Epithelial attachment alters the outcome of <i>Helicobacter pylori</i> infection

Janaki L. Guruge(Vanderbilt University), Per Falk(Vanderbilt University), Robin G. Lorenz(Vanderbilt University), Maria Dans(Vanderbilt University), Hans-Peter Wirth(Vanderbilt University), Martin J. Blaser(Vanderbilt University), Douglas E. Berg(Vanderbilt University), Jeffrey I. Gordon(Vanderbilt University)
Proceedings of the National Academy of Sciences
March 31, 1998
Cited by 292Open Access
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Abstract

Genetically defined in vivo models are needed to assess the importance of target cell attachment in bacterial pathogenesis. Gastric colonization by Helicobacter pylori in human populations is common and persistent, and has various outcomes including peptic ulcers and cancer. The impact of attachment on the course of infection was examined in transgenic mice expressing a human receptor for H. pylori in their gastric epithelium. Persistent infection by a clinical isolate occurred at comparable microbial densities in transgenic and nontransgenic littermates. However, microbial attachment in transgenic mice resulted in production of autoantibodies to Lewisx carbohydrate epitopes shared by bacteria and acid-secreting parietal cells, chronic gastritis, and parietal cell loss. This model should help identify bacterial and host genes that produce attachment-related pathology.


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