ArticleCell & bioscience2014
Genetic deletion of IL-25 (IL-17E) confers resistance to dextran sulfate sodium-induced colitis in mice.
Article in Cell & bioscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- The role of the tuft cell-interleukin-25 axis in the pathogenesis of inflammatory bowel disease.Frontiers in immunology · 2025Review
- A tuft cell - ILC2 signaling circuit provides therapeutic targets to inhibit gastric metaplasia and tumor development.Nature communications · 2023Article
- Cellular and Molecular Mechanisms of Intestinal Fibrosis.Gut and liver · 2023Review
- New insights into the function of Interleukin-25 in disease pathogenesis.Biomarker research · 2023Review
- IL25 Enhanced Colitis-Associated Tumorigenesis in Mice by Upregulating Transcription Factor GLI1.Frontiers in immunology · 2022Article
- High-Throughput On-Chip Human Mesenchymal Stromal Cell Potency Prediction.Advanced healthcare materials · 2022Article
- Epithelial cell alarmin cytokines: Frontline mediators of the asthma inflammatory response.Frontiers in immunology · 2022Review
- Interleukin 25 and its biological features and function in intestinal diseases.Central-European journal of immunology · 2022Review
- Roles of IL-25 in Type 2 Inflammation and Autoimmune Pathogenesis.Frontiers in immunology · 2021Review
- IL-33 Drives Expansion of Type 2 Innate Lymphoid Cells and Regulatory T Cells and Protects Mice From Severe, Acute Colitis.Frontiers in immunology · 2021Article
- Anti-IL-13Rα2 therapy promotes recovery in a murine model of inflammatory bowel disease.Mucosal immunology · 2019Article
- Role of interleukin-25 in development of spontaneous arthritis in interleukin-1 receptor antagonist-deficient mice.Biochemistry and biophysics reports · 2017Article
- The roles and functional mechanisms of interleukin-17 family cytokines in mucosal immunity.Cellular & molecular immunology · 2016Review
- Acute blockade of IL-25 in a colitis associated colon cancer model leads to increased tumor burden.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
backgroundIL-25 is emerging as a key regulator of inflammation in the intestinal mucosa because of its ability to promote type 2 while suppressing Th1 and Th17 responses. Several previous studies reported inconsistent results on the role of exogenous IL-25 in development of colonic inflammation and none were performed in animals with a genetic deletion of IL-25. We investigated the contribution of endogenous IL-25 to DSS-induced colitis using mice deficient in IL-25.
resultsMice were exposed to DSS in drinking water ad libitum either for seven days (acute) or for three cycles of seven days with DSS followed by 14 days without DSS (chronic) to induce colitis, respectively. The loss of body weight, appearance of diarrhea and bloody stools, and shortening of colon length were significantly less pronounced in IL-25(-/-) mice compared to WT mice after exposure to acute DSS. Histological examination showed that DSS-treated IL-25(-/-) mice had only mild inflammation in the colon, while severe inflammation developed in DSS-treated WT mice. A significant up-regulation of IL-33 was observed in acute DSS-treated WT but not in the IL-25(-/-) mice. There was significantly lower expression of pro-inflammatory cytokines in the colon of acute DSS-treated IL-25(-/-) compared to WT mice. IL-25(-/-) mice were also partially protected from chronic DSS challenge especially during the first 2 cycles of DSS exposure. In contrast to IL-25(-/-) mice, IL-13(-/-) mice were more susceptible to DSS-induced colitis. Finally, stimulation of T84 colonic epithelial cells with IL-25 up-regulated the expression of IL-33 and several pro-inflammatory cytokines.
conclusionsThese data indicate that endogenous IL-25 acts as a pro-inflammatory factor in DSS-induced colitis, which is unlikely to be mediated by IL-13 but possibly the induction of IL-33 and other pro-inflammatory mediators from colonic epithelial cells. The present study suggests that IL-25 may contribute to the pathogenesis of inflammatory bowel disease in at least a subgroup of patients.
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