ArticleWorld journal of gastroenterology2025
Keratin 1 modulates intestinal barrier and immune response
Article in World journal of gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Proteomic reprogramming of ileal epithelial cells during homologous superimposed intestinal trematode infection reveals coordinated restoration of intestinal homeostasis.PLoS neglected tropical diseases · 2026Article
- Akkermansia muciniphila affects colitis by inhibiting ferroptosis signaling pathway.Scientific reports · 2026Article
- Regulation of Keratin Chemical Modifications: Potential Molecular Mechanisms in Proliferative Diseases.International journal of molecular sciences · 2026Review
- The immunomodulatory potential of bradykinin signaling in autoimmune conditions.Frontiers in immunology · 2026Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExternal factors in ulcerative colitis (UC) exacerbate colonic epithelial permeability and inflammatory responses. Keratin 1 (KRT1) is crucial in regulating these alterations, but its specific role in the progression of UC remains to be fully elucidated.
aimTo explore the role and mechanisms of KRT1 in the regulation of colonic epithelial permeability and inflammation in UC.
methodsA KRT1 antibody concentration gradient test, along with a dextran sulfate sodium (DSS)-induced animal model, was implemented to investigate the role of KRT1 in modulating the activation of the kallikrein kinin system (KKS) and the cleavage of bradykinin (BK)/high molecular weight kininogen (HK) in UC.
resultsTreatment with KRT1 antibody in Caco-2 cells suppressed cell proliferation, induced apoptosis, reduced HK expression, and increased BK expression. It further downregulated intestinal barrier proteins, including occludin, zonula occludens-1, and claudin, and negatively impacted the coagulation factor XII. These changes led to enhanced activation of BK and HK cleavage, thereby intensifying KKS-mediated inflammation in UC. In the DSS-induced mouse model, administration of KRT1 antibody mitigated colonic injury, increased colon length, alleviated weight loss, and suppressed inflammatory cytokines such as interleukin (IL)-1, IL-6, tumor necrosis factor-α. It also facilitated repair of the intestinal barrier, reducing DSS-induced injury.
conclusionKRT1 inhibits BK expression, suppresses inflammatory cytokines, and enhances markers of intestinal barrier function, thus ameliorating colonic damage and maintaining barrier integrity. KRT1 is a viable therapeutic target for UC.
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