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Bacterial Binding in the Stomach

Helicobacter pylori is the cause of peptic ulcer disease and a contributory factor for gastric adenocarcinoma and non-Hodgkin lymphoma. Although the vast majority of H. pylori in colonized hosts is free-living, approximately 20% binds to gastric epithelial cells. This adherence is critical for induction of injury to the stomach. Decay-accelerating factor (DAF), a protein that protects epithelial cells from complement-mediated lysis, has been shown to function as the receptor for several microbial pathogens. Now, Daniel P. O'Brien and his colleagues add H. pylori to this list of DAF-binding microbes.

H. pylori adheres to CHO cells expressing DAF.

In this Paper of the Week, O'Brien et al. show that H. pylori adheres to CHO cells expressing human DAF. They also demonstrate that H. pylori induces DAF expression in cultured gastric epithelial cells and that mice lacking DAF experience attenuated stomach inflammation. These results suggest that H. pylori, like several other microbial pathogens, co-opts DAF as a receptor to induce disease. This has important implications in considering the pathogenesis of peptic ulcer disease and other related disorders.

FOOTNOTES

See referenced article, J. Biol. Chem. 2006, 281, 13317-13323

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