Matrix metalloproteinase-7 and premalignant host responses in Helicobacter pylori-infected mice.

Ogden SR, Noto JM, Allen SS, Patel DA, Romero-Gallo J, Washington MK, Fingleton B, Israel DA, Lewis ND, Wilson KT, Chaturvedi R, Zhao Z, Shyr Y, Peek RM
Cancer Res. 2010 70 (1): 30-5

PMID: 20048070 · PMCID: PMC2804939 · DOI:10.1158/0008-5472.CAN-09-2899

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.

MeSH Terms (13)

Adenocarcinoma Animals Gastric Mucosa Gastritis Helicobacter Infections Helicobacter pylori Immunohistochemistry Matrix Metalloproteinase 7 Mice Mice, Transgenic Precancerous Conditions Reverse Transcriptase Polymerase Chain Reaction Stomach Neoplasms

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