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Review
. 2014 May 21;20(19):5610-24.
doi: 10.3748/wjg.v20.i19.5610.

Factors that mediate colonization of the human stomach by Helicobacter pylori

Ciara Dunne  1 , Brendan Dolan  1 , Marguerite Clyne  1
Affiliations
Review

Factors that mediate colonization of the human stomach by Helicobacter pylori

Ciara Dunne et al. World J Gastroenterol. .

Abstract

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.

Keywords: Adhesins; CagA; Colonization; Flagella; Gastric mucosa; Helicobacter pylori; Infection; Polymorphisms; Type IV secretion system; Urease.

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Figures

Figure 1
Figure 1
Colonization and infection of the gastric mucosa by Helicobacter pylori. The majority of bacteria live in gastric mucus close to the epithelial surface. Motile, helical shaped bacteria can penetrate gastric mucus and escape the acidic conditions of the gastric lumen. Urease acts to generate ammonia in the presence of urea thus raising the pH and protecting the transiting bacteria from the effects of gastric acid. A subset of bacteria interact with gastric epithelial cells. Translocation of cytotoxin-associated gene A (CagA) from the bacteria into the host cell cytosol results in CagA phosphorylation dependent and CagA phosphorylation independent events occurring which subvert epithelial cell function.
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