ArticleOncogene2015
Matrix metalloproteinase 7 restrains Helicobacter pylori-induced gastric inflammation and premalignant lesions in the stomach by altering macrophage polarization.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 55 citations in OpenAlex.
- Conventional and Novel Approaches to Establishing Mouse Models of Gastric Cancer in the Past, Present, and Potential Post-H. Pylori Infection Era.Biological procedures online · 2026Review
- Post-booster longitudinal plasma proteomic changes following BNT162b2 COVID-19 vaccination in Qatar.Frontiers in immunology · 2026Article
- Combination detection of IgG- and IgA-related autoantibodies for the early diagnosis of gastric cancer.Cancer biomarkers : section A of Disease markers · 2025Article
- Dysregulated macrophage immunity inFrontiers in immunology · 2025Review
- Endogenous glucocorticoids are required for normal macrophage activation and gastricAmerican journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Current Knowledge about Gastric Microbiota with Special Emphasis onCurrent issues in molecular biology · 2024Review
- Strategies ofFrontiers in cellular and infection microbiology · 2024Review
- Effects and mechanisms ofFrontiers in immunology · 2024Review
- Tumour-associated macrophages in gastric cancer: From function and mechanism to application.Clinical and translational medicine · 2023Review
- Bacteria and macrophages in the tumor microenvironment.Frontiers in microbiology · 2023Review
- Linking dysbiosis to precancerous stomach through inflammation: Deeper than and beyond imaging.Frontiers in immunology · 2023Review
- Thermo-Transient Receptor Potential Channels: Therapeutic Potential in Gastric Cancer.International journal of molecular sciences · 2022Review
- Innate Immunity Crosstalk withInternational journal of molecular sciences · 2022Review
- Proteolytic Landscapes in Gastric Pathology and Cancerogenesis.International journal of molecular sciences · 2022Review
- Matrix Metalloproteinases inInternational journal of molecular sciences · 2022Review
- Emerging Role ofFrontiers in oncology · 2022Review
- Effects ofFrontiers in immunology · 2022Review
- Precision Medicine Approaches to Prevent Gastric Cancer.Gut and liver · 2021Review
- Article
- Notch Signaling Ligand Jagged1 Enhances Macrophage-Mediated Response toFrontiers in microbiology · 2021Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Helicobacter pylori is the strongest risk factor for the development of gastric cancer. Although the specific mechanisms by which this pathogen induces carcinogenesis have not been fully elucidated, high-expression interleukin (IL)-1β alleles are associated with increased gastric cancer risk among H. pylori-infected persons. In addition, loss of matrix metalloproteinase 7 (MMP7) increases mucosal inflammation in mouse models of epithelial injury, and we have shown that gastric inflammation is increased in H. pylori-infected MMP7(-/-) C57BL/6 mice. In this report, we define mechanisms that underpin such responses and extend these results into a genetic model of MMP7 deficiency and gastric cancer. Wild-type (WT) or MMP7(-/-) C57BL/6 mice were challenged with broth alone as an uninfected control or the H. pylori strain PMSS1. All H. pylori-challenged mice were successfully colonized. As expected, H. pylori-infected MMP7(-/-) C57BL/6 mice exhibited a significant increase in gastric inflammation compared with uninfected or infected WT C57BL/6 animals. Loss of MMP7 resulted in M1 macrophage polarization within H. pylori-infected stomachs, as assessed by Luminex technology and immunohistochemistry, and macrophages isolated from infected MMP7-deficient mice expressed significantly higher levels of the M1 macrophage marker IL-1β compared with macrophages isolated from WT mice. To extend these findings into a model of gastric cancer, hypergastrinemic WT INS-GAS or MMP7(-/-) INS-GAS mice were challenged with H. pylori strain PMSS1. Consistent with findings in the C57BL/6 model, H. pylori-infected MMP7-deficient INS-GAS mice exhibited a significant increase in gastric inflammation compared with either uninfected or infected WT INS-GAS mice. In addition, the incidence of gastric hyperplasia and dysplasia was significantly increased in H. pylori-infected MMP7(-/-) INS-GAS mice compared with infected WT INS-GAS mice, and loss of MMP7 promoted M1 macrophage polarization. These results suggest that MMP7 exerts a restrictive role on H. pylori-induced gastric injury and the development of premalignant lesions by suppressing M1 macrophage polarization.
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