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Updated: Jun 17, 2026

Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
Matrix metalloproteinase-7 and premalignant host responses in Helicobacter pylori-infected mice
Seth R Ogden1, Jennifer M Noto, Shannon S Allen
1Department of Medicine, Vanderbilt University, Nashville, Tennessee 37232-2279, USA.
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.
Insights
Matrix metalloproteinase-7 (MMP-7) deficiency exacerbates Helicobacter pylori-induced gastritis in mice. MMP-7 appears to protect the gastric mucosa, potentially reducing cancer risk by mitigating inflammation and cellular turnover.
Area of Science:
- Gastroenterology
- Immunology
- Oncology
Background:
- Helicobacter pylori infection is a primary cause of gastric adenocarcinoma.
- Matrix metalloproteinase-7 (MMP-7) is implicated in tumorigenesis and modulated by H. pylori.
- MMP-7 influences the gastric microbial environment and epithelial cell behavior.
Purpose of the Study:
- To investigate the role of MMP-7 in H. pylori-induced gastritis using a murine model.
- To determine if MMP-7 deficiency impacts gastric inflammation, cellular turnover, and bacterial eradication.
Main Methods:
- Utilized a transgenic murine model deficient in MMP-7 (mmp-7-/-).
- Infected mice with H. pylori to induce gastritis.
- Assessed gastric inflammation, Th1/Th17 pathways, epithelial cell turnover, proliferation, and apoptosis.
Main Results:
- MMP-7 deficient mice exhibited increased gastric inflammation upon H. pylori infection.
- Enhanced gastritis was associated with Th1 and Th17 immune responses.
- Accelerated epithelial cell turnover was observed in MMP-7 deficient mice.
- Increased inflammation, proliferation, and apoptosis were not dependent on MMP-7 for bacterial clearance.
Conclusions:
- H. pylori-induced MMP-7 expression may protect the gastric mucosa.
- MMP-7 deficiency exacerbates gastritis and associated pathophysiological processes.
- These findings suggest MMP-7 plays a protective role against H. pylori-driven carcinogenesis.
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