Helicobacter pylori alters gastric epithelial cell cycle events and gastrin secretion in Mongolian gerbils

Peek, Richard M.; Wirth§, Hans–Peter; Moss, Steven F.; Yang, Muwen; Abdalla, Abdelrahman M.; Tham, Kyi T.; Zhang, Tong; Tang, Laura H.; Modlin, Irvin; Blaser, Martin J.

doi:10.1016/s0016-5085(00)70413-6

Cited by 174 publications

(148 citation statements)

References 46 publications

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“…36,37 Finally, Th1-polarized gastric responses are linked to reduced mucosal somatostatin and elevated plasma gastrin levels in H. pylori-infected patients, 10 and increased gastrin levels are significantly associated with increased gastric epithelial cell proliferation. 38 Establishment of H. pylori as a risk factor for cancer of the stomach has permitted an approach to identify persons at increased risk; however, infection with this organism is extremely common and most colonized persons never develop cancer. Analytical tools are now available, including H. pylori, treatment, and gastric cancer J Romero-Gallo et al genome sequences (H. pylori and human), measurable phenotypes, and practical animal models, to identify high-risk subpopulations, allowing treatments to be designed and focused on individuals who are most likely to derive benefit from H. pylori eradication.…”

Section: Discussionmentioning

confidence: 99%

Effect of Helicobacter pylori eradication on gastric carcinogenesis

Romero–Gallo

Harris

Krishna

et al. 2008

Laboratory Investigation

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Chronic gastritis induced by Helicobacter pylori is the strongest known risk factor for gastric adenocarcinoma, yet the effects of bacterial eradication on carcinogenesis remain unclear. Animal models provide important insights into factors that are involved in gastric carcinogenesis, and we previously utilized such a model to demonstrate that an in vivoadapted H. pylori strain, 7.13, rapidly and reproducibly induces inflammation-mediated gastric carcinoma. In the current study, we used this bacterial strain as a prototype to define the role of targeted antimicrobial therapy in gastric carcinogenesis. Mongolian gerbils were infected with H. pylori for 4 or 8 weeks, treated with antimicrobial agents or vehicle, and then euthanized at 8 weeks after the completion of therapy. All infected gerbils developed gastritis; however, inflammation was significantly attenuated in animals receiving antimicrobial therapy. Gastric dysplasia or cancer developed in 460% of the gerbils that remained persistently colonized with H. pylori, but in none of the animals treated with antibiotics following 4 weeks of infection. Infection with H. pylori for 8 weeks prior to therapy resulted in an attenuation, but not complete prevention, of pre-malignant and malignant lesions. Similarly, antibiotic therapy initiated at 4, but not 8, weeks after H. pylori challenge significantly reduced expression of the Th1 pro-inflammatory cytokine interferon-g within colonized gastric mucosa. These results indicate that treatment of H. pylori in this model decreases the incidence and severity of lesions with carcinogenic potential. The effectiveness of eradication is dependent upon the timing of intervention, providing insights into mechanisms that may regulate the development of malignancies arising within the context of inflammatory states.

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Section: Discussionmentioning

confidence: 99%

Effect of Helicobacter pylori eradication on gastric carcinogenesis

Romero–Gallo

Harris

Krishna

et al. 2008

Laboratory Investigation

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“…When cocultured with epithelial cell lines, H. pylori are antiproliferative and proapoptotic (115, S111), although cag signaling is essentially pro-proliferative (through MAPK signaling and expression of the transcription factor AP-1) (116,117) and pro-and antiapoptotic (through NF-κB signaling) (70,118). Animal models and human studies suggest that the net effect of H. pylori colonization is pro-proliferative and proapoptotic (95,96,119,120, S87, S88). Pro-proliferative signaling increases cell replication and the chance of mutation, whereas apoptosis may be protective by inducing death of DNA-damaged cells.…”

Section: Figurementioning

confidence: 99%

Helicobacter pylori persistence: biology and disease

Blaser¹,

Atherton²

2004

J. Clin. Invest.

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776

540

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Helicobacter pylori are bacteria that have coevolved with humans to be transmitted from person to person and to persistently colonize the stomach. Their population structure is a model for the ecology of the indigenous microbiota. A well-choreographed equilibrium between bacterial effectors and host responses permits microbial persistence and health of the host but confers risk of serious diseases, including peptic ulceration and gastric neoplasia.

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“…The precise transmission route is unknown, but most individuals may become infected in childhood (Klein et al, 1991). H. pylori is an important gastrointestinal pathogen associated with chronic gastritis, gastric or duodenal ulcers, and gastric cancer (Asaka et al, 1994;Honda et al, 1998;Peek et al, 2000 ). Although the majority of H. pylori-infected patients develop asymptomatic gastritis, gastric or duodenal ulcers, only a small proportion of them suffer from gastric cancer.…”

Section: Introductionmentioning

confidence: 99%

Association Between HLA-DQ Genotypes and Haplotypes vs Helicobacter pylori Infection in an Indonesian Population

Zhao¹,

Wang²,

Tanaka³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Background: Helicobacter pylori is an important gastrointestinal pathogen related to the development of not only atrophic gastritis and peptic ulcer, but also gastric cancer. Human leukocyte antigens (HLA) may play particular roles in host immune responses to bacterial antigens. This study aimed to investigate the association between HLA-DQA1 and DQB1 genotypes and haplotypes vs H. pylori infection in an Indonesian population. Methods: We selected 294 healthy participants in Mataram, Lombok Island, Indonesia. H. pylori infection was determined by urea breath test (UBT). We analyzed HLA-DQA1 and DQB1 genotypes by PCR-RFLP and constructed haplotypes of HLA-DQA1 and DQB1 genes. Multiple comparisons were conducted according to the Bonferroni method. Results: The H. pylori infection rate was 11.2% in this Indonesian population. The DQB1*0401 genotype was noted to be associated with a high risk of H. pylori infection, compared with the DQB1*0301 genotype. None of the HLA-DQA1 or DQB1 haplotypes were related to the risk of H. pylori infection. Conclusions: The study suggests that HLADQB1 genes play important roles in H. pylori infection, but there was no statistically significant association between HLA-DQA1 or DQB1 haplotypes and H.pylori infection in our Lombok Indonesian population.

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Helicobacter pylori alters gastric epithelial cell cycle events and gastrin secretion in Mongolian gerbils

Cited by 174 publications

References 46 publications

Effect of Helicobacter pylori eradication on gastric carcinogenesis

Effect of Helicobacter pylori eradication on gastric carcinogenesis

Helicobacter pylori persistence: biology and disease

Association Between HLA-DQ Genotypes and Haplotypes vs Helicobacter pylori Infection in an Indonesian Population

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