ArticleDigestive diseases and sciences2026
TNIP3 Attenuates Colitis by Inhibiting the TAB1/NF-κB/NLRP3 Signaling Pathway in Macrophages.
Article in Digestive diseases and sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Swimming Upstream: Another Look at NF-κB Inhibition for Colitis Treatment.Digestive diseases and sciences · 2026Article
- Beyond Acupuncture: Targeting AQP1 and Glial Activation for IBS Relief.Digestive diseases and sciences · 2026Article
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Authors and funding
4 authors.
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Abstract
backgroundInflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is characterized by chronic, recurrent, and non-specific intestinal inflammation. This study aimed to elucidate the mechanism of TNIP3 (TNFAIP3-interacting protein 3) in modulating macrophage (Mφ) polarization and intestinal epithelial barrier function in IBD.
methodsLPS-induced RAW 264.7 cells and DSS-induced mouse models were used to investigate the role of TNIP3 in IBD. A coculture system of Mφ and MSIE cells was established using Transwell chambers. Mφ polarization was assessed by flow cytometry, ELISA, and Western blotting. The barrier function of MSIE cells was evaluated via transepithelial electrical resistance (TEER) and FITC-dextran permeability assays. NF-κB activation was analyzed by immunofluorescence and Western blotting. The interaction between TNIP3 and TAB1 was examinedipitation (Co-IP).
resultsTNIP3 overexpression suppressed M1 Mφ polarization and inhibited NF-κB and NLRP3 inflammasome activation. Coculture with TNIP3-overexpression Mφ, enhanced MSIE barrier function, characterized by increased TEER values and reduced membrane permeability was found. The protective effects of TNIP3 overexpression were abolished by the NLRP3 inflammasome agonist BMS-986299 and TAB1 overexpression. TNIP3 alleviated DSS-induced intestinal damage and inflammation, whereas TAB1 overexpression reversed these protective effects in DSS-induced IBD model.
conclusionThis study concludes that TNIP3 significantly attenuates inflammatory responses in Mφ by inhibiting M1 Mφ polarization through the TAB1/NF-κB/NLRP3 pathway, and enhances barrier function of IECs in microenvironment. These findings suggest TNIP3 as a potential therapeutic target for IBD treatment.
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