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).
