ArticleDigestive diseases and sciences2018
IL-17A Promotes Initiation and Development of Intestinal Fibrosis Through EMT.
Article in Digestive diseases and sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 72 citations in OpenAlex.
- Multiomics analyses revealed the roles of the epithelial-mesenchymal transition and novel early candidate diagnostic biomarkers in neonatal necrotising enterocolitis.Clinical and translational medicine · 2026Article
- Mechanisms of IL-17A Neutralisation in Alleviating Renal Fibrosis and Inflammation in Spontaneously Hypertensive Rats.Clinical and experimental pharmacology & physiology · 2026Article
- An intricate relationship between fibrosis and autoimmune diseases: a specific focus on unraveling its molecular, immunological, and epigenetic drivers.Frontiers in immunology · 2026Review
- Overexpression of mitochondrial STAT3 protein improves colonic inflammation and fibrosis in inflammatory bowel disease by enhancing mitochondrial function.Frontiers in immunology · 2026Article
- Th17/treg balance in Inflammatory Bowel Disease: the role of microbial, and genetic regulators in disease modulation.Frontiers in cell and developmental biology · 2026Review
- Th17 cell pathogenicity in autoimmune disease.Experimental & molecular medicine · 2025Review
- Intestinal fibrosis associated with inflammatory bowel disease: Known and unknown.Chinese medical journal · 2025Review
- Conventional techniques and emerging nanotechnologies for early detection of cancer metastasis via epithelial-mesenchymal transition monitoring.National science review · 2025Review
- Inflammation-fibrosis interplay in inflammatory bowel disease: mechanisms, progression, and therapeutic strategies.Frontiers in pharmacology · 2025Review
- Skullcapflavone II suppresses TGF-β-induced corneal epithelial mesenchymal transitionInternational journal of ophthalmology · 2025Article
- Inflammation accelerating intestinal fibrosis: from mechanism to clinic.European journal of medical research · 2024Review
- Single cell sequencing data identify distinct B cell and fibroblast populations in stricturing Crohn's disease.Journal of cellular and molecular medicine · 2024Article
- Review
- Role of Adipose Tissue Hormones in Pathogenesis of Cryptoglandular Anal Fistula.International journal of molecular sciences · 2024Article
- ELMO1 ameliorates intestinal epithelial cellular senescence via SIRT1/p65 signaling in inflammatory bowel disease-related fibrosis.Gastroenterology report · 2024Article
- Mechanisms and therapeutic research progress in intestinal fibrosis.Frontiers in medicine · 2024Article
- Anti-fibrotics in inflammatory bowel diseases: Challenges and successes.Advances in pharmacology (San Diego, Calif.) · 2024Review
- TH17 cell: a double-edged sword in the development of inflammatory bowel disease.Therapeutic advances in gastroenterology · 2024Review
- Targeting staphylococcal enterotoxin B binding to CD28 as a new strategy for dampening superantigen-mediated intestinal epithelial barrier dysfunctions.Frontiers in immunology · 2024Article
- A Narrative Review of Cytokine Networks: Pathophysiological and Therapeutic Implications for Inflammatory Bowel Disease Pathogenesis.Biomedicines · 2023Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntestinal fibrosis is a common complication of Crohn's disease (CD). Its exact mechanism is still unclear, and effective treatments to control or reverse the fibrosis process are unavailable. Epithelial-mesenchymal transition (EMT) may promote intestinal fibrosis by increasing deposition of extracellular matrix protein. IL-17A is a pro-inflammatory cytokine, and it has been shown as a profibrotic factor as its association with fibrosis of multiple organs was reported.
aimsTo assess the roles of IL-17A and EMT in the initiation and development of intestinal fibrosis and to verify the potential inductive effect of IL-17A on EMT.
methodsIn this study, we evaluated the expression of IL-17A and EMT-related genes in colonic mucosal biopsy tissues of CD patients and control individuals. Then, we examined the changes of EMT-related genes and fibrosis-related genes of IEC-6 cells which cultured for 72 h under increasing concentrations of IL-17A or with TGF-β1, to verify the potential inductive effect of IL-17A on EMT in vitro. We blocked the IL-17A of the mouse model of TNBS-induced experimental intestinal colitis and fibrosis to further verify the potential inductive effect of IL-17A on EMT in vivo.
resultsWe found the occurrence of EMT and high-level expression of IL-17A in intestinal mucosa of CD patients. Using IEC-6 cells, we showed that IL-17A may induce EMT in intestinal epithelial cells that come with reduced E-cadherin expression and increased expression of vimentin, snail, and α-SMA. We further found that anti-IL-17A treatment alleviated intestinal fibrosis through reducing EMT in mouse intestine.
conclusionsOur study confirmed the involvement of IL-17A in the development of intestinal fibrosis through inducing EMT.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.