Skip to main content

Receptor’s role in stopping H. pylori

Apr. 25, 2019, 10:30 AM

by Niyati Vachharajani


Helicobacter pylori infection is the most significant risk factor for stomach cancer.

Giovanni Suarez, PhD, Richard Peek, MD, and colleagues previously demonstrated that H. pylori-induced gastric injury can be reduced in vitro and in an animal model by pre-activation of the innate immune receptor, NOD1. However, the role of aberrant NOD1 activation by H. pylori in gastric carcinogenesis remains elusive.

To explore NOD1’s role in inflammation-related cancer that develops in response to H. pylori, they infected two mouse models missing the gene for NOD1. The animals developed more severe gastritis and inflammation compared to wild-type mice. Furthermore, NOD1-deficient macrophages were less effective in dampening inflammatory responses compared to wild-type macrophages.

These findings, published April 1 in Cancer Research, demonstrate that loss of NOD1 augments inflammatory and injury responses to H. pylori. They also highlight previously unreported NOD1-H. pylori interactions and point towards NOD1 as a prime target for modification for either preventing or treating H. pylori infections.

This research was supported by grants from the National Institutes of Health (DK058587, CA077955, CA116087, DK058404, CA028842).

Recent Stories from VUMC News and Communications Publications

Vanderbilt Medicine
VUMC Voice