Published online Apr 28, 2018. doi: 10.3748/wjg.v24.i16.1725
Peer-review started: March 6, 2018
First decision: March 29, 2018
Revised: April 3, 2018
Accepted: April 9, 2018
Article in press: April 9, 2018
Published online: April 28, 2018
Nucleotide-binding oligomerization domain 1 (NOD1) is an intracellular innate immune sensor for small molecules derived from bacterial cell components. NOD1 activation by its ligands leads to robust production of pro-inflammatory cytokines and chemokines by innate immune cells, thereby mediating mucosal host defense systems against microbes. Chronic gastric infection due to Helicobacter pylori (H. pylori) causes various upper gastrointestinal diseases, including atrophic gastritis, peptic ulcers, and gastric cancer. It is now generally accepted that detection of H. pylori by NOD1 expressed in gastric epithelial cells plays an indispensable role in mucosal host defense systems against this organism. Recent studies have revealed the molecular mechanism by which NOD1 activation caused by H. pylori infection is involved in the development of chronic gastritis and gastric cancer. In this review, we have discussed and summarized how sensing of H. pylori by NOD1 mediates the prevention of chronic gastritis and gastric cancer.
Core tip: Nucleotide-binding oligomerization domain 1 (NOD1), an intracellular innate immune sensor, plays a role in mucosal host defense systems against Helicobacter pylori (H. pylori) infection. NOD1 activation is involved in the generation of T helper type 1 responses against H. pylori through activation of type I IFN signaling pathways. NOD1 activation prevents gastric carcinogenesis through negative regulation of caudal-related homeobox 2 expression.