. Our data suggest that gene expression profiles of clinical isolates can discriminate strains by phylogeographic origin and that these profiles are associated with changes in expression of the proinflammatory and protumorigenic cytokine IL-8 and levels of apoptosis in host epithelial cells. These findings support the hypothesis that bacterial factors determined by the phylogeographic origin of H. pylori strains may promote increased gastric disease.

Correlation of Helicobacter pylori genotypes with gastric histopathology in the central region of a South-European country

OpenAIRE

Almeida, N; Donato, MM; Romãozinho, JM; Luxo, C; Cardoso, O; Cipriano, MA; Marinho, C; Fernandes, A; Sofia, C

2015-01-01

BACKGROUND: Outcome of Helicobacter pylori (H. pylori) infection results from interaction of multiple variables including host, environmental and bacterial-associated virulence factors. AIM: This study aimed to investigate the correlation of cagA, cagE, vacA, iceA and babA2 genotypes with gastric histopathology and disease phenotype in the central region of a South-European country. METHODS: This prospective study involved 148 infected patients (110 female; mean age 43.5 ± 13.4...

Gastritis crónica antral por Helicobacter pylori en la infancia Chronic antral gastritis induced by Helicobacter pylori in children

Directory of Open Access Journals (Sweden)

Martha M. Gámez Escalona

2008-03-01

Full Text Available INTRODUCCIÓN. La investigación tiene como objetivos conocer la frecuencia de infección por Helicobacter pylori en los niños con gastritis crónica antral, estimar las diferencias en el comportamiento histológico de esta entidad en los niños con infección por Helicobacter pylori y sin ella, e identificar la posible relación entre la edad y las características histológicas de la gastritis crónica antral por Helicobacter pylori. MÉTODO. Se tomó como universo de estudio la totalidad de biopsias gástricas procesadas en el Hospital Pediátrico Provincial de Holguín, entre enero de 1991 y diciembre del 2004. Se determinó una muestra de 192 niños con diagnóstico histológico de gastritis crónica antral. Las biopsias fueron reevaluadas para detectar infección por Helicobacter pylori y su densidad de colonización junto a la actividad y la gravedad de las lesiones de la gastritis. RESULTADOS. Se encontró infección por Helicobacter pylori en el 67,7 % de los pacientes. Las formas activas predominaron en los casos con infección por Helicobacter pylori (116/130 a diferencia de quienes no tenían infección (5/62. Se identificó una relación estadísticamente significativa (p INTRODUCTION. The objective of this investigation is to know the frequency of infection caused by Helicobacter pylori in children with chronic antral gastritis, to estimate the differences in the histological behavior of this entity in children with infection due to Helicobacter pylori and without it, and to identify the possible relation existing between age and the histgological characteristics of chronic antral gastritis caused by Helicobacter pylori. METHODS. All the gastric biopsies processed in the Provincial Pediatric Hospital of Holguin from January 1991 to December 2004 were included in the study group. A sample of 192 children with histological diagnosis of chronic antral gastritis was determined. The biopsies were reevaluated to detect Helicobacter

Anti-Helicobacter pylori and Anti-Inflammatory Effects and Constituent Analysis of Modified Xiaochaihutang for the Treatment of Chronic Gastritis and Gastric Ulcer

Directory of Open Access Journals (Sweden)

Xin Chen

2018-01-01

Full Text Available Chronic gastritis and gastric ulcers are prevalent throughout the world and are considered to be a global health problem. Modified Xiaochaihutang (MXCHT prescription is broadly used in traditional medicine hospital for the treatment of gastritis. In order to assess the anti-Helicobacter pylori (H. pylori effect of MXCHT, agar diffusion method in vitro and fluid dilution method for the minimal inhibitory concentration (MIC were established. The anti-inflammatory effects were then evaluated using mouse ear edema model and rat paw edema model. The ethanol-induced gastric ulcer method was employed to verify the gastroprotective effect of active extracts in MXCHT. HPLC-TOF-MS/MS was used for analyzing the possible active constituents after oral administration of effective extracts in ethanol-induced gastric ulcer models. MXCHT and 4 different extracts of the bacterial inhibition diameter and MIC were dramatically decreased compared with control group, showing anti-Helicobacter pylori effects. High dose groups of MXCHT, water extract, EtOAc extract, and n-BuOH extract displayed significant anti-inflammatory effects in xylene-induced mouse ear edema model and carrageenan-induced rat paw edema model test. MXCHT and all active extracts exhibited gastroprotective activity and prevented gastric lesions induced by ethanol in rats. 4 prototype components and 4 metabolites were identified after oral administration of EtOAc extract. In addition, 6 prototype components and 6 metabolites were identified in n-BuOH extract. MXCHT, EtOAc extract, and n-BuOH extract demonstrate gastroprotective effects through anti-Helicobacter pylori and anti-inflammatory activities. Thus, this prescription may be a suitable natural source for the prevention and treatment of chronic gastritis and gastric ulcers.

Helicobacter Pylori: Vías de transmisión

Directory of Open Access Journals (Sweden)

Martín Alonso Bayona Rojas

2017-09-01

Full Text Available La importancia de Helicobacter pylori como agente etiológico en diversas patologías se asocia con una alta tasa de morbimortalidad y genera un fuerte impacto en nuestra sociedad y en los sistemas de salud. En ese sentido, la presente revisión de literatura pretende analizar y comprender la ruta de transmisión de este patógeno con el objeto de prevenir su propagación. El conocimiento de la epidemiología y el modo de transmisión permite prevenir la propagación e identificar poblaciones de alto riesgo, especialmente en áreas que tienen altas tasas de linfoma gástrico, cáncer gástrico y úlcera gástrica. Helicobacter Pylori: Transmission RoutesAbstractThe importance of Helicobacter pylori as an etiological agent in several pathologies is associated with a high rate of morbi mortality, which generates a strong impact in our society and in the health systems. The present literature review sought to analize and understand the route of transmission of this pathogen to prevent its spread. Knowledge of the epidemiology and mode of transmission of this pathogen is important to prevent its spread and be useful in identifying high-risk populations, especially in areas with high rates of gastric lymphoma, gastric cancer, and gastric ulcer

Infecção por Helicobacter pylori e câncer gástrico: freqüência de cepas patogênicas cagA e vacA em pacientes com câncer gástrico Helicobacter pylori and gastric cancer: distribution of cagA and vacA genotypes in patients with gastric carcinoma

Directory of Open Access Journals (Sweden)

Cristiane Melissa Thomazini

2006-02-01

Full Text Available INTRODUÇÃO: Apesar da alta freqüência de infecção por Helicobacter pylori na população, somente uma minoria de indivíduos desenvolve câncer gástrico. É provável que a colonização da mucosa por cepas patogênicas, levando a maior agressão e inflamação da mucosa seja um dos elos da cadeia de eventos da oncogênese gástrica. OBJETIVOS: Investigar a freqüência de cepas patogênicas cagA e vacA do H. pylori em pacientes com câncer gástrico. MATERIAL E MÉTODOS: Foram estudados retrospectivamente 42 pacientes com câncer gástrico. A infecção por H. pylori foi avaliada por exame histológico e pelo PCR para identificação dos genótipos cagA e vacA em amostras de material fixado em formalina e incluído em parafina. RESULTADOS: A análise histológica permitiu a visualização direta do H. pylori em 85,7% dos casos, e o método de PCR para o gene urease C demonstrou a presença de DNA da bactéria em 95% dos casos. O gene cagA foi detectado em amostras de 23 pacientes (54,7% com câncer gástrico. O alelo s1 do gene vacA foi identificado em amostras de 24 pacientes (57,1% e o alelo m1, em amostras de 26 pacientes (61,9%. Os alelos s1 e m1 foram identificados simultaneamente em 24 pacientes (57,1%. O alelo s2 foi identificado em amostras de quatro pacientes (9,5%, e o alelo m2, em amostras de três pacientes (7,1%. A freqüência de infecção pelo Helicobacter pylori foi similar em ambos os tipos histológicos de câncer gástrico (intestinal e difuso. CONCLUSÕES: Os resultados confirmam a relevância dos genótipos patogênicos cagA e vacA do H. pylori para lesões orgânicas significativas tais como o câncer gástrico, sugerindo a participação dessa bactéria na cadeia de eventos da oncogênese gástrica.BACKGROUND: The rates of Helicobacter pylori infection are very high worldwide, but only a minority of infected patients develop gastric carcinoma. This might be related, among several factors, to the colonization of

The EPIYA-ABCC motif pattern in CagA of Helicobacter pylori is associated with peptic ulcer and gastric cancer in Mexican population.

Science.gov (United States)

Beltrán-Anaya, Fredy Omar; Poblete, Tomás Manuel; Román-Román, Adolfo; Reyes, Salomón; de Sampedro, José; Peralta-Zaragoza, Oscar; Rodríguez, Miguel Ángel; del Moral-Hernández, Oscar; Illades-Aguiar, Berenice; Fernández-Tilapa, Gloria

2014-12-24

Helicobacter pylori chronic infection is associated with chronic gastritis, peptic ulcer, and gastric cancer. Cytotoxin-associated gene A (cagA)-positive H. pylori strains increase the risk of gastric pathology. The carcinogenic potential of CagA is linked to its polymorphic EPIYA motif variants. The goals of this study were to investigate the frequency of cagA-positive Helicobacter pylori in Mexican patients with gastric pathologies and to assess the association of cagA EPIYA motif patterns with peptic ulcer and gastric cancer. A total of 499 patients were studied; of these, 402 had chronic gastritis, 77 had peptic ulcer, and 20 had gastric cancer. H. pylori DNA, cagA, and the EPIYA motifs were detected in total DNA from gastric biopsies by PCR. The type and number of EPIYA segments were determined by the electrophoretic patterns. To confirm the PCR results, 20 amplicons of the cagA 3' variable region were sequenced, and analyzed in silico, and the amino acid sequence was predicted with MEGA software, version 5. The odds ratio (OR) was calculated to determine the associations between the EPIYA motif type and gastric pathology and between the number of EPIYA-C segments and peptic ulcers and gastric cancer. H. pylori DNA was found in 287 (57.5%) of the 499 patients, and 214 (74%) of these patients were cagA-positive. The frequency of cagA-positive H. pylori was 74.6% (164/220) in chronic gastritis patients, 73.6% (39/53) in peptic ulcer patients, and 78.6% (11/14) in gastric cancer patients. The EPIYA-ABC pattern was more frequently observed in chronic gastritis patients (79.3%, 130/164), while the EPIYA-ABCC sequence was more frequently observed in peptic ulcer (64.1%, 25/39) and gastric cancer patients (54.5%, 6/11). However, the risks of peptic ulcer (OR = 7.0, 95% CI = 3.3-15.1; p peptic ulcers and gastric cancer.

Helicobacter pylori induces vascular endothelial growth factor production in gastric epithelial cells through hypoxia-inducible factor-1α-dependent pathway.

Science.gov (United States)

Kang, Min-Jung; Song, Eun-Jung; Kim, Bo-Yeon; Kim, Dong-Jae; Park, Jong-Hwan

2014-12-01

Although Helicobacter pylori have been known to induce vascular endothelial growth factor (VEGF) production in gastric epithelial cells, the precise mechanism for cellular signaling is incompletely understood. In this study, we investigated the role of bacterial virulence factor and host cellular signaling in VEGF production of H. pylori-infected gastric epithelial cells. We evaluated production of VEGF, activation of nuclear factor nuclear factor-kappaB (NF-κB) and mitogen-activated protein kinases (MAPKs) and hypoxia-inducible factor-1α (HIF-1α) stabilization in gastric epithelial cells infected with H. pylori WT or isogenic mutants deficient in type IV secretion system (T4SS). H. pylori induced VEGF production in gastric epithelial cells via both T4SS-dependent and T4SS-independent pathways, although T4SS-independent pathway seems to be the dominant signaling. The inhibitor assay implicated that activation of NF-κB and MAPKs is dispensable for H. pylori-induced VEGF production in gastric epithelial cells. H. pylori led to HIF-1α stabilization in gastric epithelial cells independently of T4SS, NF-κB, and MAPKs, which was essential for VEGF production in these cells. N-acetyl-cysteine (NAC), a reactive oxygen species (ROS) inhibitor, treatment impaired H. pylori-induced HIF-1α stabilization and VEGF production in gastric epithelial cells. We defined the important role of ROS-HIF-1α axis in VEGF production of H. pylori-infected gastric epithelial cells, and bacterial T4SS has a minor role in H. pylori-induced VEGF production of gastric epithelial cells. © 2014 John Wiley & Sons Ltd.

Medicinal plants in the treatment of Helicobacter pylori infections.

Science.gov (United States)

Safavi, Maliheh; Shams-Ardakani, Mohammadreza; Foroumadi, Alireza

2015-07-01

Helicobacter pylori is a small, spiral, Gram-negative bacillus that plays a role in the pathogenesis of a number of diseases ranging from asymptomatic gastritis to gastric cancer. Schedule compliance, antibiotic drug resistance, and side-effects of triple or quadruple therapy have led to research for novel candidates from plants. The purpose of this paper is to review the most potent medicinal plants of recently published literature with anti-H. pylori activity. For centuries, herbals have been used by traditional healers around the world to treat various gastrointestinal tract disorders such as dyspepsia, gastritis, and peptic ulcer disease. The mechanism of action by which these botanicals exert their therapeutic properties has not been completely and clearly elucidated. Anti-H. pylori properties may be one of the possible mechanisms by which gastroprotective herbs treat gastrointestinal tract disorders. Electronic databases such as PubMed, Google scholar, EBSCO, and local databases were explored for medicinal plants with anti-H. pylori properties between 1984 and 2013 using key words "medicinal plants" and "Helicobacter pylori" or "anti-Helicobacter pylori". A total of 43 medicinal plant species belonging to 27 families including Amaryllidaceae, Anacardiaceae, Apiaceae, Apocynaceae, Asclepiadoideae, Asteraceae, Bignoniaceae, Clusiaceae, Chancapiedra, Combretaceae, Cyperaceae, Euphorbiaceae, Fabaceae, Geraniaceae, Lamiaceae, Lauraceae, Lythraceae, Menispermaceae, Myristicaceae, Myrtaceae, Oleaceae, Papaveraceae, Plumbaginaceae, Poaceae, Ranunculaceae, Rosaceae, and Theaceae were studied as herbs with potent anti-H. pylori effects. Traditional folk medicinal use of some of these plants to treat gastric infections is substantiated by the antibacterial activity of their extracts against H. pylori.

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

International Nuclear Information System (INIS)

Zhao, Hangyong; Zhu, Huanghuang; Lin, Zhou; Lin, Gang; Lv, Guoqiang

2015-01-01

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

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.

Oral and gastric helicobacter pylori : Effects and associations

OpenAIRE

Veiga, Nélio; Pereira, Carlos; Resende, Carlos; Amaral, Odete; Ferreira, Manuela; Nelas, Paula; Chaves, Claudia; Duarte, João; Cirnes, Luis; Machado, José Carlos; Ferreira, Paula; Correia, Ilídio J.

2015-01-01

Introduction This study consisted in the comparison of the prevalence of Helicobacter pylori (H. pylori) present in the stomach and in saliva of a sample of Portuguese adolescents and the assessment of the association between H. pylori infection with socio-demographic variables and prevalence of dental caries. Materials and Methods A cross-sectional study was designed including a sample of 447 adolescents aged 12 to 19 years old, attending a public school in S?t?o, Portugal. A questionnaire a...

Helicobacter pylori promotes angiogenesis depending on Wnt/beta-catenin-mediated vascular endothelial growth factor via the cyclooxygenase-2 pathway in gastric cancer

International Nuclear Information System (INIS)

Liu, Ningning; Zhou, Ning; Chai, Ni; Liu, Xuan; Jiang, Haili; Wu, Qiong; Li, Qi

2016-01-01

Helicobacter pylori is an important pathogenic factor in gastric carcinogenesis. Angiogenesis (i.e., the growth of new blood vessels) is closely associated with the incidence and development of gastric cancer. Our previous study found that COX-2 stimulates gastric cancer cells to induce expression of the angiogenic growth factor VEGF through an unknown mechanism. Therefore, the aim of this study was to clarify the role of angiogenesis in H. pylori-induced gastric cancer development. To clarify the relationship between H. pylori infection and angiogenesis, we first investigated H. pylori colonization, COX-2, VEGF, beta-catenin expression, and microvessel density (MVD) in gastric cancer tissues from 106 patients. In addition, COX-2, phospho-beta-catenin, and beta-catenin expression were measured by western blotting, and VEGF expression was measured by ELISA in H. pylori-infected SGC7901 and MKN45 human gastric cancer cells. H. pylori colonization occurred in 36.8 % of gastric carcinoma samples. Furthermore, COX-2, beta-catenin, and VEGF expression, and MVD were significantly higher in H. pylori-positive gastric cancer tissues than in H. pylori-negative gastric cancer tissues (P < 0.01). H. pylori infection was not related to sex or age in gastric cancer patients, but correlated with the depth of tumor invasion, lymph node metastasis, and tumor–node–metastasis stage (P < 0.05) and correlated with the COX-2 expression and beta-catenin expression(P < 0.01). Further cell experiments confirmed that H. pylori infection upregulated VEGF in vitro. Further analysis revealed that H. pylori-induced VEGF expression was mediated by COX-2 via activation of the Wnt/beta-catenin pathway. The COX-2/Wnt/beta-catenin/VEGF pathway plays an important role in H. pylori-associated gastric cancer development. The COX-2/Wnt/beta-catenin pathway is therefore a novel therapeutic target for H. pylori-associated gastric cancers

Gastric mucosal status in populations with a low prevalence of Helicobacter pylori in Indonesia.

Directory of Open Access Journals (Sweden)

Muhammad Miftahussurur

Full Text Available In Indonesia, endoscopy services are limited and studies about gastric mucosal status by using pepsinogens (PGs are rare. We measured PG levels, and calculated the best cutoff and predictive values for discriminating gastric mucosal status among ethnic groups in Indonesia. We collected gastric biopsy specimens and sera from 233 patients with dyspepsia living in three Indonesian islands. When ≥5.5 U/mL was used as the best cutoff value of Helicobacter pylori antibody titer, 8.6% (20 of 233 were positive for H. pylori infection. PG I and II levels were higher among smokers, and PG I was higher in alcohol drinkers than in their counterparts. PG II level was significantly higher, whereas PG I/II ratios were lower in H. pylori-positive than in H. pylori-negative patients. PG I/II ratios showed a significant inverse correlation with the inflammation and atrophy scores of the antrum. The best cutoff values of PG I/II were 4.05 and 3.55 for discriminating chronic and atrophic gastritis, respectively. PG I, PG II, and PG I/II ratios were significantly lower in subjects from Bangli than in those from Makassar and Surabaya, and concordant with the ABC group distribution; however, group D (H. pylori negative/PG positive was the lowest in subjects from Bangli. In conclusion, validation of indirect methods is necessary before their application. We confirmed that serum PG level is a useful biomarker determining chronic gastritis, but a modest sensitivity for atrophic gastritis in Indonesia. The ABC method should be used with caution in areas with a low prevalence of H. pylori.

Influence of cure of Helicobacter pylori infection on gastric acidity and gastroesophageal reflux: study by 24-h pH monitoring in patients with gastric or duodenal ulcer.

Science.gov (United States)

Fukuchi, Takumi; Ashida, Kiyoshi; Yamashita, Hiroshi; Kiyota, Naomi; Tsukamoto, Reiko; Takahashi, Hajime; Ito, Dai; Nagamatsu, Ryousuke

2005-04-01

Whether or not the eradication of Helicobacter pylori is a risk factor for reflux esophagitis (RE) is a question at issue. To find an answer, it is necessary to clarify the influence of H. pylori eradication on the mechanism of RE. The authors investigated the influence of H. pylori eradication on gastric acidity and gastroesophageal reflux in ten gastric ulcer (GU) patients and ten duodenal ulcer (DU) patients by 24-h simultaneous determination of pH in the stomach and esophagus. Though the results indicated enhanced gastric acidity in GU patients at night after H. pylori eradication, no such influence was observed in DU patients. No significant changes in gastroesophageal reflux occurred in GU or DU patients before and after H. pylori eradication. RE after H. pylori eradication occurred in only one patient, with GU. This patient had several risk factors for RE, such as obesity, male sex, and dietary habits to add to the increase in gastric acidity at night that occurred after H. pylori eradication. No increase in gastroesophageal reflux occurred in any DU patients or in the other GU patients that demonstrated enhanced gastric acidity at night after H. pylori eradication. The cure of H. pylori infection does not, by itself, cause RE in patients who have few other risk factors for RE.

Urease from Helicobacter pylori is inactivated by sulforaphane and other isothiocyanates

Science.gov (United States)

Fahey, Jed W.; Stephenson, Katherine K.; Wade, Kristina L.; Talalay, Paul

2013-01-01

Infections by Helicobacter pylori are very common, causing gastroduodenal inflammation including peptic ulcers, and increasing the risk of gastric neoplasia. The isothiocyanate (ITC) sulforaphane [SF; 1-isothiocyanato-4-(methylsulfinyl)butane] derived from edible crucifers such as broccoli is potently bactericidal against Helicobacter, including antibiotic-resistant strains, suggesting a possible dietary therapy. Gastric H. pylori infections express high urease activity which generates ammonia, neutralizes gastric acidity, and promotes inflammation. The finding that SF inhibits (inactivates) urease (jack bean and Helicobacter) raised the issue of whether these properties might be functionally related. The rates of inactivation of urease activity depend on enzyme and SF concentrations and show first order kinetics. Treatment with SF results in time-dependent increases in the ultraviolet absorption of partially purified Helicobacter urease in the 280–340 nm region. This provides direct spectroscopic evidence for the formation of dithiocarbamates between the ITC group of SF and cysteine thiols of urease. The potencies of inactivation of Helicobacter urease by isothiocyanates structurally related to SF were surprisingly variable. Natural isothiocyanates closely related to SF, previously shown to be bactericidal (berteroin, hirsutin, phenethyl isothiocyanate, alyssin, and erucin), did not inactivate urease activity. Furthermore, SF is bactericidal against both urease positive and negative H. pylori strains. In contrast, some isothiocyanates such as benzoyl-ITC, are very potent urease inactivators, but are not bactericidal. The bactericidal effects of SF and other ITC against Helicobacter are therefore not obligatorily linked to urease inactivation, but may reduce the inflammatory component of Helicobacter infections. PMID:23583386

Serological response to Helicobacter pylori infection among Latin American populations with contrasting risks of gastric cancer

Science.gov (United States)

Camargo, M. Constanza; Beltran, Mauricio; Conde-Glez, Carlos; Harris, Paul R.; Michel, Angelika; Waterboer, Tim; Flórez, Astrid Carolina; Torres, Javier; Ferreccio, Catterina; Sampson, Joshua N.; Pawlita, Michael; Rabkin, Charles S.

2015-01-01

Gastric cancer is a rare outcome of chronic Helicobacter pylori infection. Serologic profiles may reveal bacterial, environmental and/or host factors associated with cancer risk. We therefore compared specific anti-H. pylori antibodies among populations with at least 2-fold differences in gastric cancer mortality from Mexico, Colombia and Chile. Our study included 1,776 adults (mean age 42 years) from three nationally representative surveys, equally divided between residents of high- and low-risk areas. Antibodies to 15 immunogenic H. pylori antigens were measured by fluorescent bead-based multiplex assays; results were summarized to identify overall H. pylori seropositivity. We used logistic regression to model associations between antibody seroreactivity and regional cancer risk (high vs. low), adjusting for country, age and sex. Both risk areas had similar H. pylori seroprevalence. Residents in high- and low-risk areas were seroreactive to a similar number of antigens (means 8.2 vs. 7.9, respectively; adjusted-odds ratio, OR: 1.02, p=0.05). Seroreactivities to Catalase and the known virulence proteins CagA and VacA were each significantly (p<0.05) associated with residence in high-risk areas, but ORs were moderate (1.26, 1.42, and 1.41, respectively) and their discriminatory power was low (ROC area under curve <0.6). The association of Catalase was independent from effects of either CagA or VacA. Sensitivity analyses for antibody associations restricted to H. pylori-seropositive individuals generally replicated significant associations. Our findings suggest that humoral responses to H. pylori are insufficient to distinguish high and low gastric cancer risk in Latin America. Factors determining population variation of gastric cancer burden remain to be identified. PMID:26178251

Helicobacter pylori SabA Adhesin in Persistent Infection and Chronic Inflammation

OpenAIRE

Mahdavi, Jafar; Sondén, Berit; Hurtig, Marina; Olfat, Farzad O.; Forsberg, Lina; Roche, Niamh; Ångström, Jonas; Larsson, Thomas; Teneberg, Susann; Karlsson, Karl-Anders; Altraja, Siiri; Wadström, Torkel; Kersulyte, Dangeruta; Berg, Douglas E.; Dubois, Andre

2002-01-01

Helicobacter pylori adherence in the human gastric mucosa involves specific bacterial adhesins and cognate host receptors. Here, we identify sialyl-dimeric-Lewis x glycosphingolipid as a receptor for H. pylori and show that H. pylori infection induced formation of sialyl-Lewis x antigens in gastric epithelium in humans and in a Rhesus monkey. The corresponding sialic acid-binding adhesin (SabA) was isolated with the "retagging" method, and the underlying sabA gene (JHP662/HP0725) wa...

Medicinal plant activity on Helicobacter pylori related diseases.

Science.gov (United States)

Wang, Yuan-Chuen

2014-08-14

More than 50% of the world population is infected with Helicobacter pylori (H. pylori). The bacterium highly links to peptic ulcer diseases and duodenal ulcer, which was classified as a group I carcinogen in 1994 by the WHO. The pathogenesis of H. pylori is contributed by its virulence factors including urease, flagella, vacuolating cytotoxin A (VacA), cytotoxin-associated gene antigen (Cag A), and others. Of those virulence factors, VacA and CagA play the key roles. Infection with H. pylori vacA-positive strains can lead to vacuolation and apoptosis, whereas infection with cagA-positive strains might result in severe gastric inflammation and gastric cancer. Numerous medicinal plants have been reported for their anti-H. pylori activity, and the relevant active compounds including polyphenols, flavonoids, quinones, coumarins, terpenoids, and alkaloids have been studied. The anti-H. pylori action mechanisms, including inhibition of enzymatic (urease, DNA gyrase, dihydrofolate reductase, N-acetyltransferase, and myeloperoxidase) and adhesive activities, high redox potential, and hydrophilic/hydrophobic natures of compounds, have also been discussed in detail. H. pylori-induced gastric inflammation may progress to superficial gastritis, atrophic gastritis, and finally gastric cancer. Many natural products have anti-H. pylori-induced inflammation activity and the relevant mechanisms include suppression of nuclear factor-κB and mitogen-activated protein kinase pathway activation and inhibition of oxidative stress. Anti-H. pylori induced gastric inflammatory effects of plant products, including quercetin, apigenin, carotenoids-rich algae, tea product, garlic extract, apple peel polyphenol, and finger-root extract, have been documented. In conclusion, many medicinal plant products possess anti-H. pylori activity as well as an anti-H. pylori-induced gastric inflammatory effect. Those plant products have showed great potential as pharmaceutical candidates for H. pylori

The Prevalence of Helicobacter pylori Virulence Factors in Bhutan, Vietnam, and Myanmar Is Related to Gastric Cancer Incidence

Directory of Open Access Journals (Sweden)

Tran Thi Huyen Trang

2015-01-01

Full Text Available Gastric cancer is a significant health problem in Asia. Although the prevalence of Helicobacter pylori infection is similar in Bhutan, Vietnam, and Myanmar, the incidence of gastric cancer is highest in Bhutan, followed by Vietnam and Myanmar. We hypothesized that H. pylori virulence factors contribute to the differences. The status of cagA, vacA, jhp0562, and β-(1,3galT(jhp0563 was examined in 371 H. pylori-infected patients from Bhutan, Vietnam, and Myanmar. Each virulence factor could not explain the difference of the incidence of gastric cancer. However, the prevalence of quadruple-positive for cagA, vacA s1, vacA m1, and jhp0562-positive/β-(1,3galT-negative was significantly higher in Bhutan than in Vietnam and Myanmar and correlated with gastric cancer incidence. Moreover, gastritis-staging scores measured by histology of gastric mucosa were significantly higher in quadruple-positive strains. We suggest that the cagA, vacA s1, vacA m1, and jhp0562-positive/β-(1,3galT-negative genotype may play a role in the development of gastric cancer.

Immunohistochemical testing for Helicobacter Pylori existence in neoplasms of the colon

Directory of Open Access Journals (Sweden)

Yasar Nurgul

2008-08-01

Full Text Available Abstract Background Helicobacter pylori is a common pathogen, and its prevalence varies with socioeconomic conditions (10–80%. It has recently been recognized as a class I carcinogen in relation to gastric cancer. The aim of this study was to investigate the presence of Helicobacter pylori in neoplasms of the colon by immunohistochemical methods. Methods The polypectomy materials of 51 patients (19 male and 32 female who had undergone colonoscopic polypectomy were retrieved for retrospective examination. The endoscopic size and colonic localization of the polyps were recorded. Hematoxylin and eosin stains were evaluated according to histological type and grade of dysplasia. Biopsy stains were immunohistochemically treated with Helicobacter pylori antibodies by the streptavidine-biotin immunoperoxidase technique. Helicobacter pylori staining in the gastric mucosa was used as the control for the immunohistochemical method. Specimens were classified according to the presence of Helicobacter pylori under an optical microscope, and Helicobacter pylori positive specimens were stratified according to the respective staining pattern. Results Mean age was 61.88 ± 10.62 (40–82 years. Polyp sizes were 1.45 ± 0.92 (1–4 cm; and 25.5% of polyps were localized in the right colon, 68.6% in the left colon and 5.9% in the transverse colon. Presence of Helicobacter pylori was not correlated with localization (p > 0.05 or size of the polyps (p > 0.05. Eleven (21.6% of all specimens included in the study were Helicobacter pylori positive by immunohistochemical methods. Of the Helicobacter pylori positive specimens, the staining pattern was diffuse: Equivocal in 90.9%, nonspecific with a finely granular type concentrated on the luminal surface in 90.9%, dot-like granular in 54.5%, and spiral in 9.1%. Of the tubular polyps, 17.9% were H. pylori positive, and the staining pattern was equivocal in 100%, luminal in 85.7%, and dot-like granular in 57.1%. Of the

Epidemiology of Helicobacter pylori infection in dyspeptic Ghanaian patients.

Science.gov (United States)

Archampong, Timothy Nii Akushe; Asmah, Richard Harry; Wiredu, Edwin Kwame; Gyasi, Richard Kwasi; Nkrumah, Kofi Nyaako; Rajakumar, Kumar

2015-01-01

Helicobacter pylori is a gram-negative urease-producing bacterium causally linked with gastritis, peptic ulcer disease and gastric adenocarcinoma. Infection is more frequent and acquired at an earlier age in developing countries compared to European populations. The incidence of Helicobacter pylori infection in dyspeptic Ghanaian patients was 75.4%. However, epidemiological factors associated with infection vary across populations. This study used a cross-sectional design to consecutively sample dyspeptic patients at the Endoscopy Unit of the Korle-Bu Teaching Hospital, Accra between 2010 and 2012. The study questionnaire elicited their epidemiological clinical characteristics. Helicobacter pylori infection was confirmed by rapid-urease examination of antral biopsies at upper Gastro-intestinal endoscopy. The sample population of dyspeptic patients attending the Endoscopy Unit for upper GI endoscopy yielded 242 patients of which 47.5% were females. The age distribution of H. pylori-infection was even across most age - groups, ranging from 69.2% (61 - 70) years to 80% (21 - 30) years. Helicobacter pylori prevalence decreased across areas mapping to the three residential classes in accordance with increasing affluence with rural areas having the highest prevalence. The unemployed and patients in farming had relatively high Helicobacter pylori infection rates of 92.3% and 91.7% respectively. Helicobacter pylori is endemic in Ghana but the persistently high prevalence across age groups despite significant community anti-microbial use suggests likely recrudescence or re-infection from multiple sources in a developing country. Socio-cultural factors such as residential class and farming may be facilitating factors for its continued prevalence.

The Prevalence of Gastric Intestinal Metaplasia and Distribution of Helicobacter pylori Infection, Atrophy, Dysplasia, and Cancer in Its Subtypes.

Science.gov (United States)

Olmez, Sehmus; Aslan, Mehmet; Erten, Remzi; Sayar, Suleyman; Bayram, Irfan

2015-01-01

Objectives. Gastric intestinal metaplasia (IM) is frequently encountered and is considered a precursor of gastric adenocarcinoma. In the Van region of Turkey, gastric adenocarcinoma incidence is high but the prevalence of gastric IM is not known. Helicobacter pylori (H. pylori) infection is a main factor leading to atrophy, IM, and cancer development in the stomach. The aim of the current study was to investigate the prevalence of IM and its subtypes and the prevalence of H. pylori infection, atrophy, dysplasia, and cancer in gastric IM subtypes. Materials and Methods. This retrospective study was conducted on 560 IM among the 4050 consecutive patients who were undergoing esophagogastroduodenoscopy (EGD) with biopsy between June 2010 and October 2014. Clinical records and endoscopic and histopathologic reports of patients with IM were analyzed. Results. The prevalence of gastric IM was 13.8%. The prevalence of incomplete IM was statistically significantly higher than complete IM. Type III IM was the most frequent subtype. Conclusions. Gastric IM is a common finding in patients undergoing EGD with biopsy in this region. High prevalence of incomplete type IM, especially type III, can be associated with the high prevalence of gastric cancer in our region.

The Prevalence of Gastric Intestinal Metaplasia and Distribution of Helicobacter pylori Infection, Atrophy, Dysplasia, and Cancer in Its Subtypes

Directory of Open Access Journals (Sweden)

Sehmus Olmez

2015-01-01

Full Text Available Objectives. Gastric intestinal metaplasia (IM is frequently encountered and is considered a precursor of gastric adenocarcinoma. In the Van region of Turkey, gastric adenocarcinoma incidence is high but the prevalence of gastric IM is not known. Helicobacter pylori (H. pylori infection is a main factor leading to atrophy, IM, and cancer development in the stomach. The aim of the current study was to investigate the prevalence of IM and its subtypes and the prevalence of H. pylori infection, atrophy, dysplasia, and cancer in gastric IM subtypes. Materials and Methods. This retrospective study was conducted on 560 IM among the 4050 consecutive patients who were undergoing esophagogastroduodenoscopy (EGD with biopsy between June 2010 and October 2014. Clinical records and endoscopic and histopathologic reports of patients with IM were analyzed. Results. The prevalence of gastric IM was 13.8%. The prevalence of incomplete IM was statistically significantly higher than complete IM. Type III IM was the most frequent subtype. Conclusions. Gastric IM is a common finding in patients undergoing EGD with biopsy in this region. High prevalence of incomplete type IM, especially type III, can be associated with the high prevalence of gastric cancer in our region.

Lanthanum Deposition in the Stomach in the Absence of Helicobacter pylori Infection.

Science.gov (United States)

Iwamuro, Masaya; Urata, Haruo; Tanaka, Takehiro; Kawano, Seiji; Kawahara, Yoshiro; Kimoto, Katsuhiko; Okada, Hiroyuki

2018-03-15

In this case report, we describe two patients who showed a diffusely whitish mucosa in the posterior wall and the lesser curvature of the gastric body. The patients were serologically- and histopathologically-negative for Helicobacter pylori. Random biopsy specimens from the stomach revealed no regenerative changes, intestinal metaplasia, and/or foveolar hyperplasia in either of the patients. Although lanthanum deposition in the gastric mucosa has been reported to occur in close association with H. pylori-associated gastritis, our patients tested negative for H. pylori. These cases suggest that lanthanum deposition presents as whitish lesions in the gastric body in H. pylori-negative patients.

Effects of Helicobacter pylori infection on the expressions of Bax and Bcl-2 in patients with chronic gastritis and gastric cancer.

Science.gov (United States)

Bartchewsky, Waldemar; Martini, Mariana R; Squassoni, Aline C; Alvarez, Marisa C; Ladeira, Marcelo S P; Salvatore, Daisy M F; Trevisan, Miriam A; Pedrazzoli, José; Ribeiro, Marcelo L

2010-01-01

The aim of the present study is to evaluate the influence of Helicobacter pylori on Bax and Bcl-2 mRNA and protein levels in patients with chronic gastritis and gastric cancer. The study included 217 patients, of which 26 were uninfected; 127 had chronic gastritis and were H. pylori-positive, and 64 had gastric cancer. Bacterial genotypes were evaluated by PCR, and the expression values were determined by quantitative real-time PCR and immunohistochemistry. Our data showed that the up-regulationary effects of H. pylori infection on the pro-apoptotic gene, Bax, were stronger than its induction of Bcl-2; this effect may increase apoptosis in patients with chronic gastritis. In patients with gastric cancer, the up-regulation of the anti-apoptotic gene, Bcl-2, counteracted the pro-apoptotic effects of Bax, leading to a deregulation of apoptosis-associated gene expression, favoring cell proliferation. Thus, the disturbance in Bax and Bcl-2 balance, induced by H. pylori, might be important in gastric cancer development.

The role of helicobacter pylori infection in the pathogenesis of chronic urticaria

International Nuclear Information System (INIS)

Ghazzawi, I.M.; Obidat, N.A.

2004-01-01

Objective: To determine the prevalence of H. pylori infection in patients with idiopathic chronic urticaria (ICU) and to see if eradication of the bacterium affects the course of the urticaria. Patients and Methods: One hundred patients with idiopathic chronic urticaria and 43 healthy subjects (matched for age and sex) underwent serological testing for H. pylori infection. All patients with idiopathic chronic urticaria were examined for Helicobacter pylori infection with the /sup 13/C-urea test as well as the serological testing. Gastric biopsy was obtained from 36 patients. Patients with proven Helicobacter pylori infection were given treatment for 2 weeks. Six weeks afterwards they were tested again for Helicobacter pylori infection, and their urticaria was clinically assessed. Results: There was no significant difference in the seroprevalence of H. pylori infection between : idiopathic chronic urticaria patients and healthy subjects. Helicobacter pylori was detected in 76% of patients and 69.8% of controls. Out of the 76 patients treated, only 24 showed complete remission of their urticaria after successfully eradicating Helicobacter pylori infection, the others only having some improvement in their symptoms. Conclusion: Patients with idiopathic chronic urticaria have similar high rates of H. pylori infection as healthy subjects. Bacterium eradication is associated with improvement of urticaria symptoms, suggesting a possible role of Helicobacter pylori in the pathogenesis of this skin disorder. (author)

A comparative study of clinicopathological features between chronic cholecystitis patients with and without Helicobacter pylori infection in gallbladder mucosa.

Directory of Open Access Journals (Sweden)

Di Zhou

Full Text Available BACKGROUND: Helicobacter pylori has been isolated from 10%-20% of human chronic cholecystitis specimens but the characteristics of "Helicobacter pylori positive cholecystitis" remains unclear. This study aims to compare the clinicopathological features between chronic cholecystitis patients with and without Helicobacter pylori infection in gallbladder mucosa. METHODS: Three hundred and twenty-six chronic cholecystitis patients were divided into two groups according to whether Helicobacter pylori could be detected by culture, staining or PCR for Helicobacter 16s rRNA gene in gallbladder mucosa. Positive samples were sequenced for Helicobacter pylori-specific identification. Clinical parameters as well as pathological characteristics including some premalignant lesions and the expression levels of iNOS and ROS in gallbladder were compared between the two groups. RESULTS: Helicobacter pylori infection in gallbladder mucosa was detected in 20.55% of cholecystitis patients. These patients had a higher prevalence of acid regurgitation symptoms (p = 0.001, more histories of chronic gastritis (p = 0.005, gastric ulcer (p = 0.042, duodenal ulcer (p = 0.026 and higher presence of Helicobacter pylori in the stomach as compared to patients without Helicobacter pylori infection in the gallbladder mucosa. Helicobacter pylori 16s rRNA in gallbladder and gastric-duodenal mucosa from the same individual patient had identical sequences. Also, higher incidences of adenomyomatosis (p = 0.012, metaplasia (p = 0.022 and higher enhanced expressions of iNOS and ROS were detected in Helicobacter pylori infected gallbladder mucosa (p<0.05. CONCLUSIONS: Helicobacter pylori infection in gallbladder mucosa is strongly associated with Helicobacter pylori existed in stomach. Helicobacter pylori is also correlated with gallbladder premalignant lesions including metaplasia and adenomyomatosis. The potential mechanism might be related with higher ROS

Trends in gastric cancer mortality and in the prevalence of Helicobacter pylori infection in Portugal.

Science.gov (United States)

Morais, Samantha; Ferro, Ana; Bastos, Ana; Castro, Clara; Lunet, Nuno; Peleteiro, Bárbara

2016-07-01

Portugal has the highest gastric cancer mortality rates in Western Europe, along with high prevalences of Helicobacter pylori infection. Monitoring their trends is essential to predict the burden of this cancer. We aimed to quantify time trends in gastric cancer mortality in Portugal and in each administrative region, and to compute short-term predictions, as well as to describe the prevalence of H. pylori infection, through a systematic review. Joinpoint analyses were used to identify significant changes in sex-specific trends in gastric cancer age-standardized mortality rates (ASMR) and to estimate annual percent changes (APC). The most recent trends were considered to compute estimates up to 2020 by adjusting Poisson regression models. We searched PubMed and IndexRMP to identify studies carried out in Portugal reporting the prevalence of H. pylori. Gastric cancer mortality has been decreasing in Portugal since 1971 in men (from ASMR=55.3/100 000; APC=-2.4, 95% confidence interval: -2.5 to -2.3) and since 1970 in women (from ASMR=28.0/100 000; APC=-2.8, 95% confidence interval: -2.9 to -2.7), although large regional differences were observed. Predicted ASMR for 2015 and 2020 were 18.8/100 000 and 16.7/100 000 for men and 8.5/100 000 and 7.4/100 000 for women, respectively. The prevalence of H. pylori varied from almost 5% at 0.5-2 years to just over 90% at 70 years or more. No consistent variation was observed since the 1990s. The downward trends in mortality rates are expected to remain in the next decades. The high prevalence of H. pylori infection across age groups and studies from different periods shows a large potential for decrease in the burden of gastric cancer in Portugal.

Helicobacter pylori

DEFF Research Database (Denmark)

Leth, Peter Mygind

1992-01-01

Helicobacter pylori (HP) are Gram-negative spiral bacteria which occur in the human stomach. The bacteria were cultured in vitro for the first time in 1983. It is suspected that the bacteria may cause chronic gastritis of type B and may also be a contributory cause of chronic ulceration and cancer...... of the stomach. The bacteria are accompanied by characteristic inflammatory changes in the gastric mucosa. The significance for gastritis, chronic ulceration, non-ulcer dyspepsia and carcinoma of the stomach is discussed. HP occurs in a great proportion of the population of the world and the frequency increases...

EXTRAGASTRIC AND ORODENTAL MANIFESTATIONS IN PEDIATRIC INFECTION WITH HELICOBACTER PYLORI. A REVIEW

OpenAIRE

Smaranda DIACONESCU; Raluca STANCA; Maria BOLAT

2015-01-01

Helicobacter pylori is a worlwide spread infection mostly manifested in childhood. Many - both invasive and non-invasive diagnostic tests - are now available,. The colonisation effect of gastric mucosa and its consequences are well known and studied. H. pylori can also induce extra-gastric manifestations, like iron-deficiency anemia. The role of oral cavity colonisation is not clearly defined, several studies stating that the oral cavity represents a reservoir for H. pyloris. The presence of ...

Relationship between caga-positive Helicobacter pylori infection and risk of gastric cancer: a case control study in Porto Alegre, RS, Brazil

Directory of Open Access Journals (Sweden)

Gilmara Coelho Meine

2011-03-01

Full Text Available CONTEXT: Gastric cancer is the second most common cause of cancer related death worldwide. Although Helicobacter pylori has been classified as a class I carcinogen, the presence of infection is not a factor that alone is able to lead to gastric cancer, and one of the possible explanations for this is the existence of different strains of H. pylori with different degrees of virulence. OBJECTIVES: To investigate the association between cagA-positive H. pylori and gastric cancer, using polymerase chain reaction (PCR for the detection of this bacterial strain. METHODS: Twenty-nine patients with gastric cancer were matched by sex and age (± 5 years with 58 patients without gastric cancer, submitted to upper gastrointestinal endoscopy. All patients were evaluated for the status of infection by H. pylori (through urease test, histological analysis and PCR for the genes ureA and 16SrRNA and by cagA-positive strain (through PCR for cagA gene. RESULTS: Evaluating the presence of infection by cagA-positive H. pylori, it was verified that the rate of infection was significantly higher in the group with gastric cancer when compared with the matched controls, occurring in 62.1% and 29.3%, respectively (OR = 3.95; CI 95% 1.543-10.096. CONCLUSIONS: There is an association between cagA-positive H. pylori strain and risk of gastric cancer.

Prevalence of Helicobacter pylori in Northern Jordan: Endoscopy based study

International Nuclear Information System (INIS)

Bani-Hani, Kamal E.; Hammouri, Shadi M.

2001-01-01

Helicobacter pylori infection is considered the most common infection worldwide and is associated with many other disorders. The aim of this study is to determine the prevalence of this infection among patients undergoing endoscopy in Northern Jordan. Between November 1998 and September 2000, all patients referred from the Gastro-esophageal Clinic to the Endoscopy Unit at Princess Basma Teaching Hospital, Irbid, Northern Jordan were enrolled in this prospective study. For each patient clinical and epidemiological data was collected and endoscopy was performed. At least 3 antral biopsies were obtained from each patient, and these were examined histologically for the presence of gastritis and stained for Helicobacter pylori using modified Giemsa stain. A total of 197 consecutive patients (113 females) with a mean age of 40.2 years (range 15-91 years) were studied. Abdominal pain was the highest presenting symptom. Gastritis 91% and esophagitis 42% were the most frequent endoscopic findings. Gastritis was documented histologically in 183 (93%) of patients. Helicobacter pylori was found in 161 patients (82%), with all of these having histological gastritis. The 11 patients with gastric ulcer, compared to the 51 out of the 59 (86%) patients with duodenal ulcer, showed Helicobacter pylori in their biopsies. The prevalence of Helicobacter pylori infection in patients subjected to an upper gastrointestinal endoscopy in Jordan is high. This study confirms that Helicobacter pylori is significantly associated with gastritis and peptic ulcer. Further studies are needed to determine the types of Helicobacter pylori strains present in Jordan. (author)

Role of Helicobacter pylori in stomach cancer after partial gastrectomy for benign ulcer disease Papel del Helicobacter pylori en el cáncer gástrico tras gastrectomía parcial por úlcera benigna

Directory of Open Access Journals (Sweden)

A. Seoane

2005-11-01

Full Text Available Objective: to determine the prevalence of Helicobacter pylori infection in patients having undergone gastrectomy for non-neoplastic disease who later developed gastric stump cancer. Material and methods: retrospective study of all patients with partial gastrectomy for non-malignant peptic disease who were submitted to an endoscopic exploration between 1995 and 2001. A comparison was made of major clinical and histological characteristics, and the presence of Helicobacter pylori among patients with and without gastric cancer in the stomach remnant. Results: a total of 73 patients were studied in this period. Fifteen patients (20.5% had remnant-stump gastric cancer. All but one were adenocarcinomas (71% intestinal and 29% diffuse, respectively. The average time between diagnosis of gastric cancer and previous gastrectomy was 32 (14-48 years. There was a higher detection rate of Helicobacter pylori in patients with cancer in the gastric remnant (100 vs. 81.5%, respectively, p Objetivo: determinar la prevalencia de la infección por Helicobacter pylori en pacientes gastrectomizados por enfermedad no neoplásica, y que han desarrollado posteriormente cáncer gástrico. Material y métodos: estudio retrospectivo con reclutamiento de todos los pacientes con gastrectomía parcial por enfermedad péptica benigna que han sido sometidos a una exploración endoscópica entre 1995-2001. Se ha realizado una comparación de las principales características clínicas e histológicas y de la presencia de Helicobacter pylori en los pacientes con y sin cáncer del remanente gástrico. Resultados: se han estudiado un total de 73 pacientes en este periodo. Se han encontrado 15 pacientes (20,5% con cáncer en el remanente gástrico, 14 adenocarcinomas (71% tipo intestinal y 29% tipo difuso y un linfoma. El tiempo transcurrido entre el diagnóstico de cáncer gástrico y la gastrectomía previa ha sido de 32 (14-48 años. Se ha detectado un alto porcentaje de infecci

empiric treatment based on helicobacter pylori serology cannot ...

African Journals Online (AJOL)

EMPIRIC TREATMENT BASED ON. HELICOBACTER PYLORI SEROLOGY. CANNOT SUBSTITUTE FOR EARLY. ENDOSCOPY IN THE. MANAGEMENT OF DYSPEPTIC. RURAL BLACK AFRICANS. Stephen JD O'Keefe, B Salvador, J Nainkin, S Majikir H. Stevens, A Atherstone. Background_ Evidence that chronic gastric ...

Infection with Helicobacter pylori strains lacking dupA is associated with an increased risk of gastric ulcer and gastric cancer development.

Science.gov (United States)

Abadi, Amin Talebi Bezmin; Taghvaei, Tarang; Wolfram, Lutz; Kusters, Johannes G

2012-01-01

Recently, dupA was reported as a new virulence factor in Helicobacter pylori, but its association with gastroduodenal disorders and its mode of action are still unclear. Here, an association of the dupA status with different disease groups was determined and a biological explanation for the observed associations was tested. In total, 216 H. pylori isolates were obtained from 232 presumed H. pylori-infected patients. A positive association was observed between the occurrence of duodenal ulcer (DU) and the presence of dupA [odds ratio (OR) 24.2; 95 % confidence interval (CI) 10.6-54.8]. In addition, an inverse association between the occurrence of gastric cancer (GC) [OR 0.16; 95 % CI 0.05-0.47] and gastric ulcer (GU) [OR 0.34; 95 % CI 0.16-0.68] with the presence of dupA was observed. A putative explanation for the observed associations might be a more corpus-located infection (pan-gastritis) by the dupA-positive strains due to their increased acid resistance. Indeed, a strong association between dupA-positive H. pylori isolated from gastritis patients and in vitro acid resistance was observed (PdupA-positive strains suggests that these strains are adapted to a stomach with high gastric acid output. This may in part explain the observed associations, as an increased gastric acid output is thought to be typical for an antrum-predominant H. pylori infection and, whilst this is associated with an increased risk of DU formation, it also decreases the risk for the genesis of GUs and GC.

Human gastric cancer, Helicobacter pylori and bracken carcinogens: A connecting hypothesis.

Science.gov (United States)

Oliveros-Bastidas, Alberto; Calcagno-Pissarelli, María Pía; Naya, Marlene; Ávila-Núñez, Jorge Luis; Alonso-Amelot, Miguel E

2016-03-01

Long term infection of Helicobacter pylori (Hp) virulent strains is a key factor in the genesis of human gastric cancer, and so are certain dietary proinflammatory and genotoxic compounds. Carcinogenic bracken fern (Pteridium spp.) is one of these. Toxins from this plant are consumed as bracken culinary preparations, through milk and meat of bracken-exposed livestock, and drain waters from bracken swards. Bracken toxin ptaquiloside (PtQ), a suspected human carcinogen, elicits complex responses in animals leading to death. PtQ and Hp might cooperate in gastric pathologies. This paper presents an hypothesis on PtQ-Hp association leading to the enhancement of carcinogenesis in the human gastric environment that might explain the high gastric cancer incidence and death rates among Hp-infected people living in bracken zones at two levels: (1) The macroscopic scale comprising the flow of PtQ in the human diet. (2) the microscopic scale encompassing (A) gastric luminal medium; (B) gastric mucus structure and mucin degradation elicited by Hp; (C) bacterial pH gradient modification of the gastric mucosa that favors PtQ survival and its penetration into epithelial tissue; (D) combined PtQ/Hp effects on gastric immune and inflammatory responses; (E) PtQ-Hp complementary activity at selected cell signaling cascades and genome disturbance. Copyright © 2015 Elsevier Ltd. All rights reserved.

Genetic Polymorphism of MDM2 SNP309 in Patients with Helicobacter Pylori-Associated Gastritis.

Science.gov (United States)

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

2015-01-01

Helicobacter pylori plays an important role in gastric cancer, which has a relatively low inciduence in Thailand. MDM2 is a major negative regulator of p53, the key tumor suppressor involved in tumorigenesis of the majority of human cancers. Whether its expression might explain the relative lack of gastric cancer in Thailand was assessed here. This single-center study was conducted in the northeast region of Thailand. Gastric mucosa from 100 patients with Helicobacter pylori associated gastritis was analyzed for MDM2 SNP309 using real-time PCR hybridization (light-cycler) probes. In the total 100 Helicobacter pylori associated gastritis cases the incidence of SNP 309 T/T homozygous was 78 % with SNP309 G/T heterozygous found in 19% and SNP309 G/G homozygous in 3%. The result show SNP 309 T/T and SNP 309 G/T to be rather common in the Thai population. Our study indicates that the MDM2 SNP309 G/G homozygous genotype might be a risk factor for gastric cancer in Thailand and the fact that it is infrequent could explain to some extent the low incidence of gastric cancer in the Thai population.

Helicobacter pylori virulence and cancer pathogenesis.

Science.gov (United States)

Yamaoka, Yoshio; Graham, David Y

2014-06-01

Helicobacter pylori is human gastric pathogen that causes chronic and progressive gastric mucosal inflammation and is responsible for the gastric inflammation-associated diseases, gastric cancer and peptic ulcer disease. Specific outcomes reflect the interplay between host-, environmental- and bacterial-specific factors. Progress in understanding putative virulence factors in disease pathogenesis has been limited and many false leads have consumed scarce resources. Few in vitro-in vivo correlations or translational applications have proved clinically relevant. Reported virulence factor-related outcomes reflect differences in relative risk of disease rather than specificity for any specific outcome. Studies of individual virulence factor associations have provided conflicting results. Since virulence factors are linked, studies of groups of putative virulence factors are needed to provide clinically useful information. Here, the authors discuss the progress made in understanding the role of H. pylori virulence factors CagA, vacuolating cytotoxin, OipA and DupA in disease pathogenesis and provide suggestions for future studies.

The Multiple Carbohydrate Binding Specificities of Helicobacter pylori

Science.gov (United States)

Teneberg, Susann

Persistent colonization of the human stomach by Helicobacter pylori is a risk factor for the development of peptic ulcer disease and gastric cancer. Adhesion of microbes to the target tissue is an important determinant for successful initiation, establishment and maintenance of infection, and a variety of different candidate carbohydrate receptors for H. pylori have been identified. Here the different the binding specifities, and their potential role in adhesion to human gastric epithelium are described. Finally, recent findings on the roles of sialic acid binding SabA adhesin in interactions with human neutrophils and erythrocytes are discussed.

Autophagy-related genes in Helicobacter pylori infection.

Science.gov (United States)

Tanaka, Shingo; Nagashima, Hiroyuki; Uotani, Takahiro; Graham, David Y; Yamaoka, Yoshio

2017-06-01

In vitro studies have shown that Helicobacter pylori (H. pylori) infection induces autophagy in gastric epithelial cells. However, prolonged exposure to H. pylori reduces autophagy by preventing maturation of the autolysosome. The alterations of the autophagy-related genes in H. pylori infection are not yet fully understood. We analyzed autophagy-related gene expression in H. pylori-infected gastric mucosa compared with uninfected gastric mucosa obtained from 136 Bhutanese volunteers with mild dyspeptic symptoms. We also studied single nucleotide polymorphisms (SNPs) of autophagy-related gene in 283 Bhutanese participants to identify the influence on susceptibility to H. pylori infection. Microarray analysis of 226 autophagy-related genes showed that 16 genes were upregulated (7%) and nine were downregulated (4%). We used quantitative reverse transcriptase polymerase chain reaction to measure mRNA levels of the downregulated genes (ATG16L1, ATG5, ATG4D, and ATG9A) that were core molecules of autophagy. ATG16L1 and ATG5 mRNA levels in H. pylori-positive specimens (n=86) were significantly less than those in H. pylori-negative specimens (n=50). ATG16L1 mRNA levels were inversely related to H. pylori density. We also compared SNPs of ATG16L1 (rs2241880) among 206 H. pylori-positive and 77 H. pylori-negative subjects. The odds ratio for the presence of H. pylori in the GG genotype was 0.40 (95% CI: 0.18-0.91) relative to the AA/AG genotypes. Autophagy-related gene expression profiling using high-throughput microarray analysis indicated that downregulation of core autophagy machinery genes may depress autophagy functions and possibly provide a better intracellular habit for H. pylori in gastric epithelial cells. © 2017 John Wiley & Sons Ltd.

A retrospective study of 5-year outcomes of radiotherapy for gastric mucosa-associated lymphoid tissue lymphoma refractory to Helicobacter pylori eradication therapy

International Nuclear Information System (INIS)

Abe, Seiichiro; Oda, Ichiro; Inaba, Koji

2013-01-01

The favorable response rate of radiotherapy for localized gastric mucosa-associated lymphoid tissue lymphoma refractory to Helicobacter pylori eradication has been demonstrated. However, there are limited data available on the long-term outcomes. The aim of this retrospective study was to evaluate the long-term outcomes of radiotherapy for localized gastric mucosa-associated lymphoid tissue lymphoma refractory to Helicobacter pylori eradication. Thirty-four consecutive patients with localized gastric mucosa-associated lymphoid tissue lymphoma that were refractory to eradication were treated with radiotherapy (a total dose of 30 Gy). The response and adverse events of radiotherapy were retrospectively analyzed as short-term outcomes, and recurrence-free, overall and disease-specific survival rates were calculated as long-term outcomes. Thirty-three (97.1%) patients achieved complete remission and radiotherapy was well tolerated. One patient underwent emergency gastrectomy due to severe hematemesis. Of the 34 patients during the median follow-up period of 7.5 (1.2-13.0) years, one patient had local recurrence after 8.8 years, one patient underwent surgery for bowel obstruction secondary to small bowel metastasis after 5.1 years and one patient had pulmonary metastasis after 10.9 years. Pathologically, all three recurrences revealed mucosa-associated lymphoid tissue lymphoma without any transformation to high-grade lymphoma. None died of gastric mucosa-associated lymphoid tissue lymphoma. The 5-year recurrence-free survival rate was 97.0%. The 5-year overall survival rates and disease-specific survival rates were 97.0 and 100%, respectively. Radiotherapy in patients with localized gastric mucosa-associated lymphoid tissue lymphoma refractory to Helicobacter pylori eradication can achieve excellent overall survival. However, long-term surveillance is necessary to identify late recurrences. (author)

A retrospective study of 5-year outcomes of radiotherapy for gastric mucosa-associated lymphoid tissue lymphoma refractory to Helicobacter pylori eradication therapy.

Science.gov (United States)

Abe, Seiichiro; Oda, Ichiro; Inaba, Koji; Suzuki, Haruhisa; Yoshinaga, Shigetaka; Nonaka, Satoru; Morota, Madoka; Murakami, Naoya; Itami, Jun; Kobayashi, Yukio; Maeshima, Akiko Miyagi; Saito, Yutaka

2013-09-01

The favorable response rate of radiotherapy for localized gastric mucosa-associated lymphoid tissue lymphoma refractory to Helicobacter pylori eradication has been demonstrated. However, there are limited data available on the long-term outcomes. The aim of this retrospective study was to evaluate the long-term outcomes of radiotherapy for localized gastric mucosa-associated lymphoid tissue lymphoma refractory to Helicobacter pylori eradication. Thirty-four consecutive patients with localized gastric mucosa-associated lymphoid tissue lymphoma that were refractory to eradication were treated with radiotherapy (a total dose of 30 Gy). The response and adverse events of radiotherapy were retrospectively analyzed as short-term outcomes, and recurrence-free, overall and disease-specific survival rates were calculated as long-term outcomes. Thirty-three (97.1%) patients achieved complete remission and radiotherapy was well tolerated. One patient underwent emergency gastrectomy due to severe hematemesis. Of the 34 patients during the median follow-up period of 7.5 (1.2-13.0) years, one patient had local recurrence after 8.8 years, one patient underwent surgery for bowel obstruction secondary to small bowel metastasis after 5.1 years and one patient had pulmonary metastasis after 10.9 years. Pathologically, all three recurrences revealed mucosa-associated lymphoid tissue lymphoma without any transformation to high-grade lymphoma. None died of gastric mucosa-associated lymphoid tissue lymphoma. The 5-year recurrence-free survival rate was 97.0%. The 5-year overall survival rates and disease-specific survival rates were 97.0 and 100%, respectively. Radiotherapy in patients with localized gastric mucosa-associated lymphoid tissue lymphoma refractory to Helicobacter pylori eradication can achieve excellent overall survival. However, long-term surveillance is necessary to identify late recurrences.

Presence of Helicobacter pylori in a Mexican Pre-Columbian Mummy

Directory of Open Access Journals (Sweden)

Cerbón Marco A

2008-07-01

Full Text Available Abstract Background Recent studies showed that Helicobacter pylori existed in the New World prior to the arrival of Columbus. The purpose of the present study was to detect the presence of Helicobacter pylori in pre-Columbian mummies from Northern Mexico. Methods Six samples were studied (four samples of gastric remains, tongue-soft palate, and brain remained as negative controls from two of the six naturally mummified corpses studied (adult male and infant male. Samples were taken from tissues suitable for DNA amplification by Polymerase chain reaction (PCR. DNA was extracted and H. pylori detection was carried out by PCR and hybridized with the pHp probe from 16S rRNA gene. The purified PCR products were cloned and sequenced in both directions. DNA sequences were analyzed with ALIGN and BLAST software. A second amplification was performed using ureB gene by real-time PCR. Results From four samples of gastric remnant, only two were H. pylori-positive for amplification of a 109 bp DNA fragment; the remaining two were negative, as were the tongue-soft palate and the brain biopsies as well. These PCR products were hybridized with a pHp probe. Nucleotide sequence analysis showed homology with H. pylori in 98 of 99% when compared with the gene bank nucleotide sequence. Only one sample of gastric remnant H. pylori-positive with 16S rRNA gene was also positive for ureB gene from H. pylori. Conclusion This data supported infection with H. pylori in Mexican pre-Columbian mummies dating from approximately 1,350 AC.

Comparative Genomics of H. pylori and Non-Pylori Helicobacter Species to Identify New Regions Associated with Its Pathogenicity and Adaptability

Directory of Open Access Journals (Sweden)

De-Min Cao

2016-01-01

Full Text Available The genus Helicobacter is a group of Gram-negative, helical-shaped pathogens consisting of at least 36 bacterial species. Helicobacter pylori (H. pylori, infecting more than 50% of the human population, is considered as the major cause of gastritis, peptic ulcer, and gastric cancer. However, the genetic underpinnings of H. pylori that are responsible for its large scale epidemic and gastrointestinal environment adaption within human beings remain unclear. Core-pan genome analysis was performed among 75 representative H. pylori and 24 non-pylori Helicobacter genomes. There were 1173 conserved protein families of H. pylori and 673 of all 99 Helicobacter genus strains. We found 79 genome unique regions, a total of 202,359bp, shared by at least 80% of the H. pylori but lacked in non-pylori Helicobacter species. The operons, genes, and sRNAs within the H. pylori unique regions were considered as potential ones associated with its pathogenicity and adaptability, and the relativity among them has been partially confirmed by functional annotation analysis. However, functions of at least 54 genes and 10 sRNAs were still unclear. Our analysis of protein-protein interaction showed that 30 genes within them may have the cooperation relationship.

Evaluation of diagnostic methods for the detection of Helicobacter pylori in gastric biopsy specimens of dyspeptic patients

Directory of Open Access Journals (Sweden)

Ivy Bastos Ramis

2012-09-01

Full Text Available Helicobacter pylori infects nearly 50% of the world's population. This microorganism is accepted as the most important agent of gastritis and as a risk factor for peptic ulcer disease and gastric adenocarcinoma. Currently many diagnostic methods exist for detecting H. pylori, however they all have limitations, thus it is recommend a combination of at least two methods. The aim of this study was to evaluate diagnostic methods, such as in-house urease test, culture and Polymerase Chain Reaction (PCR, for the detection of the H. pylori in gastric biopsy specimens of 144 dyspeptic patients, using as gold standard the association between histology and rapid urease test. According to the gold standard used in this study, 48 (33.3% patients were infected with H. pylori, while 96 (66.7% were classified as not infected. The in-house urease test and the PCR were the most sensitive methods (100%, followed by culture (85.4%. However, the in-house urease test and the culture were the most specific (100%, followed by PCR (75%. In conclusion, this study showed that, in comparison with the combination of histology and rapid urease test, the in-house urease test and the PCR presented 100% of sensitivity in the diagnosis of gastric infection by H. pylori, while the in-house urease test and the culture reached 100% of specificity. These finding suggest that the combination of two or more methods may improve the accuracy of the H. pylori detection.

Dynamic Expansion and Contraction of cagA Copy Number in Helicobacter pylori Impact Development of Gastric Disease

Directory of Open Access Journals (Sweden)

Sungil Jang

2017-02-01

Full Text Available Infection with Helicobacter pylori is a major risk factor for development of gastric disease, including gastric cancer. Patients infected with H. pylori strains that express CagA are at even greater risk of gastric carcinoma. Given the importance of CagA, this report describes a new molecular mechanism by which the cagA copy number dynamically expands and contracts in H. pylori. Analysis of strain PMSS1 revealed a heterogeneous population in terms of numbers of cagA copies; strains carried from zero to four copies of cagA that were arranged as direct repeats within the chromosome. Each of the multiple copies of cagA was expressed and encoded functional CagA; strains with more cagA repeats exhibited higher levels of CagA expression and increased levels of delivery and phosphorylation of CagA within host cells. This concomitantly resulted in more virulent phenotypes as measured by cell elongation and interleukin-8 (IL-8 induction. Sequence analysis of the repeat region revealed three cagA homologous areas (CHAs within the cagA repeats. Of these, CHA-ud flanked each of the cagA copies and is likely important for the dynamic variation of cagA copy numbers. Analysis of a large panel of clinical isolates showed that 7.5% of H. pylori strains isolated in the United States harbored multiple cagA repeats, while none of the tested Korean isolates carried more than one copy of cagA. Finally, H. pylori strains carrying multiple cagA copies were differentially associated with gastric disease. Thus, the dynamic expansion and contraction of cagA copy numbers may serve as a novel mechanism by which H. pylori modulates gastric disease development.

EXTRAGASTRIC AND ORODENTAL MANIFESTATIONS IN PEDIATRIC INFECTION WITH HELICOBACTER PYLORI. A REVIEW

Directory of Open Access Journals (Sweden)

Smaranda DIACONESCU

2015-12-01

Full Text Available Helicobacter pylori is a worlwide spread infection mostly manifested in childhood. Many - both invasive and non-invasive diagnostic tests - are now available,. The colonisation effect of gastric mucosa and its consequences are well known and studied. H. pylori can also induce extra-gastric manifestations, like iron-deficiency anemia. The role of oral cavity colonisation is not clearly defined, several studies stating that the oral cavity represents a reservoir for H. pyloris. The presence of this rod in the dental plaque may lead to periodontitis, dental caries, dental calculus and tooth loos. Dental treatment associated with eradication therapy decreases the prevalence of oral H. pylori and improves the eradication rate of gastric H. pylori. Dental treatment in H. pylori infection management should be taken into consideration, especially in children and teens.

Involvement of microRNAs-MMPs-E-cadherin in the migration and invasion of gastric cancer cells infected with Helicobacter pylori.

Science.gov (United States)

Yang, Yongmei; Li, Xiaohui; Du, Jie; Yin, Youcong; Li, Yuanjian

2018-06-15

It has been found that Helicobacter pylori （H. pylori）is not only the main cause of gastric cancer, but also closely related to its metastasis. E-cadherin cleavage induced by matrix metalloproteinases (MMPs) plays an important role in the tumor metastasis. In the present study, we investigated the role of microRNAs-MMPs-E-cadherin in migration and invasion of gastric cancer cells treated with H. pylori. The results showed that H. pylori induced migration and invasion of SGC-7901 cells with a down-regulation of E-cadherin expression, which were abolished by MMPs knock down, E-cadherin overexpression, mimics of miR128 and miR148a. MiR128/miR148a inhibitors restored MMP-3/MMP-7 expression, down-regulated E-cadherin level, and accelerated cellular migration and invasion. This study suggests that H. pylori induces migration and invasion of gastric cancer cells through reduction of E-cadherin function by activation of MMP-3, - 7. The present results also suggest that the activated MMPs/E-cadherin pathway is related with down-regulation of miR128/miR148a in the human gastric cancer cells infected with H. pylori. Copyright © 2018. Published by Elsevier Inc.

High diversity of vacA and cagA Helicobacter pylori genotypes in patients with and without gastric cancer.

Directory of Open Access Journals (Sweden)

Yolanda López-Vidal

Full Text Available BACKGROUND: Helicobacter pylori is associated with chronic gastritis, peptic ulcers, and gastric cancer. The aim of this study was to assess the topographical distribution of H. pylori in the stomach as well as the vacA and cagA genotypes in patients with and without gastric cancer. METHODOLOGY/PRINCIPAL FINDINGS: Three gastric biopsies, from predetermined regions, were evaluated in 16 patients with gastric cancer and 14 patients with dyspeptic symptoms. From cancer patients, additional biopsy specimens were obtained from tumor centers and margins; among these samples, the presence of H. pylori vacA and cagA genotypes was evaluated. Positive H. pylori was 38% and 26% in biopsies obtained from the gastric cancer and non-cancer groups, respectively (p = 0.008, and 36% in tumor sites. In cancer patients, we found a preferential distribution of H. pylori in the fundus and corpus, whereas, in the non-cancer group, the distribution was uniform (p = 0.003. A majority of the biopsies were simultaneously cagA gene-positive and -negative. The fundus and corpus demonstrated a higher positivity rate for the cagA gene in the non-cancer group (p = 0.036. A mixture of cagA gene sizes was also significantly more frequent in this group (p = 0.003. Ninety-two percent of all the subjects showed more than one vacA gene genotype; s1b and m1 vacA genotypes were predominantly found in the gastric cancer group. The highest vacA-genotype signal-sequence diversity was found in the corpus and 5 cm from tumor margins. CONCLUSION/SIGNIFICANCE: High H. pylori colonization diversity, along with the cagA gene, was found predominantly in the fundus and corpus of patients with gastric cancer. The genotype diversity observed across systematic whole-organ and tumor sampling was remarkable. We find that there is insufficient evidence to support the association of one isolate with a specific disease, due to the multistrain nature of H. pylori infection shown in this work.

Eradication of Helicobacter pylori in patients without gastric symptoms suffering from recurrent aphthous stomatitis: A pilot study

Directory of Open Access Journals (Sweden)

Latković Marina

2017-01-01

Full Text Available Background/Aim. Helicobacter (H. pylori is a widespread bacterium and its involvement in pathogenesis of gastric diseases is well-known. However, H. pylori role in etiology of other histologically similar conditions, especially recurrent aphthous stomatitis (RAS is still controversial. Research regarding H. pylori and its association with RAS, as well as the treatment options were always conducted on patients with diagnosed gastric problems. The aim of this study was to determine whether H. pylori is present in the oral cavity of patients suffering from RAS but without any symptoms or medical history of gastric disease. Methods. A total of 15 patients with RAS participated in the study. None of the participants suffered from any gastrointestinal disorders. Two dental plaque samples from each participant were collected. The first was analyzed using rapid urease test and the second one was put in transport medium and sent for cultivation. The sensitivity of H. pylori to antibiotics was established using disk diffusion method of sensitivity testing for every patient individually and adequate therapy was prescribed. Results. Before the treatment the mean annual recurrence rate of RAS was 8.1 ± 2.1, with the average number of lesions being 3.9 ± 1.9. During the 12-month observation period after the eradication therapy, none of the patients reported recurrence of aphthous lesions. The treatment was successful in all cases. Conclusion. This study shows that RAS can be effectively treated by successful eradication of oral H. pylori, and that RAS could be possibly considered as an early warning sign of potential gastric infection by H. pilory.

Effects of Helicobacter pylori infection and smoking on gastric cancer incidence in China: a population-level analysis of trends and projections

Science.gov (United States)

Goldie, Sue J.; Kuntz, Karen M.; Ezzati, Majid

2010-01-01

Objective Although gastric cancer incidence is declining in China, trends may differ from historical patterns in developed countries. Our aim was to (1) retrospectively estimate the effects of Helicobacter pylori (H. pylori) and smoking on past gastric cancer incidence and (2) project how interventions on these two risk factors can reduce future incidence. Methods We used a population-based model of intestinal-type gastric cancer to estimate gastric cancer incidence between 1985 and 2050. Disease and risk factor data in the model were from community-based epidemiological studies and national prevalence surveys. Results Between 1985 and 2005, age-standardized gastric cancer incidence among Chinese men declined from 30.8 to 27.2 per 100,000 (12%); trends in H. pylori and smoking prevalences accounted for >30% of overall decline. If past risk factor trends continue, gastric cancer incidence will decline an additional 30% by 2050. Yet, annual cases will increase from 116,000 to 201,000 due to population growth and aging. Assuming that H. pylori prevention/treatment and tobacco control are implemented in 2010, the decline in gastric cancer incidence is projected to increase to 33% with universal H. pylori treatment for 20-year-olds, 42% for a hypothetical childhood H. pylori vaccine, and 34% for aggressive tobacco control. Conclusions The decline in gastric cancer incidence has been slower than in developed countries and will be offset by population growth and aging. Public health interventions should be implemented to reduce the total number of cases. PMID:19642005

Helicobacter Pylori Infection in the Elderly

Directory of Open Access Journals (Sweden)

Jyh-Ming Liou

2008-12-01

Full Text Available The elderly often seek medical attention because of gastroduodenal diseases. Helicobacter pylori (H. pylori infection is associated with several gastroduodenal diseases and its prevalence increases with age worldwide. It is estimated that 10–15% of infected patients will have peptic ulcer disease and 1% of patients will have gastric cancer or mucosa-associated lymphoid tissue lymphoma. Notably, the most severe clinical outcomes, i.e., gastric cancer and complicated peptic ulcer diseases, usually occur in elderly patients. Thus the test-and-treatment strategy is not recommended for elderly patients with uninvestigated dyspepsia. However, biopsy specimens for the rapid urease test and histology should be taken from both the antrum and corpus to increase the detection rate in elderly patients, especially in those with atrophic gastritis. The urea breath test may increase the detection rate if the rapid urease test or histology are negative in elderly patients with atrophic gastritis. Standard triple therapy and sequential therapy can achieve satisfactory eradication rates for H. pylori in elderly patients. Elderly patients with peptic ulcers may have a similar benefit from treatment of H. pylori infection as non-elderly patients. Eradication of H. pylori infection may also lead to improvement in histologic grading of gastritis, but the risk of gastric cancer cannot be completely reduced, especially in patients with existing premalignant lesions.

Immune Reactions Against Elongation Factor 2 Kinase: Specific Pathogenesis of Gastric Ulcer from Helicobacter pylori Infection

Directory of Open Access Journals (Sweden)

Kiyoshi Ayada

2009-01-01

Full Text Available Helicobacter pylori (H. pylori infection is a definite causative factor for gastric ulcers (GUs. In the present study we detected a specific antigen of gastric epithelial cells (HGC-27 using cell ELISA, which was recognized by the sera of GU patients (n=20 but not in patients with chronic gastritis (CG; n=20 or in healthy volunteers (HC; n=10. This antigen was over-expressed by a stressful (heat-stressed environment, and was identified as elongation factor 2 kinase (EF-2K by western blotting. The GU patients' lymphocytes stimulated by H. pylori specifically disrupted heat-stressed HGC-27 cells in a cytotoxic assay. In flow cytometry, the effector cells (lymphocytes from GU patients were significantly differentiated to T helper type 1 lymphocyte (Th1 and cytotoxic T lymphocyte (CTL as opposed to those from CG patients. The target cells (HGC-27 expressed EF-2K and MHC-class I together with costimulatory molecules from heat stress. This antigen specific immune mechanism could have a prominent role in the pathogenesis of GU.

3rd BRAZILIAN CONSENSUS ON Helicobacter pylori

Directory of Open Access Journals (Sweden)

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.

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

Science.gov (United States)

Lee, Sun-Young

2016-09-01

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 fundus, and thickened gastric folds are common endoscopic findings. The secreting ability of the gastric mucosa cells is usually intact in both noninfected and actively infected stomachs, and the intragastric condition becomes hyperacidic upon inflammation. Increased serum pepsinogen II concentration correlates well with active H. pylori infection, and also indicates an increased risk of diffuse-type gastric cancer. In chronic inactive H. pylori infection, metaplastic gastritis and atrophic gastritis extending from the antrum (closed-type chronic atrophic gastritis) toward the corpus (open-type chronic atrophic gastritis) are common endoscopic findings. The intragastric environment is hypoacidic and the risk of intestinal-type gastric cancer is increased in such conditions. Furthermore, there is a decrease in serum pepsinogen I concentration when the secreting ability of the gastric mucosa cells is damaged. Serologic and endoscopic changes that occur upon H. pylori infection are important findings for estimating the secreting ability of the gastric mucosa cells, and could be applied for the secondary prevention of gastric cancer.

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

Alcohol consumption and Helicobacter pylori infection

DEFF Research Database (Denmark)

Brenner, H; Berg, Gabriele; Lappus, N

1999-01-01

Alcohol has strong antimicrobial activity and stimulates gastric acid secretion. Alcohol consumption may therefore compromise the living conditions of Helicobacter pylori in the stomach. We assessed the relation of alcohol consumption with H. pylori infection among 1,785 participants ages 18...... prevalence of H. pylori infection was 39.2%. There was a clear inverse dose-response-relation between reported alcohol consumption and H. pylori infection. The relation persisted after control for potential confounding factors. The adjusted prevalence ratios (95% confidence intervals) for H. pylori infection...... among persons who consumed up to 10, 10 to 20, and more than 20 gm of alcohol per day compared with non-drinkers were 0.93 (0.77-1.13), 0.82 (0.65-1.04), and 0.71 (0.55-0.92). The inverse relation between alcohol consumption and H. pylori infection was even stronger when individuals with an indication...

Host Epithelial Interactions with Helicobacter Pylori: A Role for Disrupted Gastric Barrier Function in the Clinical Outcome of Infection?

Directory of Open Access Journals (Sweden)

Andre G Buret

2005-01-01

Full Text Available Infection of the human stomach with Helicobacter pylori may develop into gastritis, ulceration, adenocarcinoma and mucosal lymphomas. The pathogenic mechanisms that determine the clinical outcome from this microbial-epithelial interaction remain poorly understood. An increasing number of reports suggests that disruptions of epithelial barrier function may contribute to pathology and postinfectious complications in a variety of gastrointestinal infections. The aim of this review is to critically discuss the implications of H pylori persistence on gastric disease, with emphasis on the role of myosin light chain kinase, claudins and matrix metalloproteinases in gastric permeability defects, and their contribution to the development of cancer. These mechanisms and the associated signalling events may represent novel therapeutic targets to control disease processes induced by H pylori, a microbial pathogen that colonizes the stomach of over 50% of the human population.

Helicobacter pylori vacA and cagA genotype diversity and interferon gamma expression in patients with chronic gastritis and patients with gastric cancer.

Science.gov (United States)

Martínez-Carrillo, D N; Atrisco-Morales, J; Hernández-Pando, R; Reyes-Navarrete, S; Betancourt-Linares, R; Cruz-del Carmen, I; Illades Aguiar, B; Román-Román, A; Fernández-Tilapa, G

2014-01-01

Helicobacter pylori (H. pylori) is the main risk factor for the development of chronic gastritis, gastric ulcer, and gastric cancer. In H. pylori-infected individuals, the clinical result is dependent on various factors, among which are bacterial components, the immune response, and environmental influence. To compare IFN-γ expression with the H. pylori vacA and cagA genotypes in patients with chronic gastritis and patients with gastric cancer. Ninety-five patients diagnosed with chronic gastritis and 20 with gastric cancer were included in the study. Three gastric biopsies were taken; one was used for the molecular detection and genotyping of H. pylori; another was fixed in absolute alcohol and histologic sections were made for determining IFN-γ expression through immunohistochemistry. No differences were found in the cells that expressed IFN-γ between the patients with chronic gastritis (median percentage of positive cells: 82.6% in patients without H. pylori and 82% in infected persons) and those with gastric cancer (70.5% in H. pylori-negative patients and 78.5% in infected persons). IFN-γ expression was 69% in chronic gastritis patients infected with H. pylori vacAs2m2/cagA⁻ it was 86.5% in patients infected with H. pylori vacAs1m2/cagA⁻, 86.5% in vacAs1m1/cagA⁻, and 82% in vacAs1m1/cagA⁺. Similar data were found in the patients with gastric cancer. IFN-γ expression varied depending on the H. pylori vacA and cagA genotype, but not in accordance with the presence of chronic gastritis or gastric cancer.

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.

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

Directory of Open Access Journals (Sweden)

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.

A study on the effect of Helicobacter pylori infection on p53 expression in gastric cancer and gastritis tissues.

Science.gov (United States)

Salih, Barik A; Gucin, Zuhal; Bayyurt, Nizamettin

2013-09-16

Helicobacter pylori cause damage to gastric epithelial cells and alterations in the p53 gene that lead to cancer development. This study aimed to determine the correlation of p53 expression with H. pylori using immunohistochemistry, RFLP-PCR, and histopathology. Gastric biopsy samples from gastric cancer (GC) (n = 54) and gastritis (n = 31) patients were examined for histopathological changes and expression of p53 protein by immunohistochemistry. Immunohistochemical analysis of p53 protein expression in H. pylori-positive GC sections showed an average of 44.3% positive cells in tumors and 6.9% in normal tissues, as compared to 16.4% and 4.4% in H. pylori-negative sections. P53 expression showed significant association with H. pylori (P = 0.005), invasion depth (P = 0.029) and inflammation reaction (P = 0.008). In gastritis sections, no difference in the average p53 staining in H. pylori-positive or -negative sections was seen. PCR-RFLP results also showed no difference in genotype frequencies of p53 in H. pylori-positive or -negative gastritis sections. Histopathology study of H. pylori-positive GC sections showed that 97.2% were the intestinal type and 2.8% the diffuse type, while in H. pylori-negative sections 35.2% were the intestinal type and 64.8% the diffuse type. Biopsy sections from H. pylori-positive gastritis patients revealed more severe inflammation than those of H. pylori-negative patients. Our results show that H. pylori infection affects p53 expression in GC. The average p53 expression was significantly higher in tumor than in normal tissues. In gastritis sections p53 expression was significantly associated with H. pylori.

Controversies in the Helicobacter pylori/duodenal ulcer story.

Science.gov (United States)

Hobsley, Michael; Tovey, Frank I; Holton, John

2008-12-01

In patients with Helicobacter pylori-positive duodenal ulcer (DU), the organism must be eradicated to achieve rapid, stable healing. However, evidence is against much else that is commonly accepted. (1) Does H. pylori cause the ulcer? Evidence against includes archaeopathology, geographical prevalence, temporal relationships and H. pylori-negative DU patients. DU can recur after eradication of H. pylori infection, and DUs may remain healed after reduction of acid secretion despite persistent infection. The faster healing of ulcers when H. pylori has been eradicated is due to the organism's interference with neoangiogenesis and the healing of wounded epithelial cells. (2) Does H. pylori infection persist until pharmacologically eradicated? Studies based on current infection show that H. pylori infection is a labile state that can change in 3 months. High rates of gastric acid secretion result in spontaneous cure, whereas low rates permit re-infection. Hydrochloric acid, necessary for producing a DU, is strongly associated with the likelihood of an ulcer. At the start, patients owe their ulcer to gastric hypersecretion of hydrochloric acid; approximately 60% may be H. pylori-negative. If acid is suppressed, the less acid milieu encourages invasion by H. pylori, especially if the strain is virulent.

Prospective study on effect of Helicobacter pylori on gastroesophageal reflux disease

Directory of Open Access Journals (Sweden)

Sabah Jalal Shareef

2017-08-01

Full Text Available Background and objective: The Helicobacter pylori infections role in etiology of peptic ulcer is well known, but its role in gastroesophageal reflux disease is one of the important issues which has to be confirmed. We tried to find out the effect of Helicobacter pylori infection on gastroesophageal reflux disease. Methods: The current study was done on 100 patients with gastroesophageal reflux disease from January 1st to June 30th, 2014 in Rizgary Teaching Hospital, Erbil city. The diagnosis was made by history, clinical examination, and endoscopy. Helicobacter pylori infection was confirmed by gastric biopsy and histopathological examination. We tried to find out the effects of Helicobacter pylori infection in gastroesophageal reflux disease patients and its eradication on their symptoms. The data was analyzed with the statistical package for the social sciences (version 18. Results: The mean age ± SD of participants was 37.13 ± 12.5 (17-75 years. The prevalence of Helicobacter pylori infection was 75%. The endoscopy showed that 50 out of 75 patients had erosive esophagitis and 25 out of 75 patients had normal appearance known as non-erosive esophagitis. The study showed no significance of its eradication on symptoms of gastroesophageal reflux disease. Conclusion: The effect of Helicobacter pylori infection in gastroesophageal reflux disease patients was significant regarding endoscopic finding while inversely related to symptoms severity. The eradication of infection did not cause improvement in symptom severity i.e. triple therapy not advised in the course of treatment.

Consecutive regression of MALT lymphomas coexisting in the pharyngeal and gastric tissue after the eradication of Helicobacter pylori

Directory of Open Access Journals (Sweden)

Giuseppe Ivan Potente

2012-09-01

Full Text Available The stomach is one of the most common organs in which mucosa-associated lymphoid tissue (MALT lymphoma develops. It is well established that Helicobacter pylori (Hp infection plays a major role in the development of gastric MALT lymphoma and that the presence of Hp in the gastric mucosa is connected with mucosa-associated lymphatic tissue (MALT.The same tissue is located in the oral cavity and pharynx in Waldayer’s circuit. Recently, the oral cavity was proposed as an extragastric reservoir of Hp infection. We report the case of a 79-year-old female patient with concomitant pharyngeal (MALT lymphoma and Hp-related gastric MALT lymphoma. Gastric MALT lymphoma was detected both through endoscopic examination as well as in biopsies. Pharyngeal MALT lymphoma was also detected in biopsies. Hp has been recognized in the gastric mucosa by positive serum H. pylori antibody and urease tests. Treatment of the Hp infection in our patient using antibiotics led to the regression of both lesions. This is the first case report on the regression of a pharyngeal MALT lymphoma after Hp eradication.

Special licorice extracts containing lowered glycyrrhizin and enhanced licochalcone A prevented Helicobacter pylori-initiated, salt diet-promoted gastric tumorigenesis.

Science.gov (United States)

Park, Jong-Min; Park, Sang-Ho; Hong, Kyung-Sook; Han, Young-Min; Jang, Sang-Ho; Kim, Eun-Hee; Hahm, Ki-Baik

2014-06-01

In spite of cytoprotective and anti-inflammatory actions, conventional licorice extracts (c-lico) were limitedly used due to serious side effects of glycyrrhizin. As our group had successfully isolated special licorice extracts (s-lico) lowering troublesome glycyrrhizin, but increasing licochalcone A, we have compared anti-inflammatory, antioxidative, and cytoprotective actions of s-lico and c-lico against either in vitro or in vivo Helicobacter pylori infection. RT-PCR and Western blot were performed to check anti-inflammatory action and electron spin resonance (ESR) and DCFDA spectroscopy to check antioxidative action. s-lico or c-lico was pretreated 1 hours before H. pylori infection on AGS cells. Interleukin-10 deficient mice inoculated H. pylori and followed with high salt containing pallet diets to produce H. pylori-associated chronic atrophic gastritis and gastric tumors, during which s-lico or c-lico-containing pellet diets were administered up to 24 weeks. s-lico had fabulous efficacy on scavenging ROS which was further confirmed by DCFDA study and ESR measurement. The expressions of COX-2, iNOS, VEGF, and IL-8 were increased after H. pylori infection, of which levels were significantly decreased with s-lico in a dose-dependent manner. s-lico significantly ameliorated hypoxia-induced or H. pylori-induced angiogenic activities. s-lico significantly ameliorated H. pylori-induced gastric damages as well as gastritis. Our animal model showed significant development of gastric tumors including adenoma and dysplasia relevant to H. pylori infection, and s-lico administration significantly attenuated incidence of H. pylori-induced gastric tumorigenesis. Special licorice extracts can be anticipating substance afforded significant attenuation of either H. pylori-induced gastritis or tumorigenesis based on potent antioxidative, anti-inflammatory, and antimutagenic actions. © 2014 John Wiley & Sons Ltd.

The immunohistochemical demonstration of Helicobacter pylori in rectal ectopia.

LENUS (Irish Health Repository)

Corrigan, Mark Anthony

2009-08-01

The finding of heterotopic gastric mucosa in the rectum is rare, with less than 40 reported cases in the literature. A condition of unknown etiology, several hypotheses exist including infectious and congenital. We report a case of ectopic gastric tissue in the rectum of a 47-year-old female, and her subsequent clinical course. Furthermore for the first time, we present immunohistologic evidence of the presence of Helicobacter pylori in rectal ectopic gastric tissue.

Two distinct etiologies of gastric cardia adenocarcinoma: interactions among pH, Helicobacter pylori, and bile acids

Directory of Open Access Journals (Sweden)

Ken-ichi eMukaisho

2015-05-01

Full Text Available Gastric cancer can be classified as cardia and noncardia subtypes according to the anatomic site. Although the gastric cancer incidence has decreased steadily in several countries over the past 50 years, the incidence of cardia cancers and esophageal adenocarcinoma (EAC continue to increase. The etiological factors involved in the development of both cardia cancers and EACs are associated with high animal fat intake, which causes severe obesity. Central obesity plays roles in cardiac-type mucosa lengthening and partial hiatus hernia development. There are two distinct etiologies of cardia cancer subtypes: one associated with gastroesophageal reflux (GER, which predominantly occurs in patients without Helicobacter pylori (H. pylori infection and resembles EAC, and the other associated with H. pylori atrophic gastritis, which resembles noncardia cancer. The former can be developed in the environment of high volume duodenal content reflux, including bile acids and a higher acid production in H. pylori–negative patients. N-nitroso compounds, which are generated from the refluxate that includes a large volume of bile acids and are stabilized in the stomach (which has high levels of gastric acid, play a pivotal role in this carcinogenesis. The latter can be associated with the changing colonization of H. pylori from the distal to the proximal stomach with atrophic gastritis because a high concentration of soluble bile acids in an environment of low acid production is likely to act as a bactericide or chemorepellent for H. pylori in the distal stomach with H. pylori infection. The manuscript introduces new insights in causative factors of adenocarcinoma of the cardia about the role of bile acids in gastro-esophageal refluxate based upon robust evidences supporting interactions among pH, H. pylori, and bile acids.

Factors that mediate colonization of the human stomach by Helicobacter pylori.

Science.gov (United States)

Dunne, Ciara; Dolan, Brendan; Clyne, Marguerite

2014-05-21

Helicobacter pylori (H. pylori) colonizes the stomach of humans and causes chronic infection. The majority of bacteria live in the mucus layer overlying the gastric epithelial cells and only a small proportion of bacteria are found interacting with the epithelial cells. The bacteria living in the gastric mucus may act as a reservoir of infection for the underlying cells which is essential for the development of disease. Colonization of gastric mucus is likely to be key to the establishment of chronic infection. How H. pylori manages to colonise and survive in the hostile environment of the human stomach and avoid removal by mucus flow and killing by gastric acid is the subject of this review. We also discuss how bacterial and host factors may together go some way to explaining the susceptibility to colonization and the outcome of infection in different individuals. H. pylori infection of the gastric mucosa has become a paradigm for chronic infection. Understanding of why H. pylori is such a successful pathogen may help us understand how other bacterial species colonise mucosal surfaces and cause disease.

Outer membrane vesicles enhance the carcinogenic potential of Helicobacter pylori.

Science.gov (United States)

Chitcholtan, Kenny; Hampton, Mark B; Keenan, Jacqueline I

2008-12-01

Chronic Helicobacter pylori infection is associated with an increased risk of gastric carcinogenesis. These non-invasive bacteria colonize the gastric mucosa and constitutively shed small outer membrane vesicles (OMV). In this study, we investigated the direct effect of H.pylori OMV on cellular events associated with carcinogenesis. We observed increased micronuclei formation in AGS human gastric epithelial cells treated with OMV isolated from a toxigenic H.pylori strain (60190). This effect was absent in OMV from strain 60190v:1 that has a mutant vacA, indicating VacA-dependent micronuclei formation. VacA induces intracellular vacuolation, and reduced acridine orange staining indicated disruption in the integrity of these vacuoles. This was accompanied by an alteration in iron metabolism and glutathione (GSH) loss, suggesting a role for oxidative stress in genomic damage. Increasing intracellular GSH levels with a GSH ester abrogated the VacA-mediated increase in micronuclei formation. In conclusion, OMV-mediated delivery of VacA to the gastric epithelium may constitute a new mechanism for H.pylori-induced gastric carcinogenesis.

A Possible Link between Gastric Mucosal Atrophy and Gastric Cancer after Helicobacter pylori Eradication.

Directory of Open Access Journals (Sweden)

Tomomitsu Tahara

Full Text Available The effect of H. pylori eradication in gastric cancer prevention can be attributed to the improvement of atrophic gastritis, which is a known risk of gastric cancer. However, gastric cancer has also been diagnosed after long-term H. pylori eradication. This study aimed to clarify the association between gastric atrophy and gastric cancer after H. pylori eradication, including its clinicopathological features.A total of 55 consecutive patients with 64 early gastric cancers (EGCs diagnosed after H. pylori eradication were enrolled. The degree of endoscopic atrophy and the histological degrees of mononuclear cell infiltration, atrophy, and metaplasia in the corpus and adjacent mucosa of the EGCs were determined and scored.The majority of EGCs (63/64 were located within the endoscopically assessed atrophic mucosa or along the atrophic border. The adjacent mucosa of the EGCs presented significantly higher degrees of all histological parameters than in the corpus (mononuclear cell infiltration, 0.86+/-0.09 vs. 0.51+/-0.11, P = 0.016; atrophy, 1.77+/-0.13 vs. 0.65+/-0.14, P<0.0001; metaplasia, 1.68+/-0.13 vs. 0.48+/-0.1, P<0.0001. The degree of endoscopic atrophy improved in the patients with longer post-H. pylori eradication periods; however, this trend was not observed for the histological parameters, and high degrees of atrophy and metaplasia were observed in the adjacent mucosa of the EGCs compared with the corpus during all periods (all P<0.05. The histological degrees of atrophy and metaplasia in the adjacent mucosa were particularly higher in the patients who underwent eradication due to gastric ulcers.Severe gastric atrophy remained in the adjacent mucosa of the EGCs after H. pylori eradication, which may be linked to gastric carcinogenesis.

Changes in gastric microbiota induced by Helicobacter pylori infection and preventive effects of Lactobacillus plantarum ZDY 2013 against such infection.

Science.gov (United States)

Pan, Mingfang; Wan, Cuixiang; Xie, Qiong; Huang, Renhui; Tao, Xueying; Shah, Nagendra P; Wei, Hua

2016-02-01

Helicobacter pylori is a gram-negative pathogen linked to gastric ulcers and stomach cancer. Gastric microbiota might play an essential role in the pathogenesis of these stomach diseases. In this study, we investigated the preventive effect of a probiotic candidate Lactobacillus plantarum ZDY 2013 as a protective agent against the gastric mucosal inflammation and alteration of gastric microbiota induced by H. pylori infection in a mouse model. Prior to infection, mice were pretreated with or without 400 µL of L. plantarum ZDY 2013 at a concentration of 10(9) cfu/mL per mouse. At 6 wk postinfection, gastric mucosal immune response and alteration in gastric microbiota mice were examined by quantitative real-time PCR and high-throughput 16S rRNA gene amplicon sequencing, respectively. The results showed that L. plantarum ZDY 2013 pretreatment prevented increase in inflammatory cytokines (e.g., IL-1β and IFN-γ) and inflammatory cell infiltration in gastric lamina propria induced by H. pylori infection. Weighted UniFrac principal coordinate analysis showed that L. plantarum ZDY 2013 pretreatment prevented the alteration in gastric microbiota post-H. pylori infection. Linear discriminant analysis coupled with effect size identified 22 bacterial taxa (e.g., Pasteurellaceae, Erysipelotrichaceae, Halomonadaceae, Helicobacteraceae, and Spirochaetaceae) that overgrew in the gastric microbiota of H. pylori-infected mice, and most of them belonged to the Proteobacteria phylum. Lactobacillus plantarum ZDY 2013 pretreatment prevented this alteration; only 6 taxa (e.g., Lachnospiraceae, Ruminococcaceae, and Clostridiaceae), mainly from the taxa of Firmicutes and Bacteroidetes, were dominant in the gastric microbiota of the L. plantarum ZDY 2013 pretreated mice. Administration of L. plantarum ZDY 2013 for 3 wk led to increase in several bacterial taxa (e.g., Rikenella, Staphylococcus, Bifidobacterium), although a nonsignificant alteration was found in the gastric microbiota

Influence of duodenogastric reflux in the gastric mucosa histological changes of rats infected with Helicobacter pylori.

Science.gov (United States)

Araujo, José Carlos Ribeiro DE; Carvalho, Jorge José DE; Serra, Humberto Oliveira

2016-01-01

to evaluate the influence of Duodenal reflux in histological changes of the gastric mucosa of rats infected with Helicobacter pylori submitted to pyloroplasty. after two weeks of acclimation, we infected 30 male Wistar rats with Helicobacter pylori. We randomly divided them into three groups: one submitted to pyloroplasty, another to partial gastrectomy and the third, only infected, was not operated. After six months of surgery, euthanasia was carried out. Gastric fragments were studied by light microscopy to count the number of H. pylori, and to observe the histological changes (gastritis, metaplasia, dysplasia and neoplasia). We confirmed these changes by immunohistochemistry using the molecular markers PCNA and TGF-beta. the animals submitted to pyloroplasty had higher percentage of colonization by H. pylori (median=58.5; gastrectomy=16.5; control=14.5). There was a positive correlation between the amount of H. pylori and the occurrence of chronic gastritis present in the antral fragments. Neoplasia occurred in 40% of rats from the group submitted to pyloroplasty. The staining with PCNA and TGF-ß confirmed the histopathological changes visualized by optical microscopy. the antral region was the one with the highest concentration of H. pylori, regardless of the group. There was a positive correlation between the appearance of benign disorders (chronic gastritis, metaplasia, dysplasia) and cancer in mice infected with H. pylori submitted to pyloroplasty. avaliar a influência do refluxo duodenogástrico nas alterações histológicas da mucosa gástrica de ratos, infectados por Helicobacter pylori, submetidos à piloroplastia. após duas semanas de aclimatação, 30 ratos machos da raça Wistar, foram infectados com o microorganismo patogênico H. pylori. De forma aleatória, foram divididos em três grupos: um submetido à piloroplastia, outro à gastrectomia parcial e o terceiro, apenas infectados, não foi operado. Após seis meses de operados, procedeu-se a

Clinical Manifestations of Helicobacter pylori-Negative Gastritis.

Science.gov (United States)

Shiota, Seiji; Thrift, Aaron P; Green, Linda; Shah, Rajesh; Verstovsek, Gordana; Rugge, Massimo; Graham, David Y; El-Serag, Hashem B

2017-07-01

There are data to suggest the existence of non-Helicobacter pylori gastritis. However, the risk factors and clinical course for H pylori-negative gastritis remain unclear. We aimed to examine the prevalence and determinants of H pylori-negative gastritis in a large multiethnic clinical population. We conducted a cross-sectional study among patents scheduled for an elective esophagastroduodenoscopy or attending selected primary care clinics and eligible for screening colonoscopy at a single Veterans Affairs medical center. We identified cases of H pylor-negative gastritis, H pylori-positive gastritis, and H pylori-negative nongastritis, where gastritis was defined by the presence of neutrophils and/or mononuclear cells. Risk factors for H pylori-negative gastritis were analyzed in logistic regression models. A total of 1240 patients had information from all biopsy sites, of whom 695 (56.0%) had gastritis. H pylori-negative gastritis was present in 123 patients (9.9% of all study subjects and 17.7% of all patients with gastritis). Among all patients with gastritis, African Americans were statistically significantly less likely than non-Hispanic whites to have H pylori-negative gastritis (odds ratio, 0.25; 95% confidence interval, 0.14-0.43). Conversely, PPI users were more likely to have H pylori-negative gastritis than H pylori-positive gastritis compared with nonusers (odds ratio, 2.02; 95% confidence interval, 1.17-3.49). The cumulative incidence of gastric erosions and ulcers were higher in patients with H pylori-negative gastritis than H pylori-negative nongastritis. We found that H pylori-negative gastritis was present in approximately 18% of patients with gastritis. The potential for H pylori-negative gastritis to progress or the risk of gastric cancer of those with gastric mucosal atrophy/intestinal metaplasia remains unclear. Copyright © 2017 AGA Institute. Published by Elsevier Inc. All rights reserved.

Role of microRNAs and Exosomes in Helicobacter pylori and Epstein-Barr Virus Associated Gastric Cancers

Science.gov (United States)

Polakovicova, Iva; Jerez, Sofia; Wichmann, Ignacio A.; Sandoval-Bórquez, Alejandra; Carrasco-Véliz, Nicolás; Corvalán, Alejandro H.

2018-01-01

Emerging evidence suggests that chronic inflammation caused by pathogen infection is connected to the development of various types of cancer. It is estimated that up to 20% of all cancer deaths is linked to infections and inflammation. In gastric cancer, such triggers can be infection of the gastric epithelium by either Helicobacter pylori (H. pylori), a bacterium present in half of the world population; or by Epstein-Barr virus (EBV), a double-stranded DNA virus which has recently been associated with gastric cancer. Both agents can establish lifelong inflammation by evolving to escape immune surveillance and, under certain conditions, contribute to the development of gastric cancer. Non-coding RNAs, mainly microRNAs (miRNAs), influence the host innate and adaptive immune responses, though long non-coding RNAs and viral miRNAs also alter these processes. Reports suggest that chronic infection results in altered expression of host miRNAs. In turn, dysregulated miRNAs modulate the host inflammatory immune response, favoring bacterial survival and persistence within the gastric mucosa. Given the established roles of miRNAs in tumorigenesis and innate immunity, they may serve as an important link between H. pylori- and EBV-associated inflammation and carcinogenesis. Example of this is up-regulation of miR-155 in H. pylori and EBV infection. The tumor environment contains a variety of cells that need to communicate with each other. Extracellular vesicles, especially exosomes, allow these cells to deliver certain type of information to other cells promoting cancer growth and metastasis. Exosomes have been shown to deliver not only various types of genetic information, mainly miRNAs, but also cytotoxin-associated gene A (CagA), a major H. pylori virulence factor. In addition, a growing body of evidence demonstrates that exosomes contain genetic material of viruses and viral miRNAs and proteins such as EBV latent membrane protein 1 (LMP1) which are delivered into

Role of microRNAs and Exosomes in Helicobacter pylori and Epstein-Barr Virus Associated Gastric Cancers

Directory of Open Access Journals (Sweden)

Iva Polakovicova

2018-04-01

Full Text Available Emerging evidence suggests that chronic inflammation caused by pathogen infection is connected to the development of various types of cancer. It is estimated that up to 20% of all cancer deaths is linked to infections and inflammation. In gastric cancer, such triggers can be infection of the gastric epithelium by either Helicobacter pylori (H. pylori, a bacterium present in half of the world population; or by Epstein-Barr virus (EBV, a double-stranded DNA virus which has recently been associated with gastric cancer. Both agents can establish lifelong inflammation by evolving to escape immune surveillance and, under certain conditions, contribute to the development of gastric cancer. Non-coding RNAs, mainly microRNAs (miRNAs, influence the host innate and adaptive immune responses, though long non-coding RNAs and viral miRNAs also alter these processes. Reports suggest that chronic infection results in altered expression of host miRNAs. In turn, dysregulated miRNAs modulate the host inflammatory immune response, favoring bacterial survival and persistence within the gastric mucosa. Given the established roles of miRNAs in tumorigenesis and innate immunity, they may serve as an important link between H. pylori- and EBV-associated inflammation and carcinogenesis. Example of this is up-regulation of miR-155 in H. pylori and EBV infection. The tumor environment contains a variety of cells that need to communicate with each other. Extracellular vesicles, especially exosomes, allow these cells to deliver certain type of information to other cells promoting cancer growth and metastasis. Exosomes have been shown to deliver not only various types of genetic information, mainly miRNAs, but also cytotoxin-associated gene A (CagA, a major H. pylori virulence factor. In addition, a growing body of evidence demonstrates that exosomes contain genetic material of viruses and viral miRNAs and proteins such as EBV latent membrane protein 1 (LMP1 which are

Helicobacter pylori Antibody Titer and Gastric Cancer Screening

Directory of Open Access Journals (Sweden)

Hiroshi Kishikawa

2015-01-01

Full Text Available The “ABC method” is a serum gastric cancer screening method, and the subjects were divided based on H. pylori serology and atrophic gastritis as detected by serum pepsinogen (PG: Group A [H. pylori (− PG (−], Group B [H. pylori (+ PG (−], Group C [H. pylori (+ PG (+], and Group D [H. pylori (− PG (+]. The risk of gastric cancer is highest in Group D, followed by Groups C, B, and A. Groups B, C, and D are advised to undergo endoscopy, and the recommended surveillance is every three years, every two years, and annually, respectively. In this report, the reported results with respect to further risk stratification by anti-H. pylori antibody titer in each subgroup are reviewed: (1 high-negative antibody titer subjects in Group A, representing posteradicated individuals with high risk for intestinal-type cancer; (2 high-positive antibody titer subjects in Group B, representing active inflammation with high risk for diffuse-type cancer; and (3 low-positive antibody titer subjects in Group C, representing advanced atrophy with increased risk for intestinal-type cancer. In these subjects, careful follow-up with intervals of surveillance of every three years in (1, every two years in (2, and annually in (3 should be considered.

Treatment of Helicobacter pylori infections: Mitigating factors and ...

African Journals Online (AJOL)

Helicobacter pylori is a Gram-negative, microaerophilic spiral or motile rod that infects about half the world's population with a very high prevalence in the developing world. It is an important aetiological factor in the development of gastritis, peptic ulcer disease, gastric atrophy and B cell mucosa associated lymphoid tissue ...

Helicobacter pylori eradication as the sole treatment for gastric and duodenal ulcers.

Science.gov (United States)

Arkkila, Perttu Et; Seppälä, Kari; Kosunen, Timo U; Sipponen, Pentti; Mäkinen, Judit; Rautelin, Hilpi; Färkkilä, Martti

2005-01-01

It is uncertain whether eradication of Helicobacter pylori--without a prolonged suppression of acid secretion--is sufficient to allow healing of peptic ulcers. We evaluated whether eradication of H. pylori with no following anti-secretory medication then administered is sufficient for treatment of peptic ulcers. We also looked at the impact of non-steroidal anti-inflammatory drug (NSAID) and acetylsalicylic acid (ASA) use on ulcer relapses. The effect of eradication on ulcer healing and relapse rate was analysed in 115 patients, randomly allocated to four treatment groups: (1) quadruple therapy (28); (2) dual therapy (n-30); (3) triple therapy (n=27); and (4) lansoprazole and placebo (n=30). Endoscopic assessment was performed at 0, 8, and 52 weeks. The ulcer healing rate was 100% [95% confidence interval (CI), 95-100%] in H. pylori-negative and 83% (95% CI, 67-94%) in H. pylori-positive patients (PUlcer relapses occurred in 5% (95% CI, 1-13%) of H. pylori-negative and in 36% (95% CI, 19-56%) of H. pylori-positive patients (P ulcer relapse rate was 30% (95% CI, 7-65%), whereas the ulcer relapse rate was 2% (95% CI, 0.4-10%) in patients who did not use NSAIDs or ASA (P ulcer relapse rate in H. pylori-positive patients who used or did not use NSAIDs or ASA was found. The eradication rate of H. pylori was 93% (95% CI, 76-99%) in the quadruple therapy group, 83% (95% CI, 64-94%) in the dual therapy group, 100% (95% CI, 87-100%) in the triple therapy group, and 0% (95% CI, 0-12%) in the lansoprazole and placebo group. Eradication treatment for H. pylori-positive gastric or duodenal ulcer is sufficient, with no need to follow it with anti-secretory medication. Cure of the infection reduces ulcer relapses in patients who did not use NSAIDs or ASA.

Association between interleukin-1 β polymorphisms and gastric disease in children: A correlation with Helicobacter pylori

Directory of Open Access Journals (Sweden)

Luanna Munhoz Zabaglia

2016-09-01

Full Text Available Objective: To investigate an association between the interleukin-1β (IL-1β -511 T>C (rs16944, -31 C>T (rs1143627, and/or interleukin-1 receptor antagonist (IL-1RA polymorphisms and gastritis and then to correlate any associations with the presence of Helicobacter pylori (H. pylori, cagA and vacA genes. Methods: Gastric biopsies were obtained from 377 children with gastric symptoms including 152 males and 225 females aging from 1–15 years with the mean age of (9.41 ± 4.29 years. To characterize the -511 T>C, -31 C>T, and IL-1RA polymorphisms, the PCR-RFLP and PCRVNTR methods were used. PCR was also used for the diagnosis of H. pylori and to determine whether cagA and vacA genes were present. Results: The histopathological analysis revealed 206 patients (54.6% with gastritis and 171 patients (45.4% with normal gastric tissue. Subjects carrying the -511 T/T genotype were associated with a risk of gastritis (odds ratio (OR = 2.75, 95% confidence interval (CI 1.45– 5.18, P = 0.0035. Similar results were found in subjects carrying -31 C/C (OR= 2.27, 95% CI 1.13–4.54, P = 0.0440. However, the IL-1RA polymorphism did not seem to be associated with gastric disease (OR= 1.38, 95% CI 0.58–3.26, P = 0.2400. Conclusions: This data suggests that IL-1β gene cluster polymorphisms and, more specifically, interactions between these polymorphisms and H. pylori may be predictors of gastritis risks, which possibly play a relevant role in the susceptibility to or the development of gastric disease early in life.

Study on Urea Breath Test (UBT) a tool for helicobacter pylori infection

International Nuclear Information System (INIS)

Kolekar, R.V.; Bhade, S.P.D.; Reddy, Priyanka; Singh, Rajvir; Gadgil, Anita; Bhandarkar, Prashant; Roy, N.; Patil, S.P.

2016-01-01

Helicobacter pylori commonly called as H. pylori resides in the gastric epithelial mucosa and induces an inflammatory response leading to gastritis, peptic nicer disease and gastric malignancies. Detection and eradication of H.pylori infection is thus an important measure to prevent these. H.pylori has a worldwide prevalence rate of about 50%, with a higher prevalence in developing countries. Urea breath test, an outpatient noninvasive technique achieves up to 95% sensitivity and specificity at half the cost compared to histology, in detecting H. Pylori infection. Indian studies on the use of UBT and its standard protocol are sparse. The present paper discusses the application of Carbon-14 Urea breath test for the diagnosis of H pylori bacterial infection in 261 adult patients

Seven-day PPI-triple therapy with levofloxacin is very effective for Helicobacter pylori eradication.

NARCIS (Netherlands)

Schrauwen, R.W.; Janssen, M.J.R.; Boer, W.A. de

2009-01-01

BACKGROUND: Helicobacter pylori infection causes lifelong gastritis and is associated with the development of peptic ulcer disease, MALT lymphoma and gastric cancer. Many patients benefit from H. pylori eradication therapy. PPI-triple therapy is recommended as initial therapy. Quadruple therapy,

Piperine treatment suppresses Helicobacter pylori toxin entry in to gastric epithelium and minimizes β-catenin mediated oncogenesis and IL-8 secretion in vitro

OpenAIRE

Tharmalingam, Nagendran; Park, Min; Lee, Min Ho; Woo, Hyun Jun; Kim, Hyun Woo; Yang, Ji Yeong; Rhee, Ki-Jong; Kim, Jong-Bae

2016-01-01

Helicobacter pylori related gastric cancer initiation has been studied widely. The objective of our present study was to evaluate the effect of a single compound piperine on H. pylori infection and its anti-inflammatory and anti-cancer effects in vitro. Cytotoxicity was tested by Ez-cytox cell viability assay kit. Effects of piperine on H. pylori toxin gene expression and IL-8 expression in mammalian cells during infection were assessed by RT-PCR. Effects of piperine on toxin entry into host ...

Re-annotation of the genome sequence of Helicobacter pylori 26695

Directory of Open Access Journals (Sweden)

Resende Tiago

2013-12-01

Full Text Available Helicobacter pylori is a pathogenic bacterium that colonizes the human epithelia, causing duodenal and gastric ulcers, and gastric cancer. The genome of H. pylori 26695 has been previously sequenced and annotated. In addition, two genome-scale metabolic models have been developed. In order to maintain accurate and relevant information on coding sequences (CDS and to retrieve new information, the assignment of new functions to Helicobacter pylori 26695s genes was performed in this work. The use of software tools, on-line databases and an annotation pipeline for inspecting each gene allowed the attribution of validated EC numbers and TC numbers to metabolic genes encoding enzymes and transport proteins, respectively. 1212 genes encoding proteins were identified in this annotation, being 712 metabolic genes and 500 non-metabolic, while 191 new functions were assignment to the CDS of this bacterium. This information provides relevant biological information for the scientific community dealing with this organism and can be used as the basis for a new metabolic model reconstruction.

Seroprevalence of Helicobacter pylori in Hispanics living in Puerto Rico: A population-based study.

Science.gov (United States)

González-Pons, María; Soto-Salgado, Marievelisse; Sevilla, Javier; Márquez-Lespier, Juan M; Morgan, Douglas; Pérez, Cynthia M; Cruz-Correa, Marcia

2018-02-01

Helicobacter pylori is an important etiologic factor for peptic ulcers and gastric cancer, one of the top ten leading causes of cancer death in Puerto Rico. However, the prevalence of H. pylori infections in this population was previously unknown. The aim of this study was to examine the seroprevalence of H. pylori and its associated risk factors in Puerto Rico. A cross-sectional study was designed using an existing population-based biorepository. Seropositivity was determined using the Premier ™ H. pylori immunoassay. Helicobacter pylori seroprevalence was estimated with 95% confidence using marginal standardization following logistic regression. To assess the risk factors associated with H. pylori seropositivity, a multivariable log-binomial model was fitted to estimate the prevalence ratio (PR) and its 95% confidence interval (95% CI). A total of 528 population-based serum samples were analyzed. The mean age of the study population was 41 ± 12 years, of whom 55.3% were females. The overall seroprevalence of H. pylori was 33.0% (95% CI = 28.3%-38.1%). Increasing age and having Puerto Rico. The H. pylori seroprevalence observed in Puerto Rico is similar to the seroprevalence reported in the overall population of the United States. The association between H. pylori seroprevalence and the risk factors analyzed offers insight into the epidemiology of gastric cancer in Puerto Rico and warrants further investigation. © 2017 The Authors. Helicobacter Published by John Wiley & Sons Ltd.

Piperine treatment suppresses Helicobacter pylori toxin entry in to gastric epithelium and minimizes β-catenin mediated oncogenesis and IL-8 secretion in vitro

Science.gov (United States)

Tharmalingam, Nagendran; Park, Min; Lee, Min Ho; Woo, Hyun Jun; Kim, Hyun Woo; Yang, Ji Yeong; Rhee, Ki-Jong; Kim, Jong-Bae

2016-01-01

Helicobacter pylori related gastric cancer initiation has been studied widely. The objective of our present study was to evaluate the effect of a single compound piperine on H. pylori infection and its anti-inflammatory and anti-cancer effects in vitro. Cytotoxicity was tested by Ez-cytox cell viability assay kit. Effects of piperine on H. pylori toxin gene expression and IL-8 expression in mammalian cells during infection were assessed by RT-PCR. Effects of piperine on toxin entry into host cells, E-cadherin cleavage by H. pylori, and the changes in H. pylori mediated β-catenin expression and IL-8 secretion were determined by immunoblotting. Piperine treatment restrained the entry of CagA and VacA into AGS cells. Piperine administration in H. pylori infection reduced E-cadherin cleavage in stomach epithelium. In addition, H. pylori induced β-catenin up-regulation was reduced. Piperine administration impaired IL-8 secretion in H. pylori-infected gastric epithelial cells. As we reported previously piperine restrained H. pylori motility. The possible reason behind the H. pylori inhibition mechanism of piperine could be the dwindled motility, which weakened H. pylori adhesion to gastric epithelial cells. The reduced adhesion decreased the toxin entry thereby secreting less amount of IL-8. In addition, piperine treatment suppressed H. pylori protease led to reduction of E-cadherin cleavage and β-catenin expression resulting in diminished β-catenin translocation into the nucleus thus decreasing the risk of oncogenesis. To our knowledge, this is the preliminary report of piperine mediated H. pylori infection control on gastric epithelial cells in-vitro. PMID:27158376

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. Copyright © 2014 Elsevier Inc. All rights reserved.

An association between Helicobacter pylori and upper respiratory tract disease: Fact or fiction?

Science.gov (United States)

Kariya, Shin; Okano, Mitsuhiro; Nishizaki, Kazunori

2014-01-01

Helicobacter pylori (H. pylori) is a major cause of chronic gastritis and gastric ulcers and considerable evidence supports the notion that infection with this bacterium is also associated with gastric malignancy in addition to various other conditions including pulmonary, vascular and autoimmune disorders. Gastric juice infected with H. pylori might play an important role in upper respiratory tract infection. Although direct and/or indirect mechanisms might be involved in the association between H. pylori and upper respiratory tract diseases, the etiological role of H. pylori in upper respiratory tract disorders has not yet been fully elucidated. Although various studies over the past two decades have suggested a relationship between H. pylori and upper respiratory tract diseases, the findings are inconsistent. The present overview describes the outcomes of recent investigations into the impact of H. pylori on upper respiratory tract and adjacent lesions. PMID:24587622

Treatment of helicobacter pylori infection; a controlled randomized comparative clinical trial

International Nuclear Information System (INIS)

Mehmood, A.; Usmanghani, K.; Mohiuddin, E.; Akram, M.

2010-01-01

Helicobacter pylori induces chronic inflammation of the underlying gastric mucosa and is strongly linked to the development of duodenal and gastric carcinoma. A study was conducted to evaluate the efficacy of Pylorex, a herbal formulation, for treatment of H. pylori infection as compared to triple allopathic therapy (Omeprazole, Amoxicillin, Metronidazole). The therapeutic evaluations of these medicines were conducted on 97 clinically and immunologically diagnosed cases of H. pylori infection. H. pylori was eradicated in 16 (32.6%) out of 49 patients by the use of triple allopathic therapy (Control drugs), and in 9 (18.7%) out of 48 patients by the use of Pylorex (Test drug). Pylorex possesses a therapeutic value for the treatment of H. pylori associated symptoms but the eradication rate is superior in triple allopathic therapy. (author)

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

Cell-cycle inhibition by Helicobacter pylori L-asparaginase.

Directory of Open Access Journals (Sweden)

Claudia Scotti

Full Text Available Helicobacter pylori (H. pylori is a major human pathogen causing chronic gastritis, peptic ulcer, gastric cancer, and mucosa-associated lymphoid tissue lymphoma. One of the mechanisms whereby it induces damage depends on its interference with proliferation of host tissues. We here describe the discovery of a novel bacterial factor able to inhibit the cell-cycle of exposed cells, both of gastric and non-gastric origin. An integrated approach was adopted to isolate and characterise the molecule from the bacterial culture filtrate produced in a protein-free medium: size-exclusion chromatography, non-reducing gel electrophoresis, mass spectrometry, mutant analysis, recombinant protein expression and enzymatic assays. L-asparaginase was identified as the factor responsible for cell-cycle inhibition of fibroblasts and gastric cell lines. Its effect on cell-cycle was confirmed by inhibitors, a knockout strain and the action of recombinant L-asparaginase on cell lines. Interference with cell-cycle in vitro depended on cell genotype and was related to the expression levels of the concurrent enzyme asparagine synthetase. Bacterial subcellular distribution of L-asparaginase was also analysed along with its immunogenicity. H. pylori L-asparaginase is a novel antigen that functions as a cell-cycle inhibitor of fibroblasts and gastric cell lines. We give evidence supporting a role in the pathogenesis of H. pylori-related diseases and discuss its potential diagnostic application.

Did transmission of Helicobacter pylori from humans cause a disease outbreak in a colony of Stripe-faced Dunnarts (Sminthopsis macroura?

Directory of Open Access Journals (Sweden)

Every Alison L

2011-02-01

Full Text Available Abstract Since the discovery that Helicobacter pylori causes a range of pathologies in the stomachs of infected humans, it has become apparent that Helicobacters are found in a diverse range of animal species where they are frequently associated with disease. In 2003 and 2004, there were two outbreaks of increased mortality associated with gastric bleeding and weight-loss in a captive colony of the Australian marsupial, the Stripe-faced Dunnart (Sminthopsis macroura. The presence of gastric pathology led to an investigation of potential Helicobacter pathogenesis in these animals. Histological examination revealed the presence of gastritis, and PCR analysis confirmed the presence of Helicobacter infection in the stomachs of these marsupials. Surprisingly, sequencing of 16S rRNA from these bacteria identified the species as H. pylori and PCR confirmed the strain to be positive for the important pathogenesis factor, cagA. We therefore describe, for the first time, an apparent reverse zoonotic infection of Stripe-faced Dunnarts with H. pylori. Already prone to pathological effects of stress (as experienced during breeding season, concomitant H. pylori infection appears to be a possible essential but not sufficient co-factor in prototypic gastric bleeding and weight loss in these marsupials. The Stripe-faced Dunnart could represent a new model for investigating Helicobacter-driven gastric pathology. Infections from their human handlers, specifically of H. pylori, may be a potential risk to captive colonies of marsupials.

Helicobacter pylori in First Nations and Recent Immigrant Populations in Canada

Directory of Open Access Journals (Sweden)

Nicola L Jones

2012-01-01

Full Text Available The diminishing prevalence of Helicobacter pylori infection among most segments of the Canadian population has led to changes in the etiologies and patterns of associated upper gastrointestinal diseases, including fewer peptic ulcers and their complications. Canadian Aboriginals and recent immigrants are among populations in which the prevalence of H pylori infection remains high and, therefore, the health risks imposed by H pylori remain a significant concern. Population-based strategies for H pylori eradication in groups with a low prevalence of infection are unlikely to be cost effective, but such measures are attractive in groups in which the prevalence rates of infection remain substantial. In addition to a lower prevalence of peptic ulcers and dyspepsia, the public health value of eradication may be particularly important if this leads to a reduction in the prevalence of gastric cancer in high prevalence groups. Therefore The Canadian Helicobacter Study Group held a conference that brought together experts in the field to address these issues, the results of which are reviewed in the present article. Canadians with the highest prevalence of H pylori infection are an appropriate focus for considering the health advantages of eradicating persistent infection. In Canadian communities with a high prevalence of both H pylori and gastric cancer, there remains an opportunity to test the hypothesis that H pylori infection is a treatable risk factor for malignancy.

Invasive Tests for Helicobacter Pylori in Children

Directory of Open Access Journals (Sweden)

Hien Q Huynh

2005-01-01

Full Text Available One of the primary indications for upper gastrointestinal (GI endoscopy in children is the presence of persistent and severe upper abdominal symptoms. Upper GI endoscopies are performed to allow the physician to confirm or rule out upper GI pathology. Additionally, upper GI endoscopies with mucosal biopsies are the gold standard for the diagnosis of Helicobacter pylori infection and its complications in children. The gastric biopsies can be used for the rapid urease test, histological examination and bacterial culture to determine antibiotic sensitivity. DNA extracted in these biopsies can also be subjected to genotyping using molecular methods to determine the presence of H pylori infection, antibiotic resistance mutations and H pylori virulence factors.

Prevalence of Helicobacter Pylori in Gastric Fluid in the Surgical Patient

Science.gov (United States)

1998-05-01

highest rates of H. pylori infection occur in areas with the highest rates of stomach cancer, such as China, Japan, Peru and Scotland. However, even in the...Mahoney, D.H. (1997). Helicobacter pylori gastritis in a child with sickle cell anemia and recurrent abdominal pain. Journal of Hematology and

[Overview of researches for Helicobacter pylori in oral cavity and stomach].

Science.gov (United States)

Yang, Kaiyu; Li, Yuqing; Zhou, Xuedong

2014-06-01

Helicobacter pylori (H. pylori) is one of the most common pathogens in human and it is closely related to gastrointestinal diseases. It is essential for us to understand the transmission process of H. pylori to prevent its spreading. The oral cavity has been proposed as a reservoir for gastric H. pylori, which has been detected by culture and polymerase chain reaction (PCR) in both dental plaque and saliva. Some researchers have proposed H. pylori in oral cavity may play an important role in its transmission and reinfection. Oral-oral or fecal-oral transmission are thought to be the most possible transmit way. This review will discuss the evidence for the role of the oral cavity in the transmission of H. pylori, the difficulties encountered in addressing this topic and possible directions for future research. Oral H. pylori may also play a role in the diagnosis and prevention of deceases related to H. pylori such as gastritis, gastric ulcer and gastric carcinoma. The recent progresses in this area are also reviewed. Moreover, we also discussed the relationship between oral H. pylori and oral deceases like periodontal disease and oral ulcer.

Gastric polyps diagnosed by double-contrast upper gastrointestinal barium X-ray radiography mostly arise from the Helicobacter pylori-negative stomach with low risk of gastric cancer in Japan.

Science.gov (United States)

Takeuchi, Chihiro; Yamamichi, Nobutake; Shimamoto, Takeshi; Takahashi, Yu; Mitsushima, Toru; Koike, Kazuhiko

2017-03-01

Double-contrast upper gastrointestinal barium X-ray radiography (UGI-XR) is a method broadly used for gastric cancer screening in Japan. Gastric polyp is one of the most frequent findings detected by UGI-XR, but how to handle it remains controversial. Gastric polyps of the 17,264 generally healthy subjects in Japan who underwent UGI-XR or upper gastrointestinal endoscopy (UGI-ES) in 2010 were analyzed. Of the 6,433 UGI-XR examinees (3,405 men and 3,028 women, 47.4 ± 9.0 years old), gastric polyps were detected in 464 men (13.6 %) and 733 women (24.2 %) and were predominantly developed on the non-atrophic gastric mucosa (p gastric polyps has significant association with lower value of serum anti-Helicobacter pylori IgG titer, female gender, lighter smoking habit, older age, and normal range of body mass index (≥18.5 and gastric cancer occurred in 7 subjects (0.11 %), but none of them had gastric polyps at the beginning of the follow-up period. Of the 2,722 subjects with gastric polyps among the 10,831 UGI-ES examinees in the same period, 2,446 (89.9 %) had fundic, 267 (9.8 %) had hyperplastic, and 9 (0.3 %) had adenomatous/cancerous polyps. Gastric polyps diagnosed by UGI-XR predominantly arise on the Helicobacter pylori-negative gastric mucosa with a low risk of gastric cancer in Japan. In the prospective observation, none of the UGI-XR examinees with gastric polyps developed gastric cancer for at least 3 years subsequently.

[Clinical significance of infection with cag A and vac A positive Helicobacter pylori strains].

Science.gov (United States)

Sokić-Milutinović, Aleksandra; Todorović, Vera; Milosavljević, Tomica

2004-01-01

Clinical relevance of infection with different Helicobacter pylori strains was reviewed in this paper. Helicobacter pylori (H. pylori) infection plays a role in pathogenesis of chronic gastritis, peptic ulcer disease, gastric adenocarcinoma and MALT lymphoma. Extragastric manifestations of H. pylori infection most probably include acne rosacea and chronic urticaria, while the importance of H. pylori infection for pathogenesis of growth retardation in children, iron deficiency anemia, coronary heart disease, stroke and idiopathic thrombocytopenic purpura remains vague. The expression of two H. pylori proteins, cytotoxin associated protein (cag A) and vacuolization cytotoxin (vac A) is considered to be related with pathogenicity of the bacterium. It is clear that presence of cag A+ strains is important for development of peptic ulcer; nevertheless, it is also protective against esophageal reflux disease. On the other hand, cag A+ strains are common in gastric adenocarcinoma and MALT lymphoma patients, but it seems that certain subtypes of vac A cytotoxin are more important risk factors. Infection with cag A+ strains is more common in patients with acne rosacea, stroke and coronary heart disease.

Clinical significance of infection with cag A and vac A positive helicobacter pylori strains

Directory of Open Access Journals (Sweden)

Sokić-Milutinović Aleksandra

2004-01-01

Full Text Available Clinical relevance of infection with different Helicobacter pylori strains was reviewed in this paper. Helicobacter pylori (H. pylori infection plays a role in pathogenesis of chronic gastritis, peptic ulcer disease, gastric adenocarcinoma and MALT lymphoma. Extragastric manifestations of H. pylori infection most probably include acne rosacea and chronic urticaria, while the importance of H. pylori infection for pathogenesis of growth retardation in children, iron deficiency anemia, coronary heart disease, stroke and idiopathic thrombocytopenic purpura remains vague. The expression of two H. pylori proteins, cytotoxin associated protein (cag A and vacuolization cytotoxin (vac A is considered to be related with pathogenicity of the bacterium. It is clear that presence of cag A+ strains is important for development of peptic ulcer; nevertheless, it is also protective against esophageal reflux disease. On the other hand, cag A+ strains are common in gastric adenocarcinoma and MALT lymphoma patients, but it seems that certain subtypes of vac A cytotoxin are more important risk factors. Infection with cag A+ strains is more common in patients with acne rosacea, stroke and coronary heart disease.

Severe gastritis decreases success rate of Helicobacter pylori eradication.

Science.gov (United States)

Kalkan, Ismail Hakki; Sapmaz, Ferdane; Güliter, Sefa; Atasoy, Pınar

2016-05-01

In several studies, different risk factors other than antibiotic resistance have been documented with Helicobacter pylori eradication failure. We aimed in this study to investigate the relationship of gastric density of H. pylori, the occurrence/degree of gastric atrophy, and intestinal metaplasia (IM) with success rate of H. pylori eradication. Two hundred consecutive treatment naive patients who received bismuth containing standart quadruple treatment due to H. pylori infection documented by histopathological examination of two antral or two corpal biopsies entered this retrospective study. The updated Sydney system was used to grade the activity of gastritis, density of H. pylori colonization, atrophy, and IM. Stages III and IV of operative link for gastritis assessment (OLGA) or the operative link on gastric intestinal metaplasia assessment (OLGIM) stages was considered as severe gastritis. H. pylori eradication was determined via stool H. pylori antigen test performed 4 weeks after the end of therapy. The presence of gastric atrophy and IM was significantly higher in patients with eradication failure (p = 0.001 and 0.01, respectively). Severe gastritis (OLGA III-IV and OLGIM III-IV) rates were higher in eradication failure group. A multiple linear regression analysis showed that OLGA and OLGIM stages were to be independent risk factors for eradication failure (p = 0.03 and 0.01, respectively). Our results suggested that histopathologically severe gastritis may cause H. pylori eradication failure. In addition, we found that H. pylori density was not a risk factor for treatment failure in patients who receive quadruple treatment.

Phenotypic and genotypic characterization of Helicobacter pylori from patients with and without peptic ulcer disease

DEFF Research Database (Denmark)

Petersen, A M; Fussing, V; Colding, H

2000-01-01

BACKGROUND: Helicobacter pylori plays an important role in peptic ulcer disease, although not all H. pylori-infected persons will develop a peptic ulcer. Currently, H. pylori strains cannot be divided into commensals and pathogens. METHODS: Fifty H. pylori strains were cultured from patients......) profile of H. pylori strains were recorded; randomly amplified polymorphic DNA (RAPD) and urease gene typing were performed and correlated with diagnostic groups. RESULTS: Electron micrographs showed that H. pylori strains from patients with gastric ulcers adhered more frequently through filamentous...... strands and were less frequently found free in mucus than any other diagnostic group (P pylori strains from patients with gastric...

Helicobacter heilmannii-associated Gastritis: Clinicopathologic Findings and Comparison with Helicobacter pylori-associated Gastritis

Science.gov (United States)

Kwak, Ji Eun; Chang, Sun Hee; Kim, Hanseong; Chi, Je G.; Kim, Kyung-Ah; Yang, Jeon Ho; Lee, June Sung; Moon, Young-Soo; Kim, Kyoung-Mee

2007-01-01

The aims of this study were to evaluate the clinicopathologic features of Helicobacter heilmannii-associated gastritis and to compare H. heilmannii-associated gastritis with H. pylori-associated gastritis. We reviewed 5,985 consecutive gastric biopsy specimens. All cases of chronic gastritis with Helicobacter infection were evaluated with the Updated Sydney System, and the grades of all gastritis variables were compared between H. heilmannii-associated gastritis and H. pylori-associated gastritis groups. There were 10 cases of H. heilmannii-associated gastritis (0.17%) and 3,285 cases of H. pylori-associated gastritis (54.9%). The organisms were superficially located within the mucous layer without adhesion to epithelial cells. Interestingly, in one case many intracytoplasmic H. heilmannii organisms were observed in parietal cells with cell damage. A case of low-grade mucosa-associated lymphoid tissue (MALT) lymphoma concomitant with H. heilmannii infection was detected. Compared to H. pylori-associated gastritis, H. heilmannii-associated gastritis showed less severe neutrophilic activity (pgastritis devoid of erosion or ulcer (p=0.0309). In conclusion, we present the detailed clinicopathologic findings of H. heilmannii-associated gastritis compared to H. pylori-associated gastritis. H. heilmannii-associated gastritis is uncommon and milder than H. pylori-associated gastritis, however it may be noteworthy with respect to the development of MALT lymphoma. PMID:17297253

Analysis of the microflora in the stomach of Mongolian gerbils infected with Helicobacter pylori.

Science.gov (United States)

Zaman, Cynthia; Osaki, Takako; Hanawa, Tomoko; Yonezawa, Hideo; Kurata, Satoshi; Kamiya, Shigeru

2010-05-01

Mongolian gerbils are frequently used to study Helicobacter pylori-induced gastritis and its consequences. The presence of some gastric flora with a suppressive effect on H. pylori suggests inhibitory microflora against H. pylori infection. The aim of the present study was to analyze the microflora in the stomach of Mongolian gerbils with H. pylori infection. H. pylori ureA was detected by polymerase chain reaction (PCR) in the fecal samples of infected Mongolian gerbils. H. pylori was isolated from the gastric mucosa of the gerbils by microaerophilic cultivation. Gastric microflora were isolated by aerobic and anaerobic culture, and the identification of gastric bacterial species was performed by API20E and API20A. Oral administration of H. pylori TK1402 induced colonization and gastric inflammation of the stomach of the Mongolian gerbils. According to the frequency of detection of H. pylori ureA in fecal samples, the gerbils were divided into three groups (frequently detected, moderately detected and infrequently detected). According to the analysis of the gastric microflora in the frequently and infrequently detected groups, Lactobacillus spp. and Eubacterium limosum were isolated from the former and latter group, respectively. Some gastric flora, such as Lactobacillus spp., may inhibit colonization by H. pylori.

Molecular alterations in early gastric carcinomas. No apparent correlation with Helicobacter pylori status

NARCIS (Netherlands)

Blok, P.; Craanen, M. E.; Offerhaus, G. J.; Dekker, W.; Kuipers, E. J.; Meuwissen, S. G.; Tytgat, G. N.

1999-01-01

Data on the differences in molecular profile between H pylori-positive and H pylori-negative early gastric carcinomas, if any, are almost nonexistent. We therefore investigated whether molecular differences can be observed between H pylori-positive and H pylori-negative early gastric carcinomas.

vacA genotypes of Helicobacter pylori in the oral cavity and stomach of patients with chronic gastritis and gastric ulcer.

Science.gov (United States)

Román-Román, Adolfo; Giono-Cerezo, Silvia; Camorlinga-Ponce, Margarita; Martínez-Carrillo, Dinorah Nashely; Loaiza-Loeza, Salome; Fernández-Tilapa, Gloria

2013-03-01

Helicobacter pylori adheres to various components of the human saliva. Therefore, the objective of this research was to simultaneously detect H. pylori in saliva and in gastric biopsy, and to determine the agreement between the vacA genotypes in both saliva and gastric biopsy. A total of 162 patients with chronic gastritis and 34 with gastric ulcer were studied, and saliva and biopsy samples were collected from each patient. H. pylori DNA was detected by conventional PCR and nested PCR was used for vacA genotyping. In 24% of the patients (47/196) H. pylori DNA was found in saliva and in biopsy; 52.5% (103/196) were saliva(negative)/biopsy(positive) and 6.6% (13/196) were saliva(positive)/biopsy(negative). In either or both H. pylori vacAs1m1 or s1m2 genotypes were detected in saliva in 41.5% of the patients with chronic gastritis. Forty-seven percent had >1 genotype, and the s1m1/s1m2 combination was found in 36% of them. H. pylori vacAs1m1 and s1m2 were also found in the saliva and biopsy of patients with gastric ulcer. The genotypes found in saliva and biopsy of the same patient had 51.1% agreement. In 27.6% of the 47 patients saliva(positive)/biopsy(positive) two genotypes were found in saliva, and one or both in the stomach. The s1m1/s1m2 genotypes, alone or together, are found simultaneously in saliva and gastric biopsy of the same patient. These results suggest that H. pylori reaches the oral cavity by various ways, and that saliva can be the transmitting and re-infecting vector. Copyright © 2012 Elsevier España, S.L. All rights reserved.

Antimicrobial and anti-inflammatory activities of Apis mellifera honey on the Helicobacter pylori infection of Wistar rats gastric mucosa

Directory of Open Access Journals (Sweden)

Thiago Yamamoto AMARAL

Full Text Available Abstract Considering that Helicobacter pylori, a bacterium able to colonize the upper gastrointestinal tract and cause mucosal injury, not always can be effectively eradicated by the traditional approaches, there is an interest in alternative therapies until a vaccine be available. Honey is a food supplement with high carbohydrate content and antioxidant activity, as well as broad antimicrobial spectrum. After analyzing the physicochemical and in vitro antimicrobial properties of an Apis mellifera honey from the Atlantic forest of Alagoas / Brazil, the purpose of the present work was evaluate its in vivo effects against Helicobacter pylori in the gastric mucosa of Wistar rats. First, it was verified the success of inoculation/infection of the pathogen in the gastric mucosa of the rats, through the subsequent removal of their stomachs for histological analysis (hematoxylin and eosin stain and Giemsa stain. Then, four groups of animals were treated with sterilized distilled deionized water, the Apis mellifera honey, a combination of omeprazole, amoxicillin and clarithromycin, and an association of such medicines and honey (1:1. Except the control, all treatments were effective in combating infection, however, honey reduced the inflammatory process, whilst the antibiotics increase the number of eosinophils.

The co-evolved Helicobacter pylori and gastric cancer: trinity of bacterial virulence, host susceptibility and lifestyle

Directory of Open Access Journals (Sweden)

Devi S Manjulata

2007-01-01

Full Text Available Abstract Helicobacter pylori is an important yet unproven etiological agent of gastric cancer. H. pylori infection is more prevalent in developing Asian countries like India and it is usually acquired at an early age. It has been two decades since Marshall and Warren (1984 first described curved bacilli in the stomach of ulcer and gastritis patients. This discovery has won them the Nobel Prize recently, but the debate whether H. pylori is a pathogen or a commensal organism is still hot. Associations with disease-specific factors remain illusive years after the genome sequences were made available. Cytotoxin-associated antigen A (CagA and the so-called plasticity region cluster genes are implicated in pathogenesis of the carcinoma of stomach. Another virulence factor VacA whose role is still debatable, has recently been projected in pathology of gastric cancer. Studies of the evolution through genetic variation in H. pylori populations have provided a window into the history of human population migrations and a possible co-evolution of this pathogen with its human host. Possible symbiotic relationships were seriously debated since the discovery of this pathogen. The debate has been further intensified as some studies proposed H. pylori infection to be beneficial in some humans. In this commentary, we attempt to briefly discuss about H. pylori as a human pathogen, and some of the important issues linked to its pathophysiology in different hosts. 'We dance around in a ring and suppose, the secret sits in the middle and knows' – Robert Frost

Indications for treatment of Helicobacter pylori infection: a systematic overview.

Science.gov (United States)

Veldhuyzen van Zanten, S J; Sherman, P M

1994-01-15

To determine (a) the advantages and disadvantages of treatment options for the eradication of Helicobacter pylori and (b) whether eradication of H. pylori is indicated in patients with duodenal ulcer, nonucler dyspepsia and gastric cancer. A MEDLINE search for articles published in English between January 1983 and December 1992 with the use of MeSH terms Helicobacter pylori (called Campylobacter pylori before 1990) and duodenal ulcer, gastric cancer, dyspepsia and clinical trial. Six journals and Current Contents were searched manually for pertinent articles published in that time frame. For duodenal ulcer the search was limited to studies involving adults, studies of H. pylori eradication and randomized clinical trials comparing anti-H. pylori therapy with conventional ulcer treatment. For nonulcer dyspepsia with H. pylori infection the search was limited to placebo-controlled randomized clinical trials. The quality of each study was rated independently on a four-point scale by each author. For the studies of duodenal ulcer the outcome measures assessed were acute ulcer healing and time required for healing, H. pylori eradication and ulcer relapse. For the studies of nonulcer dyspepsia with H. pylori infection the authors assessed H. pylori eradication, the symptoms used as outcome measures and whether validated outcome measures had been used. Eight trials involving duodenal ulcer met our inclusion criteria: five were considered high quality, two were of reasonable quality, and one was weak. Six trials involving nonulcer dyspepsia met the criteria, but all were rated as weak. Among treatment options triple therapy with a bismuth compound, metronidazole and either amoxicillin or tetracycline achieved the highest eradication rates (73% to 94%). Results concerning treatment indications for duodenal ulcer were consistent among all of the studies: when anti-H. pylori therapy was added to conventional ulcer treatment acute ulcers healed more rapidly. Ulcer relapse rates

Role of dupA in virulence of Helicobacter pylori.

Science.gov (United States)

Talebi Bezmin Abadi, Amin; Perez-Perez, Guillermo

2016-12-14

Helicobacter pylori ( H. pylori ) is a gastric human pathogen associated with acute and chronic gastritis, 70% of all gastric ulcers, 85% of all duodenal ulcers, and both forms of stomach cancer, mucosal-associated lymphoid tissue (MALT) lymphoma and adenocarcinoma. Recently, attention has focused on possible relationship between presence of certain virulence factor and H. pylori -associated diseases. Some contradictory data between this bacterium and related disorders has been observed since not all the colonized individuals develop to severe disease. The reported diseases plausibility related to H. pylori specific virulence factors became an interesting story about this organism. Although a number of putative virulence factors have been identified including cytotoxin-associated gene a ( cagA ) and vacA , there are conflicting data about their actual participation as specific risk factor for H. pylori -related diseases. Duodenal ulcer promoting gene a ( dupA ) is a virulence factor of H. pylori that is highly associated with duodenal ulcer development and reduced risk of gastric cancer. The prevalence of dupA in H. pylori strains isolated from western countries is relatively higher than in H. pylori strains from Asian countries. Current confusing epidemiological reports will continue unless future sophisticated and molecular studies provide data on functional and complete dupA cluster in H. pylori infected individuals. This paper elucidates available knowledge concerning role of dupA in virulence of H. pylori after a decade of its discovery.

Relationship between childhood asthma and Helicobacter pylori infection

Directory of Open Access Journals (Sweden)

Ying Wu

2016-07-01

Full Text Available Objective: To investigate the correlation between childhood asthma and Helicobacter pylori infection. Methods: A total of 80 children with asthma who were treated in our hospital from May 2012 to May 2015 were selected as the research subjects, and 40 cases of healthy children were selected as control group, the Helicobacter pylori infection of the two groups of patients were compared, the double antibody sandwich enzyme-linked immunosorbent assay was used to detect the serum Helicobacter pylori-IgG, Helicobacter pylori-CagAIgG, IL-4, Helicobacter pylori, IFN-γ and IL-1β, etc., and the correlation between Helicobacter pylori infection and asthma was analyzed. Results: The positive rates of Helicobacter pylori infection in asthma group and children in attack stage were significantly higher than those in control group and children in remission stage (P<0.05. The positive rates of serum Helicobacter pylori-IgG and Helicobacter pylori-CagAIgG in asthma group and children in attack stage were significantly lower than those in control group and children in remission stage (P<0.05. The serum levels of IFN-γ in asthma group and children in attack stage were significantly lower than those in control group and children in remission stage, IL-4 and IL-1β levels in the former were significantly higher than those in the latter (P<0.05. Helicobacter pylori infection positive had significant positive correlation with IL-1β concentration (r=0.75, P<0.05. Conclusions: Helicobacter pylori infection in children has significant positive correlation with the incidence of asthma, suggesting that Helicobacter pylori infection has a certain protective effect on childhood asthma, but persistent Helicobacter pylori infection in children with asthma can aggravate the immune disorder, which is the main reason for the difficulty of treatment of asthma.

Chemical structure of bismuth compounds determines their gastric ulcer healing efficacy and anti-Helicobacter pylori activity.

Science.gov (United States)

Sandha, G S; LeBlanc, R; Van Zanten, S J; Sitland, T D; Agocs, L; Burford, N; Best, L; Mahoney, D; Hoffman, P; Leddin, D J

1998-12-01

The recognition of the role of Helicobacter pylori in the pathogenesis of peptic ulcer disease has led to renewed interest in bismuth pharmacology since bismuth compounds have both anti-Helicobacter pylori and ulcer healing properties. The precise chemical structure of current bismuth compounds is not known. This has hindered the development of new and potentially more efficacious formulations. We have created two new compounds, 2-chloro-1,3-dithia-2-bismolane (CDTB) and 1,2-[bis(1,3-dithia-2-bismolane)thio]ethane (BTBT), with known structure. In a rat model of gastric ulceration, BTBT was comparable to, and CDTB was significantly less effective than colloidal bismuth subcitrate in healing cryoprobe-induced ulcers. However, both BTBT and CDTB inhibited H. pylori growth in vitro at concentrations <1/10 that of colloidal bismuth subcitrate. The effects on ulcer healing are not mediated by suppression of acid secretion, pepsin inhibition, or prostaglandin production. Since all treated animals received the same amount of elemental bismuth, it appears that the efficacy of bismuth compounds varies with compound structure and is not simply dependent on the delivery of bismuth ion. Because the structure of the novel compounds is known, our understanding of the relationship of bismuth compound structure and to biologic activity will increase. In the future it may be possible to design other novel bismuth compounds with more potent anti-H. pylori and ulcer healing effects.

[Gastric cancer risk estimate in patients with chronic gastritis associated with Helicobacter pylori infection in a clinical setting].

Science.gov (United States)

Arismendi-Morillo, G; Hernández, I; Mengual, E; Abreu, N; Molero, N; Fuenmayor, A; Romero, G; Lizarzábal, M

2013-01-01

Severity of chronic gastritis associated with Helicobacter pylori infection (CGAHpI) could play a role in evaluating the potential risk to develop gastric cancer. Our aim was to estimate the risk for gastric cancer in a clinical setting, according to histopathologic criteria, by applying the gastric cancer risk index (GCRI) METHODS: Histopathologic study of the gastric biopsies (corpus-antrum) from consecutive adult patients that underwent gastroesophageal duodenoscopy was carried out, and the GCRI was applied in patients presenting with CGAHpI. One hundred eleven patients (77% female) with a mean age of 38.6±13.1 years were included. Active Helicobacter pylori infection (aHpi) was diagnosed in 77 cases (69.40%). In 45% of the cases with aHpi, pangastritis (23%) or corpus-predominant gastritis (22%) was diagnosed. Nine cases were diagnosed with intestinal metaplasia (8%), 7 of which (77.70%) were in the aHpi group. Twenty one percent of the patients with aHpi had a GCRI of 2 (18.10%) or 3 (2.50%) points (high risk index), while 79.10% accumulated a GCRI of 0 or 1 points (low risk index). Of the patients with no aHpi, none of them had 3 points (p=0.001). Of the 18 patients that accumulated 2 or 3 points, 6 (33.30%) presented with intestinal metaplasia (all with pangastritis and corpus-predominant gastritis), of which 4 cases (66.60%) had aHpi. The estimated gastric cancer risk in patients with CGAHpI in the clinical setting studied was relatively low and 5% of the patients had a histopathologic phenotype associated with an elevated risk for developing gastric cancer. Copyright © 2012 Asociación Mexicana de Gastroenterología. Published by Masson Doyma México S.A. All rights reserved.

PREVALENCE OF HELICOBACTER PYLORI IN PATIENTS WITH DYSPEPSIA UNDERGOING UPPER GASTRO INTESTINAL ENDOSCOPY IN TERTIARY CARE HOSPITAL

Directory of Open Access Journals (Sweden)

Ajay Babu K

2017-12-01

Full Text Available BACKGROUND Acid peptic disease comprises of a wide spectrum of diseases, which cause considerable morbidity. Helicobacter pylori, a curved rod-shaped bacterium, has been consistently associated with patients suffering from acid peptic diseases, more in ulcer disease than in non-ulcer disease. Due to this high association, it is now believed that Helicobacter pylori plays an important role in the aetiopathogenesis of acid peptic disease. Several studies have revealed the association of Helicobacter pylori in 70-75 percent of patients with dyspepsia. Endoscopic studies have shown that, Helicobacter pylori is found in 80-100% of patients with duodenal ulcers and 60-75 per cent of patients with gastric ulcers. Amidst these profound variations proposed by many workers in the previous studies, we have attempted to study the prevalence of Helicobacter pylori in patients undergoing upper gastrointestinal endoscopy at our hospital and its association with acid-peptic disease. The objectives of this study were- 1. To study the prevalence of Helicobacter pylori in patients with dyspepsia undergoing upper gastrointestinal endoscopy. 2. To study the association of Helicobacter pylori with acid peptic Diseases. MATERIALS AND METHODS 344 cases of dyspepsia were studied clinically as per the proforma over a period of one and half years from July 2014 to October 2015. The inclusion and exclusion criteria were as follows; RESULTS Out of 344 patients, there were 224 male patients and 120 female patients, age ranging from 19 years to 60 years (Mean44.8. Out of 344 patients, 156 patients were diagnosed to have been infected with Helicobacter pylori (45.3%. CONCLUSION This was a prospective study conducted to determine the role of Helicobacter pylori in acid-peptic diseases. This study design was based on clinical study and endoscopic biopsy of gastric mucosa (and duodenal mucosa whenever necessary in 344 patients with a history of dyspepsia. Endoscopy confirmed the

Immune Evasion Strategies and Persistence of Helicobacter pylori.

Science.gov (United States)

Mejías-Luque, Raquel; Gerhard, Markus

Helicobacter pylori infection is commonly acquired during childhood, can persist lifelong if not treated, and can cause different gastric pathologies, including chronic gastritis, peptic ulcer disease, and eventually gastric cancer. H. pylori has developed a number of strategies in order to cope with the hostile conditions found in the human stomach as well as successful mechanisms to evade the strong innate and adaptive immune responses elicited upon infection. Thus, by manipulating innate immune receptors and related signaling pathways, inducing tolerogenic dendritic cells and inhibiting effector T cell responses, H. pylori ensures low recognition by the host immune system as well as its persistence in the gastric epithelium. Bacterial virulence factors such as cytotoxin-associated gene A, vacuolating cytotoxin A, or gamma-glutamyltranspeptidase have been extensively studied in the context of bacterial immune escape and persistence. Further, the bacterium possesses other factors that contribute to immune evasion. In this chapter, we discuss in detail the main evasion and persistence strategies evolved by the bacterium as well as the specific bacterial virulence factors involved.

Prediction of Helicobacter pylori status by conventional endoscopy, narrow-band imaging magnifying endoscopy in stomach after endoscopic resection of gastric cancer.

Science.gov (United States)

Yagi, Kazuyoshi; Saka, Akiko; Nozawa, Yujiro; Nakamura, Atsuo

2014-04-01

To reduce the incidence of metachronous gastric carcinoma after endoscopic resection of early gastric cancer, Helicobacter pylori eradication therapy has been endorsed. It is not unusual for such patients to be H. pylori negative after eradication or for other reasons. If it were possible to predict H. pylori status using endoscopy alone, it would be very useful in clinical practice. To clarify the accuracy of endoscopic judgment of H. pylori status, we evaluated it in the stomach after endoscopic submucosal dissection (ESD) of gastric cancer. Fifty-six patients treated by ESD were enrolled. The diagnostic criteria for H. pylori status by conventional endoscopy and narrow-band imaging (NBI)-magnifying endoscopy were decided, and H. pylori status was judged by two endoscopists. Based on the H. pylori stool antigen test as a diagnostic gold standard, conventional endoscopy and NBI-magnifying endoscopy were compared for their sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV). Interobserver agreement was assessed in terms of κ value. Interobserver agreement was moderate (0.56) for conventional endoscopy and substantial (0.77) for NBI-magnifying endoscopy. The sensitivity, specificity, PPV, and NPV were 0.79, 0.52, 0.70, and 0.63 for conventional endoscopy and 0.91, 0.83, 0.88, and 0.86 for NBI-magnifying endoscopy, respectively. Prediction of H. pylori status using NBI-magnifying endoscopy is practical, and interobserver agreement is substantial. © 2013 John Wiley & Sons Ltd.

The Possible Role of Helicobacter pylori Infection in Non-alcoholic Fatty Liver Disease

Directory of Open Access Journals (Sweden)

Dan-dan Cheng

2017-05-01

Full Text Available Helicobacter pylori (H. pylori which colonizes the stomach can cause a wide array of gastric disorders, including chronic gastritis, peptic ulcer, and gastric cancer. Recently, accumulating evidence has implicated H. pylori infection in extragastrointestinal diseases such as cardiovascular diseases, neurological disorders, and metabolic diseases. At the same time, many scholars have noted the relationship between H. pylori infection and non-alcoholic fatty liver disease (NAFLD. Despite the positive association between H. pylori and NAFLD reported in some researches, there are opposite perspectives denying their relationship. Due to high prevalence, unclear etiology and difficult treatment of NAFLD, confirming the pathogenicity of H. pylori infection in NAFLD will undoubtedly provide insights for novel treatment strategies for NAFLD. This paper will review the relationship between H. pylori infection and NAFLD and the possible pathogenic mechanisms.

Gene expression profiling in gastric mucosa from Helicobacter pylori-infected and uninfected patients undergoing chronic superficial gastritis.

Directory of Open Access Journals (Sweden)

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.

The need for using fluoroscopic guidance to obtain gastric biopsies when in search of Helicobacter pylori with a nonendoscopic method

International Nuclear Information System (INIS)

Bender, Greg N.; Mullins, Daniel J.; Makuch, Richard S.

1999-01-01

Purpose: Nonendoscopic, fluoroscopic biopsy of the gastric mucosa, following barium examination of the stomach, has gained attention with its ease of performance and cost savings potential over endoscopy. Endoscopic research concerning the efficacy of biopsy sites has revealed an increased sensitivity of antral biopsies over greater curvature biopsies for the detection of Helicobacter pylori. Fluoroscopically guided biopsies of the gastric mucosal are studied to determine whether such a difference between site sensitivity held true. If not, blind biopsy through a nasogastric tube, which traditionally samples only the greater curvature, might prove an even less expensive alternative. Materials and methods: Seventy-two patients underwent nonendoscopic, fluoroscopically guided, mucosal biopsy of both the gastric antrum and the greater curvature of the stomach. Pathologic reports from both sites, using each patient as their own control, are compared to assess site sensitivity in the diagnosis of H. pylori gastritis. Results: The sensitivity for the detection of H. pylori gastritis by antral biopsy is 89% whereas the sensitivity of greater curvature biopsy is 62%. The difference is considered clinically significant at P≤0.05. Conclusions: This study confirms the need for antral biopsies when desiring a nonendoscopic approach to gastric mucosal sampling, in order to obtain a reasonable yield of data in dyspeptic patients with H. pylori gastritis. Blind techniques cannot reliably reach the antrum. Fluoroscopy can, and remains a less expensive alternative to endoscopy

The need for using fluoroscopic guidance to obtain gastric biopsies when in search of Helicobacter pylori with a nonendoscopic method

Energy Technology Data Exchange (ETDEWEB)

Bender, Greg N.; Mullins, Daniel J.; Makuch, Richard S

1999-12-01

Purpose: Nonendoscopic, fluoroscopic biopsy of the gastric mucosa, following barium examination of the stomach, has gained attention with its ease of performance and cost savings potential over endoscopy. Endoscopic research concerning the efficacy of biopsy sites has revealed an increased sensitivity of antral biopsies over greater curvature biopsies for the detection of Helicobacter pylori. Fluoroscopically guided biopsies of the gastric mucosal are studied to determine whether such a difference between site sensitivity held true. If not, blind biopsy through a nasogastric tube, which traditionally samples only the greater curvature, might prove an even less expensive alternative. Materials and methods: Seventy-two patients underwent nonendoscopic, fluoroscopically guided, mucosal biopsy of both the gastric antrum and the greater curvature of the stomach. Pathologic reports from both sites, using each patient as their own control, are compared to assess site sensitivity in the diagnosis of H. pylori gastritis. Results: The sensitivity for the detection of H. pylori gastritis by antral biopsy is 89% whereas the sensitivity of greater curvature biopsy is 62%. The difference is considered clinically significant at P{<=}0.05. Conclusions: This study confirms the need for antral biopsies when desiring a nonendoscopic approach to gastric mucosal sampling, in order to obtain a reasonable yield of data in dyspeptic patients with H. pylori gastritis. Blind techniques cannot reliably reach the antrum. Fluoroscopy can, and remains a less expensive alternative to endoscopy.

Novel and Effective Therapeutic Regimens for Helicobacter pylori in an Era of Increasing Antibiotic Resistance

Directory of Open Access Journals (Sweden)

Yi Hu

2017-05-01

Full Text Available Helicobacter pylori (H. pylori is a common gastrointestinal bacterial strain closely associated with the incidence of chronic gastritis, peptic ulcers, gastric mucosa-associated lymphoid tissue lymphoma, and gastric cancer. A current research and clinical challenge is the increased rate of antibiotic resistance in H. pylori, which has led to a decreased H. pylori eradication rate. In this article, we review recent H. pylori infection and reinfection rates and H. pylori resistance to antibiotics, and we discuss the pertinent treatments. A PubMed literature search was performed using the following keywords: Helicobacter pylori, infection, reinfection, antibiotic resistance, bismuth, proton pump inhibitors, vonoprazan, susceptibility, quintuple therapy, dual therapy, and probiotic. The prevalence of H. pylori has remained high in some areas despite the decreasing trend of H. pylori prevalence observed over time. Additionally, the H. pylori reinfection rate has varied in different countries due to socioeconomic and hygienic conditions. Helicobacter pylori monoresistance to clarithromycin, metronidazole or levofloxacin was common in most countries. However, the prevalence of amoxicillin and tetracycline resistance has remained low. Because H. pylori infection and reinfection present serious challenges and because H. pylori resistance to clarithromycin, metronidazole or levofloxacin remains high in most countries, the selection of an efficient regimen to eradicate H. pylori is critical. Currently, bismuth-containing quadruple therapies still achieve high eradication rates. Moreover, susceptibility-based therapies are alternatives because they may avoid the use of unnecessary antibiotics. Novel regimens, e.g., vonoprazan-containing triple therapies, quintuple therapies, high-dose dual therapies, and standard triple therapies with probiotics, require further studies concerning their efficiency and safety for treating H. pylori.

A Novel Assay for Easy and Rapid Quantification of Helicobacter pylori Adhesion.

Science.gov (United States)

Skindersoe, Mette E; Rasmussen, Lone; Andersen, Leif P; Krogfelt, Karen A

2015-06-01

Reducing adhesion of Helicobacter pylori to gastric epithelial cells could be a new way to counteract infections with this organism. We here present a novel method for quantification of Helicobacter pylori adhesion to cells. Helicobacter pylori is allowed to adhere to AGS or MKN45g cells in a 96-well microtiter plate. Then wells are added saponin, which lyses the cells without affecting the bacteria. After addition of alamarBlue(®) (resazurin) and 1- to 2-hour incubation, fluorescence measurements can be used to quantify the number of adherent bacteria. By use of the method, we demonstrate that adhesion of both a sabA and babA deletion mutant of H. pylori is significantly reduced compared to the wild type. The method offers a number of applications and may be used to compare the adherence potential of different strains of H. pylori to either cells or different materials or to screen for potential anti-adhesive compounds. The results presented here suggest that this easy and reproducible assay is well suited for quantitative investigation of H. pylori adhesion. © 2015 John Wiley & Sons Ltd.

The significance of virulence factors in Helicobacter pylori.

Science.gov (United States)

Shiota, Seiji; Suzuki, Rumiko; Yamaoka, Yoshio

2013-07-01

Helicobacter pylori (H. pylori) infection is linked to various gastroduodenal diseases; however, only a small fraction of these patients develop associated diseases. Despite the high prevalence of H. pylori infection in Africa and South Asia, the incidence of gastric cancer in these areas is much lower than those in other countries. The incidence of gastric cancer tends to decrease from north to south in East Asia. Such geographical differences in the pathology can be explained, at least in part, by the presence of different types of H. pylori virulence factors in addition to host and environmental factors. Virulence factors of H. pylori, such as CagA, VacA, DupA, IceA, OipA and BabA, have been demonstrated to be the predictors of severe clinical outcomes. Interestingly, a meta-analysis showed that CagA seropositivity was associated with gastric cancer compared with gastritis, even in East Asian countries where almost the strains possess cagA. Another meta-analysis also confirmed the significance of vacA, dupA and iceA. However, it is possible that additional important pathogenic genes may exist because H. pylori consists of approximately 1600 genes. Despite the advances in our understanding of the development of H. pylori infection-related diseases, further work is required to clarify the roles of H. pylori virulence factors. © 2013 The Authors. Journal of Digestive Diseases © 2013 Wiley Publishing Asia Pty Ltd and Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine.

14C-urea breath test for the detection of Helicobacter pylori

International Nuclear Information System (INIS)

Veldhuyzen van Zanten, S.J.; Tytgat, K.M.; Hollingsworth, J.; Jalali, S.; Rshid, F.A.; Bowen, B.M.; Goldie, J.; Goodacre, R.L.; Riddell, R.H.; Hunt, R.H.

1990-01-01

The high urease activity of Helicobacter pylori can be used to detect this bacterium by noninvasive breath tests. We have developed a 14 C-urea breath test which uses 5 microCi 14 C with 50 mg nonradioactive urea. Breath samples are collected at baseline and every 30 min for 2 h. Our study compared the outcome of the breath test to the results of histology and culture of endoscopically obtained gastric biopsies in 84 patients. The breath test discriminated well between the 50 positive patients and the 34 patients negative for Helicobacter pylori: the calculated sensitivity was 100%, specificity 88%, positive predictive value 93%, and negative predictive value 100%. Treatment with bismuth subsalicylate and/or ampicillin resulted in lower counts of exhaled 14 CO 2 which correlated with histological improvement in gastritis. The 14 C-urea breath test is a better gold standard for the detection of Helicobacter pylori than histology and/or culture

Culturable Bacterial Microbiota of the Stomach of Helicobacter pylori Positive and Negative Gastric Disease Patients

Directory of Open Access Journals (Sweden)

Yalda Khosravi

2014-01-01

Full Text Available Human stomach is the only known natural habitat of Helicobacter pylori (Hp, a major bacterial pathogen that causes different gastroduodenal diseases. Despite this, the impact of Hp on the diversity and the composition of the gastric microbiota has been poorly studied. In this study, we have analyzed the culturable gastric microbiota of 215 Malaysian patients, including 131 Hp positive and 84 Hp negative individuals that were affected by different gastric diseases. Non-Hp bacteria isolated from biopsy samples were identified by matrix assisted laser desorption ionization-time of flight mass spectrometry based biotyping and 16SrRNA sequencing. The presence of Hp did not significantly modify the diversity of the gastric microbiota. However, correlation was observed between the isolation of Streptococci and peptic ulcer disease. In addition, as a first report, Burkholderia pseudomallei was also isolated from the gastric samples of the local population. This study suggested that there may be geographical variations in the diversity of the human gastric microbiome. Geographically linked diversity in the gastric microbiome and possible interactions between Hp and other bacterial species from stomach microbiota in pathogenesis are proposed for further investigations.

Assessment of p21, p53 expression, and Ki-67 proliferative activities in the gastric mucosa of children with Helicobacter pylori gastritis.

Science.gov (United States)

Saf, Coskun; Gulcan, Enver Mahir; Ozkan, Ferda; Cobanoglu Saf, Seyhan Perihan; Vitrinel, Ayca

2015-02-01

Helicobacter pylori that is generally acquired in childhood and infects the gastric mucosa is considered to be responsible for many pathobiological changes that are linked to the pathogenesis of gastric cancer. Although the majority of studies on the subject have been carried out in adults, there are a limited number of studies on children that reflect the early period of infection and may be of greater significance. We aimed to determine the role of H. pylori infection and/or gastritis in several histopathological changes, p53, p21, and cell proliferation-associated Ki-67 antigen expression in the gastric mucosa. We studied 60 patients with a mean age of 7.5 ± 4.5 years at referral. On the basis of endoscopic appearance and the evaluation of the gastric antral specimens, the patients were divided into three groups: patients without gastritis, patients with H. pylori-positive gastritis, and patients with H. pylori-negative gastritis. To determine the expression of p53, Ki-67, and p21 in gastric biopsy specimens, immunohistochemical stains were performed. The incidence of neutrophil activity, which was one of our histopathologic parameters, was significantly higher in the H. pylori-positive gastritis group than the other two groups. The presence of lymphoid aggregate was more frequent in H. pylori ± gastritis groups than the nongastritis group. p53 expression was found to be significantly higher in the H. pylori-positive gastritis group than the nongastritis group. Ki-67 and p21 expressions were significantly more frequent in the H. pylori-positive gastritis group than the other two groups. When we evaluated the density of H. pylori, as the density of bacteria increases, we found that the expressions of p53, p21, and Ki-67 increased significantly. Expression of the studied precancerous markers in significant amounts indicates the importance of childhood H. pylori infection in the constitution of gastric cancer in adulthood.

Polymorphisms at Locus 4p14 of Toll-Like Receptors TLR-1 and TLR-10 Confer Susceptibility to Gastric Carcinoma in Helicobacter pylori Infection.

Directory of Open Access Journals (Sweden)

M Ravishankar Ram

Full Text Available Helicobacter pylori (H. pylori -induced gastric inflammation impacts the functions of leptin- and ghrelin-producing cells in the gastroduodenum. Inflammation resulting from H. pylori sensing via Toll-like receptors (TLRs and the associated downstream signaling largely remain ambiguous. Here, we investigated the role of gut hormones, pro-inflammatory cytokines and single nucleotide polymorphisms (SNPs associated with TLR 4p14 in H. pylori disease in 30 subjects with non-ulcer dyspepsia (NUD, 40 with peptic ulcer disease (PUD and 15 with gastric cancer (GC subjects positive and negative for H. pylori infection. The level of pro-inflammatory cytokines was directly proportional to the severity of gastritis, and disease status influenced the levels of gut hormones and pro-inflammatory cytokines. TLR-1 SNPs rs4833095 and TLR-10 SNPs rs10004195 and were directly associated with H. pylori disease, and were up-regulated in the presence of H. pylori in a genotype-independent manner. We concluded that TLR-1 rs4833095 and TLR10 rs10004195 confer susceptibility to development of gastroduodenal disease, especially GC in H.pylori disease.

CEACAM6 is upregulated by Helicobacter pylori CagA and is a biomarker for early gastric cancer

Science.gov (United States)

Srivastava, Supriya; Samanta, Animesh; Sharma, Neel; Tan, Kar Tong; Yang, Henry; Voon, Dominic C.; Pang, Brendan; Teh, Ming; Murata-Kamiya, Naoko; Hatakeyama, Masanori; Chang, Young-Tae; Yong, Wei Peng; Ito, Yoshiaki; Ho, Khek Yu; Tan, Patrick; Soong, Richie; Koeffler, Phillip H.; Yeoh, Khay Guan; Jeyasekharan, Anand D.

2016-01-01

Early detection of gastric cancers saves lives, but remains a diagnostic challenge. In this study, we aimed to identify cell-surface biomarkers of early gastric cancer. We hypothesized that a subset of plasma membrane proteins induced by the Helicobacter pylori oncoprotein CagA will be retained in early gastric cancers through non-oncogene addiction. An inducible system for expression of CagA was used to identify differentially upregulated membrane protein transcripts in vitro. The top hits were then analyzed in gene expression datasets comparing transcriptome of gastric cancer with normal tissue, to focus on markers retained in cancer. Among the transcripts enriched upon CagA induction in vitro, a significant elevation of CEACAM6 was noted in gene expression datasets of gastric cancer. We used quantitative digital immunohistochemistry to measure CEACAM6 protein levels in tissue microarrays of gastric cancer. We demonstrate an increase in CEACAM6 in early gastric cancers, when compared to matched normal tissue, with an AUC of 0.83 for diagnostic validity. Finally, we show that a fluorescently conjugated CEACAM6 antibody binds avidly to freshly resected gastric cancer xenograft samples and can be detected by endoscopy in real time. Together, these results suggest that CEACAM6 upregulation is a cell surface response to H. pylori CagA, and is retained in early gastric cancers. They highlight a novel link between CEACAM6 expression and CagA in gastric cancer, and suggest CEACAM6 to be a promising biomarker to aid with the fluorescent endoscopic diagnosis of early neoplastic lesions in the stomach. PMID:27421133

Interleukin-1 gene polymorphisms in chronic gastritis patients infected with Helicobacter pylori as risk factors of gastric cancer development.

Science.gov (United States)

Hnatyszyn, Andrzej; Wielgus, Karolina; Kaczmarek-Rys, Marta; Skrzypczak-Zielinska, Marzena; Szalata, Marlena; Mikolajczyk-Stecyna, Joanna; Stanczyk, Jerzy; Dziuba, Ireneusz; Mikstacki, Adam; Slomski, Ryszard

2013-12-01

Epidemiological investigations indicated association of the Helicobacter pylori infections with the occurrence of inflammatory conditions of the gastric mucosa and development of chronic gastritis and intestinal type of gastric cancer. IL1A and IL1B genes have been proposed as key factors in determining risk of gastritis and malignant transformation. The aim of this paper was to evaluate association of interleukin-1 gene polymorphisms with chronic gastritis, atrophy, intestinal metaplasia, dysplasia and intestinal type of gastric cancer in H. pylori-infected patients. Patients subjected to analysis represent group of 144 consecutive cases that suffered from dyspepsia with coexisting infection of H. pylori and chronic gastritis, chronic atrophic gastritis, intestinal metaplasia, dysplasia or gastric cancer. Molecular studies involved analysis of -889C>T polymorphism of IL1A gene and +3954C>T polymorphism of IL1B gene. Statistical analysis of association of polymorphism -889C>T of gene IL1A with changes in gastric mucosa showed lack of significance, whereas +3954C>T polymorphism of IL1B gene showed significant association. Frequency of allele T of +3954C>T polymorphism of IL1B gene was higher in group of patients with chronic gastritis, atrophy, intestinal metaplasia, dysplasia or intestinal type of gastric cancer (32.1 %) as compared with population group (23 %), χ(2) = 4.61 and p = 0.03. This corresponds to odds ratio: 1.58, 95 % CI: 1.04-2.4. Our results indicate that +3954C>T polymorphism of IL1B gene increase susceptibility to inflammatory response of gastric mucosa H. pylori-infected patients and plays a significant role in the development of chronic gastritis, atrophy, intestinal metaplasia, dysplasia and the initiation of carcinogenesis.

Responsiveness to acidity via metal ion regulators mediates virulence in the gastric pathogen Helicobacter pylori.

Science.gov (United States)

Bury-Moné, Stéphanie; Thiberge, Jean-Michel; Contreras, Monica; Maitournam, Aboubakar; Labigne, Agnès; De Reuse, Hilde

2004-07-01

The virulence of pathogenic bacteria is dependent on their adaptation to and survival in the stressful conditions encountered in their hosts. Helicobacter pylori exclusively colonizes the acid stomach of primates, making it an ideal study model. Little is known about how H. pylori responds to the moderately acidic conditions encountered at its colonization site, the gastric mucus layer. Thus, we compared gene expression profiles of H. pylori 26695 grown at neutral and acidic pH, and validated the data for a selection of genes by real-time polymerase chain reaction, dot-blots or enzymatic assays. During growth in acidic conditions, 56 genes were upregulated and 45 genes downregulated. We found that acidity is a signal modulating the expression of several virulence factors. Regulation of genes related to metal ion homeostasis suggests protective mechanisms involving diminished transport and enhanced storage. Genes encoding subunits of the F0F1 ATPase and of a newly identified Na+/H+ antiporter (NhaC-HP0946) were downregulated, revealing that this bacterium uses original mechanisms to control proton entry. Five of the upregulated genes encoded proteins controlling intracellular ammonia synthesis, including urease, amidase and formamidase, underlining the major role of this buffering compound in the protection against acidity in H. pylori. Regulatory networks and transcriptome analysis as well as enzymatic assays implicated two metal-responsive transcriptional regulators (NikR and Fur) and an essential two-component response regulator (HP0166, OmpR-like) as effectors of the H. pylori acid response. Finally, a nikR-fur mutant is attenuated in the mouse model, emphasizing the link between response to acidity, metal metabolism and virulence in this gastric pathogen.

Colonization and infection by Helicobacter pylori in humans.

Science.gov (United States)

Andersen, Leif Percival

2007-11-01

When Helicobacter pylori arrives in the human stomach, it may penetrate the mucin layer and adhere to the gastric epithelial cells or it may pass through the stomach without colonizing the mucosa. In this paper, the colonization process and the ensuing immunological response will be briefly described. Urease production is necessary for H. pylori to establish a pH-neutral microenvironment around the bacteria. The flagella enable the bacteria to move and the shape of H. pylori makes it possible to penetrate the mucin layer where it comes into contact with the gastric epithelial cells. H. pylori contains several adhesins that enable it to adhere to the epithelial cells. This adherence activates IL-8 which, together with bacterial antigens, attracts polymorphs and monocytes and causes acute gastritis. Antigen-presenting cells activate lymphocytes and other mononuclear cells that are attracted to the inflamed mucosa, causing chronic superficial gastritis and initiating a cytotoxic or an antigen-producing Th response. The infection is established within a few weeks after the primary exposure to H. pylori. After this initial colonization, many chemical, biochemical, and immunologic reactions take place that are of importance in the progress of the infection and the development of disease.

Gastric bicarbonate secretion and release of prostaglandin E2 are increased in duodenal ulcer patients, but not in Helicobacter pylori positive healthy subjects

DEFF Research Database (Denmark)

A, Mertz-Nielsen; Hillingsø, Jens; Frøkiær, Hanne

1996-01-01

Background: Duodenal ulcer (DU) patients have impaired proximal duodenal mucosal bicarbonate secretion at rest and in response to luminal acid with higher acid-stimulated mucosal release of prostaglandin (PG) E(2) than healthy subjects. Our purpose was to determine whether this abnormality...... was present also in the stomach of DU patients. Methods: Simultaneous determinations of gastric and duodenal bicarbonate secretion and luminal release of PGE(2) were performed in 16 healthy volunteers (5 Helicobacter pylori-positive) and 8 inactive DU patients (all H. pylori-positivr). Results: In healthy...... be responsible for the abnormally high gastric secretion of bicarbonate in inactive DU patients. Th; defective duodenal secretion of bicarbonate observed in these patients may be a consequence of previous ulceration rather than the mere presence of H. pylori infection....

Helicobacter pylori vacA and cagA genotypes in patients from northeastern Brazil with upper gastrointestinal diseases

Directory of Open Access Journals (Sweden)

Meyssa Quezado de Figueiredo Cavalcante

2012-06-01

Full Text Available Helicobacter pylori causes chronic gastric inflammation and significantly increases the risk of duodenal and gastric ulcer disease and distal gastric carcinoma. In this study, we evaluated the Helicobacter pylori vacA and cagA genotypes in patients from a Brazilian region where there is a high prevalence of gastric cancer. Polymerase chain reaction (PCR was used to investigate vacA mosaicism and cagA status in the gastric mucosa of 134 H. pylori-positive patients, including 76 with gastritis: 28 with peptic ulcer disease and 30 with gastric cancer. The s1m1 variant was the predominant vacA genotype observed, whereas the s1 allele was more frequently observed in patients with more severe diseases associated with H. pylori infection [p = 0.03, odds ratio (OR = 5.72, 95% confidence interval (CI = 1.15-38.60]. Furthermore, all of the s1 alleles were s1b. Mixed vacA m1/m2 strains were found more frequently in patients with gastric cancer and a cagA-positive status was significantly associated with gastric cancer (p = 0.016, OR = 10.36, 95% CI = 1.35-217.31. Patients with gastric cancer (21/21, 100%, p = 0.006 or peptic ulcers (20/21, 95%, p = 0.02 were more frequently colonised by more virulent H. pylori strains compared to gastritis patients (41/61, 67.2%. In conclusion, in the northeastern of Brazil, which is one of the regions with the highest prevalence of gastric cancer in the country, infection with the most virulent H. pylori strains, carrying the cagA gene and s1m1 vacA alleles, predominates and is correlated with more severe H. pylori-associated diseases.

Prevalence and Correlation with Clinical Diseases of Helicobacter pylori cagA and vacA Genotype among Gastric Patients from Northeast China

Directory of Open Access Journals (Sweden)

Faisal Aziz

2014-01-01

Full Text Available Helicobacter pylori vacA and cagA genes have significant genetic heterogenicity, resulting in different clinical outcomes. Northeast part of China has reported high prevalence of H. pylori infections and gastric cancer. Hence, we investigated the H. pylori cagA and vacA genotypes with clinical outcomes in Northeast China. Gastric tissue samples (n=169, chronic gastritis (GIs, gastric ulcer (GU, and gastric cancer (GC were analysed for 16S rRNA ureA, cagA, and cagA genotypes by PCR. A total of 141 (84% cases were found positive for H. pylori by 16S rRNA and ureA. GC showed high H. pylori infection (93% compared with GIs (72% and GU (84%. The vacAs1am1 was highly found in GC (40% and GU (36%, vacAs1am2 in GIs (33%, vacAs1bm1 (14% and vacAs1bm2 (8% in GU cases, and s2m1 in normal cases (33%, while vacAs1cm1 showed low frequency in GIs (2% and GU (3% and GC showed negative result. The East-Asian cagA strain was highly observed in GC (43%, as compared to GIs (41% and GU (20%. The East-Asian cagA/vacAs1am1 was significantly higher in GC (23% than in GU (22% and GIs (145 patients. The East-Asian type cagA with vacAs1a and vacAm1 is the most predominant genotype in H. pylori strains of Northeast China.

The investigation of Helicobacter pylori in the dental biofilm and saliva samples of children with dyspeptic complaints

OpenAIRE

Aksit B?cak, Damla; Akyuz, Serap; K?ratl?, Binnur; Usta, Merve; Urganci, Nafiye; Alev, Burcin; Yarat, Aysen; Sahin, Fikrettin

2017-01-01

Background The oral cavity can be an extra-gastric reservoir for Helicobacter pylori (H.pylori). This can play a role in the pathogenesis of halitosis, glossitis, recurrent aphthous stomatitis, and dental caries. The present study was conducted to detect the presence of H.pylori within the dental biofilm and in saliva samples collected from children suffering from dyspepsia and children without any gastrointestinal complaints. Associations with gastric infection, halitosis, and some oral para...

Helicobacter pylori and non-malignant diseases.

Science.gov (United States)

Matysiak-Budnik, Tamara; Laszewicz, Wiktor; Lamarque, Dominique; Chaussade, Stanislas

2006-10-01

The prevalence of Helicobacter pylori-associated peptic ulcers, in particular duodenal ulcers, is decreasing following decreasing prevalence of H. pylori infection, while the frequency of non-steroidal anti-inflammatory drugs (NSAIDs)-induced and H. pylori-negative idiopathic ulcers is increasing. The incidence of bleeding ulcers has been stable during the last decades. Several putative H. pylori virulence genes, i.e., cag, vacA, babA, or dupA, as well as host-related genetic factors like IL-1beta and TNFalpha-gene polymorphism, have been proposed as risk factors for duodenal ulcer. H. pylori eradication may prevent NSAID complications, in particular, when it is performed before introduction of NSAIDs. There is a complex association between H. pylori and gastroesophageal reflux disease (GERD), and the impact of H. pylori eradication on the appearance of GERD symptoms depends on various host- and bacteria-related factors. Eradication of H. pylori in GERD is recommended in patients before instauration of a long-term PPI treatment to prevent the development of gastric atrophy. A small proportion (10%) of non-ulcer dyspepsia cases may be attributed to H. pylori and may benefit from eradication treatment. A test-and-treat strategy is more cost-effective than prompt endoscopy in the initial management of dyspepsia.

Helicobacter pylori colonization of the oral cavity: A milestone discovery

Science.gov (United States)

Yee, John KC

2016-01-01

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. PMID:26811613

The Relationship between Oral Hygiene Index and Gastric Helicobacter Pylori Positivity

Directory of Open Access Journals (Sweden)

Tolga Önder

2016-03-01

Full Text Available Objective: Helicobacter pylori (HP is a bacterial patho­gen that leads to gastroduodenal inflammation, gastric and duodenal ulcer and atrophic gastritis. Colonization of bacteria can be shown by using rapid-urease test during endoscopy. There are conflicting data about the route of transmission and reservoir. It’s thought to be transmitted primarily by oral route. Many studies showed results sup­porting that the presence of bacteria in dental plaques has effects on gastric colonization and eradication. There are data about the potential inhibitory effect of oral flora on HP. We aimed to analyze the association of simplified oral hygiene index -a possible representation of a healthy oral flora- with HP positivity. Methods: Patients undergoing upper gastrointestinal system endoscopy for symptoms of dyspepsia were as­sessed by a dentist for the simplified oral hygiene index (OHI. Patients were classified as good, poor and bad groups based on oral hygiene index scale. Pre-pyloric biopsy materials were assessed using rapid-urease test. Oral hygiene indexes were analyzed retrospectively, groups were compared for HP positivity. Results: 66 patients (30 females, 45.5% were included. Mean age of patients was 34.17±14.7 years. 11 (16.7%, 29 (43.9% and 26 (39.4% patients were classified as in good, poor and bad hygiene index groups, respectively. In patients with good OHI gastric HP positivity was less frequent. Conclusion: Decreased frequency in gastric HP may be observed with maintaining an ideal oral hygiene.

Morphological and Cellular Features of Innate Immune Reaction in Helicobacter pylori Gastritis: A Brief Review

Directory of Open Access Journals (Sweden)

Antonio Ieni

2016-01-01

Full Text Available 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.

[On the rating of Helicobacter pylori in drinking water].

Science.gov (United States)

Fedichkina, T P; Solenova, L G; Zykova, I E

2014-01-01

There are considered the issues related to the possibility to rate of Helicobacter pylori (H. pylori) content in drinking water. There is described the mechanism of of biofilm formation. The description refers to the biofilm formation mechanism in water supply systems and the existence of H. pylori in those systems. The objective premises of the definition of H. pylori as a potential limiting factor for assessing the quality of drinking water have been validated as follows: H. pylori is an etiologic factor associated to the development of chronic antral gastritis, gastric ulcer and duodenal ulcer, and gastric cancer either, in the Russian population the rate of infection with H. pylori falls within range of 56 - 90%, water supply pathway now can be considered as a source of infection of the population with H. pylori, the existence of WHO regulatory documents considering H. pylori as a candidate for standardization of the quality of the drinking water quite common occurrence of biocorrosion, the reduction of sanitary water network reliability, that creates the possibility of concentrating H. pylori in some areas of the water system and its delivery to the consumer of drinking water, and causes the necessity of the prevention of H. pylori-associated gastric pathology of the population. A comprehensive and harmonized approach to H. pylori is required to consider it as a candidate to its rating in drinking water. Bearing in mind the large economic losses due to, on the one hand, the prevalence of disease caused by H. pylori, and, on the other hand, the biocorrosion of water supply system, the problem is both relevant in terms of communal hygiene and economy.

Anti-Bacterial Properties of Herbs against Helicobacter Pylori Infection: A Review

Directory of Open Access Journals (Sweden)

Hedieh Yousef-Nezhad

2017-09-01

Full Text Available Helicobacter pylori is a gram-negative bacterium that lives in human stomach. This bacterium is the most important cause of chronic gastritis, peptic and duodenal ulcers and gastric cancer. The therapies include the use of antibiotics and a proton pump inhibitor, but unfortunately, these therapeutic methods are not always responsive due to resistance to antibiotics. In recent years, use of alternative treatment, including medicinal herbs was shown to have anti-H. Pylori properties. So, in this review, anti-H. Pylori features of herbals were investigated including ginger, garlic, cranberry, curcumin, green tea and broccoli sprouts derived through the search in Google Scholar search engine, and PubMed scientific database using English keywords such as Helicobacter pylori, anti-H. pylori, ginger, garlic, cranberry, curcumin, broccoli and green tea, between 1984 -2016. Results showed that ginger, garlic, cranberry, curcumin, broccoli and green tea have antibacterial, antioxidant and anti-inflammatory potential properties, and because of their role in protecting the stomach against H. pylori infection, it seems, they can be an appropriate treatment option for patients with this infection.

Helicobacter pylori and autoimmune disease: Cause or bystander

Science.gov (United States)

Smyk, Daniel S; Koutsoumpas, Andreas L; Mytilinaiou, Maria G; Rigopoulou, Eirini I; Sakkas, Lazaros I; Bogdanos, Dimitrios P

2014-01-01

Helicobacter pylori (H. pylori) is the main cause of chronic gastritis and a major risk factor for gastric cancer. This pathogen has also been considered a potential trigger of gastric autoimmunity, and in particular of autoimmune gastritis. However, a considerable number of reports have attempted to link H. pylori infection with the development of extra-gastrointestinal autoimmune disorders, affecting organs not immediately relevant to the stomach. This review discusses the current evidence in support or against the role of H. pylori as a potential trigger of autoimmune rheumatic and skin diseases, as well as organ specific autoimmune diseases. We discuss epidemiological, serological, immunological and experimental evidence associating this pathogen with autoimmune diseases. Although over one hundred autoimmune diseases have been investigated in relation to H. pylori, we discuss a select number of papers with a larger literature base, and include Sjögrens syndrome, rheumatoid arthritis, systemic lupus erythematosus, vasculitides, autoimmune skin conditions, idiopathic thrombocytopenic purpura, autoimmune thyroid disease, multiple sclerosis, neuromyelitis optica and autoimmune liver diseases. Specific mention is given to those studies reporting an association of anti-H. pylori antibodies with the presence of autoimmune disease-specific clinical parameters, as well as those failing to find such associations. We also provide helpful hints for future research. PMID:24574735

Reflux esophagitis triggered after Helicobacter pylori eradication: a noteworthy demerit of eradication therapy among the Japanese?

Directory of Open Access Journals (Sweden)

Katsunori eIijima

2015-06-01

Full Text Available In the February 2013 Revision of Insured Medical Treatment, bacterial eradication for all Helicobacter pylori-positive individuals in Japan was covered under the insurance scheme. However, reflux esophagitis is believed to occur in approximately 10% of Japanese patients who undergo eradication therapy. Hence, the risk of reflux esophagitis among such cases should be carefully considered, particularly in the treatment for H. pylori-positive patients who are otherwise healthy. The eradication of Helicobacter pylori in cases of H. pylori-positive gastritis markedly suppresses gastric inflammation, and inhibits gastric mucosal atrophy and its progression to intestinal metaplasia. In a long-term follow-up study (10-20 years, eradication treatment was found to reduce the risk of subsequent gastric cancer. However, the fact that eradication-induced reflux esophagitis could increase the long-term risk of Barrett’s esophagus and esophageal adenocarcinoma should also be considered in the Japanese population. Appropriate treatment with proton pump inhibitors should be taken into consideration for patients undergoing eradication therapy in clinical practice.