ArticleCellular & molecular immunology2023
Tubulointerstitial nephritis antigen-like 1 is a novel matricellular protein that promotes gastric bacterial colonization and gastritis in the setting of Helicobacter pylori infection.
Article in Cellular & molecular immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Review
- Article
- Integrated transcriptomics and molecular docking identify hub genes and statin regulators inFrontiers in cellular and infection microbiology · 2026Article
- The association of the advanced lung cancer inflammation index with the risk ofFrontiers in cellular and infection microbiology · 2026Article
- Disruption of the biorhythm in gastric epithelial cell triggers inflammation in Helicobacter pylori-associated gastritis by aberrantly regulating NFIL3 via CagA activated ERK-SP1 pathway.Cell communication and signaling : CCS · 2025Article
- Mesenteric adipose-derived exosomal TINAGL1 enhances intestinal fibrosis in Crohn's Disease via SMAD4.Journal of advanced research · 2025Article
- Helicobacter pylori and gastric cancer: mechanisms and new perspectives.Journal of hematology & oncology · 2025Review
- Article
- Tubulointerstitial nephritis antigen-like 1 promotes the progression of liver fibrosis after HCV eradication with direct-acting antivirals.International journal of biological sciences · 2025Article
- Inflammatory factors collaboratively linkFrontiers in immunology · 2025Review
- Identifying gastric intestinal metaplasia risk based on clinical indicators: a machine learning predictive model based on the SHAP methodology.Frontiers in pharmacology · 2025Article
- Leishmania regulates host YY1: Comparative proteomic analysis identifies infection modulated YY1 dependent proteins.PloS one · 2025Article
- Article
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The interaction between the gastric epithelium and immune cells plays key roles in H. pylori-associated pathology. Here, we demonstrate a procolonization and proinflammatory role of tubulointerstitial nephritis antigen-like 1 (TINAGL1), a newly discovered matricellular protein, in H. pylori infection. Increased TINAGL1 production by gastric epithelial cells (GECs) in the infected gastric mucosa was synergistically induced by H. pylori and IL-1β via the ERK-SP1 pathway in a cagA-dependent manner. Elevated human gastric TINAGL1 correlated with H. pylori colonization and the severity of gastritis, and mouse TINAGL1 derived from non-bone marrow-derived cells promoted bacterial colonization and inflammation. Importantly, H. pylori colonization and inflammation were attenuated in Tinagl1
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Registered trials
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