Alimentary TractHelicobacter pylori alters gastric epithelial cell cycle events and gastrin secretion in Mongolian gerbils☆,☆☆
Section snippets
Animals and housing and H. pylori challenge
Outbred Mongolian gerbils of 30-50 g body weight, corresponding to an age of approximately 4-8 weeks, were purchased either from Harlan Sprague Dawley, Inc. (Indianapolis, IN) (Hsd:MON) or Charles River Laboratories (Wilmington, MA) (Crl:[MON]BR[outbred]), exactly as described previously.24 All experiments and procedures carried out on the animals were approved by the Institutional Animal Care Committee of Vanderbilt University. The mouse-passaged cagA+, vacA s1a toxigenic strain CPY340124 was
Colonization efficiency of wild-type and isogenic mutant H. pylori strains
The population of animals examined in the current study has been described previously by Wirth et al.24 In total, 120 gerbils had been challenged either with H. pylori strain G1.1 WT (n = 60), G1.1 C− (n = 23), G1.1 V− (n = 17), or brucella broth alone (n = 20).24 Because indices of cell turnover and gastrin levels in uninfected gerbils did not vary by age, the control animals were analyzed together as a single group. Of the 100 gerbils challenged with H. pylori, 93 (57 WT, 22 C−, 14 V−) were
Discussion
Apoptosis is a normal component of epithelial cell turnover in the gastrointestinal tract, and most studies show that persons colonized with H. pylori have increased rates of gastric mucosal proliferation and apoptosis compared with uninfected persons.11, 12, 13, 14, 29 However, within clinical populations, there is substantial overlap in these measures of gastric epithelial cell growth and death. H. pylori strain–specific characteristics may contribute to this heterogeneity; persons carrying
Acknowledgements
The authors thank Uma Krishna and Annuapama Voodarla for excellent technical assistance.
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Cited by (165)
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2021, Research and Clinical Applications of Targeting Gastric NeoplasmsEpithelial cell ADAM17 activation by Helicobacter pylori: Role of ADAM17 C-terminus and Threonine-735 phosphorylation
2015, Microbes and InfectionCitation Excerpt :Potential contributory factors linking H. pylori with development of gastric cancer include the chronic inflammatory response to infection, H. pylori induced perturbations in gastric epithelial cell signalling [2–5] and disruption of gastric epithelial cell intercellular and cell-matrix junctions [6]. Gastric epithelial hyperproliferation is observed both clinically [7,8] and in animal models [9,10]. One of the potential mechanisms by which H. pylori induces hyperproliferative epithelial responses involves H. pylori stimulated transactivation of the Epidermal Growth Factor Receptor (EGFR).
Helicobacter pylori and Other Gastric Helicobacter Species
2014, Mandell, Douglas, and Bennett's Principles and Practice of Infectious DiseasesGastrointestinal malignancy and the microbiome
2014, GastroenterologyHelicobacter pylori decreases p27 expression through the delta opioid receptor-mediated inhibition of histone acetylation within the p27 promoter
2012, Cancer LettersCitation Excerpt :Both the accelerated cell turnover and decrease in p27 can be reversed to normal following the successful eradication of H. pylori in patients with chronic gastritis [21,22]. In animal [23] and cell culture [24] models of chronic H. pylori infection, the long-term exposure of H. pylori to gastric epithelial cells leads to the emergence of epithelial cells that are relatively apoptosis resistant. The levels of p27 and p27 mRNA transcripts in these cells are low when compared to parental AGS cells [24].
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Address requests for reprints to: Richard M. Peek, Jr., M.D., Division of Gastroenterology, Vanderbilt University School of Medicine, C-2104 Medical Center North, Nashville, Tennessee 37232-2279. e-mail: [email protected]; fax: (615) 343-6229.
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Supported in part by the National Institutes of Health grants KO8 DK02381-01A3, R29 CA77955, and R01 DK50837 and the Medical Research Service of the Department of Veterans Affairs.