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Bacterial pathogenesis

Exterior detection

Nature Reviews Microbiology volume 2, page 925 (2004)Cite this article

Approximately one in every two individuals worldwide carries H. pylori in their gastric mucosa, and H. pylori infection is a known risk factor for the development of gastroduodenal disease. H. pylori infection of gastric epithelial cells causes major changes in cellular morphology; these changes are stimulated by the CagA virulence factor, which is secreted across the host cell membrane by the H. pylori T4SS encoded on the cag pathogenicity island (cag PAI). H. pylori also stimulates a pro-inflammatory response by activating the transcription factor nuclear factor (NF)-κB but, until now, the mechanism underlying this activation has been unknown, as neither CagA nor any other gene product encoded by the cag PAI stimulates the pro-inflammatory response, and the evidence for the involvement of the Toll-like receptors (TLRs) in innate immune detection of H. pylori has been controversial.

In this study, Viala et al. first examined the effects of H. pylori on NF-κB signalling in the HEK293 epithelial cell line, in which the two TLRs that are important for detection of Gram-negative bacteria, TLR2 and TLR4, are non-functional. Using an NF-κB-dependent assay with a luciferase reporter gene, several H. pylori strains were analysed and it was shown that the H. pylori-mediated activation of NF-κB was strictly dependent on the cag PAI.

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References

ORIGINAL RESEARCH PAPER

  1. Viala, J. et al. Nod1 responds to peptidoglycan delivered by the Helicobacter pylori cag pathogenicity island. Nature Immunol. 5, 1166–1174 (2004)

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FURTHER READING

  1. Cascales, E & Christie, P. J. The versatile bacterial type IV secretion systems Nature Rev. Microbiol. 1, 137–149 (2003)

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Authors
  1. Sheilagh Molloy
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Molloy, S. Exterior detection. Nat Rev Microbiol 2, 925 (2004). https://doi.org/10.1038/nrmicro1058

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