Matrix Metalloproteinase-7 and Premalignant Host Responses in Helicobacter pylori-Infected Mice

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...

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Veröffentlicht in:Cancer research (Chicago, Ill.) Ill.), 2010, Vol.70 (1), p.30-35
Hauptverfasser: OGDEN, Seth R, NOTO, Jennifer M, CHATURVEDI, Rupesh, ZHIGUO ZHAO, SHYR, Yu, PEEK, Richard M, ALLEN, Shannon S, PATEL, Dilan A, ROMERO-GALLO, Judith, WASHINGTON, M. Kay, FINGLETON, Barbara, ISRAEL, Dawn A, LEWIS, Nuruddeen D, WILSON, Keith T
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Sprache:eng
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Zusammenfassung: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.
ISSN:0008-5472
1538-7445
DOI:10.1158/0008-5472.can-09-2899