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Updated: Jan 26, 2026

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance
Published on: March 7, 2025
Helicobacter pylori-induced matrix metallopeptidase-10 promotes gastric bacterial colonization and gastritis
Yi-Pin Lv1, Ping Cheng1, Jin-Yu Zhang1
1National Engineering Research Center of Immunological Products, Department of Microbiology and Biochemical Pharmacy, College of Pharmacy, Third Military Medical University, Chongqing, China.
Abstract:
The interaction between gastric epithelium and immune response plays key roles in H. pylori-associated pathology. We demonstrated a procolonization and proinflammation role of MMP-10 in H. pylori infection. MMP-10 is elevated in gastric mucosa and is produced by gastric epithelial cells synergistically induced by H. pylori and IL-22 via the ERK pathway. Human gastric MMP-10 was correlated with H. pylori colonization and the severity of gastritis, and mouse MMP-10 from non-BM-derived cells promoted bacteria colonization and inflammation. H. pylori colonization and inflammation were attenuated in IL-22-/-, MMP-10-/-, and IL-22-/-MMP-10-/- mice. MMP-10-associated inflammation is characterized by the influx of CD8+ T cells, whose migration is induced via MMP-10-CXCL16 axis by gastric epithelial cells. Under the influence of MMP-10, Reg3a, E-cadherin, and zonula occludens-1 proteins decrease, resulting in impaired host defense and increased H. pylori colonization. Our results suggest that MMP-10 facilitates H. pylori persistence and promotes gastritis.
Insights
Matrix metalloproteinase-10 (MMP-10) promotes Helicobacter pylori colonization and gastritis by affecting immune cells and epithelial barrier function. Reducing MMP-10 could be a therapeutic strategy against H. pylori infection.
Area of Science:
- Gastroenterology
- Immunology
- Molecular Biology
Background:
- Helicobacter pylori infection is a major cause of gastritis and other gastric pathologies.
- The interplay between gastric epithelium and the immune system is crucial in H. pylori-associated diseases.
Purpose of the Study:
- To investigate the role of Matrix metalloproteinase-10 (MMP-10) in H. pylori infection and associated gastric pathology.
- To elucidate the mechanisms by which MMP-10 influences bacterial colonization and inflammation.
Main Methods:
- Analysis of MMP-10 levels in human gastric mucosa.
- Studies in genetically modified mice (IL-22-/-, MMP-10-/-, and combined knockouts) to assess H. pylori colonization and inflammation.
- Investigation of the MMP-10-CXCL16 axis and its effect on CD8+ T cell migration.
- Assessment of protein expression (Reg3a, E-cadherin, zonula occludens-1) under MMP-10 influence.
Main Results:
- MMP-10 is elevated in H. pylori-infected gastric mucosa and produced by epithelial cells.
- MMP-10 deficiency or IL-22 deficiency attenuated H. pylori colonization and inflammation in mice.
- MMP-10 promotes CD8+ T cell influx via the MMP-10-CXCL16 axis.
- MMP-10 downregulates Reg3a, E-cadherin, and zonula occludens-1, impairing host defense.
Conclusions:
- MMP-10 plays a significant pro-colonization and pro-inflammation role in H. pylori infection.
- MMP-10 facilitates H. pylori persistence and exacerbates gastritis by compromising epithelial barrier function and modulating immune cell infiltration.
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