Abstract:
: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.
journal_name
Cancer Resjournal_title
Cancer researchauthors
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 Jrdoi
10.1158/0008-5472.CAN-09-2899subject
Has Abstractpub_date
2010-01-01 00:00:00pages
30-5issue
1eissn
0008-5472issn
1538-7445pii
0008-5472.CAN-09-2899journal_volume
70pub_type
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