Helicobacter pylori−induced gastritis is the strongest singular risk factor for gastric adenocarcinoma. Matrix metalloproteinase−7 (MMP−7) is a proteolytic enzyme that can modify the intestinal microbial replicative niche as well as affect tumorigenesis, and H. pylori stimulates expression of MMP−7 in gastric epithelial cells in vitro. Utilizing a transgenic murine model of H. pylori−mediated injury, our experiments now show that gastric inflammation is increased within the context of MMP−7 deficiency, which involves both Th1− and Th17−mediated pathways. Enhanced gastritis in H. pylori−infected mmp−7−/− mice is strongly linked to accelerated epithelial cellular turnover. However, more severe inflammation and heightened proliferation and apoptosis are not dependent on MMP−7−mediated bacterial eradication. Collectively, these studies indicate that H. pylori−mediated induction of MMP−7 may serve to protect the gastric mucosa from pathophysiologic processes that promote carcinogenesis.

PMID: 20048070 [PubMed − indexed for MEDLINE] Source: National Library of Medicine.
PMCID: PMC2804939 [Available on 2011/1/1]