ArticleDigestive diseases and sciences2020
Role of Interleukin-17 in Pathogenesis of Intestinal Fibrosis in Mice.
Article in Digestive diseases and sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Pooled it
- Targeting Molecular Dysregulation in Ulcerative Colitis: A Paired Cellular Perspective on CD4International journal of molecular sciences · 2025Observational
- Inflammation-fibrosis interplay in inflammatory bowel disease: mechanisms, progression, and therapeutic strategies.Frontiers in pharmacology · 2025Review
- Fibroblast-derived interleukin-11 as a potential biomarker for intestinal fibrostenosis in Crohn's disease.Therapeutic advances in gastroenterology · 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
- Anti-fibrotics in inflammatory bowel diseases: Challenges and successes.Advances in pharmacology (San Diego, Calif.) · 2024Review
- Cellular and Molecular Mechanisms of Intestinal Fibrosis.Gut and liver · 2023Review
- Molecular Basis of Intestinal Fibrosis in Inflammatory Bowel Disease.Inflammatory intestinal diseases · 2023Review
- Th17 Cell-Derived Amphiregulin Promotes Colitis-Associated Intestinal Fibrosis Through Activation of mTOR and MEK in Intestinal Myofibroblasts.Gastroenterology · 2023Article
- Immunological Regulation of Intestinal Fibrosis in Inflammatory Bowel Disease.Inflammatory bowel diseases · 2022Review
- Intestinal ischemia-reperfusion induces the release of IL-17A to regulate cell inflammation, apoptosis and barrier damage.Experimental and therapeutic medicine · 2022Article
- Review
- Intestinal Fibrosis in Inflammatory Bowel Disease and the Prospects of Mesenchymal Stem Cell Therapy.Frontiers in immunology · 2022Review
- The Molecular Mechanisms of Intestinal Inflammation and Fibrosis in Crohn's Disease.Frontiers in physiology · 2022Review
- Immunology of Inflammatory Bowel Disease: Molecular Mechanisms and Therapeutics.Journal of inflammation research · 2022Review
- Co-expression of fibrotic genes in inflammatory bowel disease; A localized event?Frontiers in immunology · 2022Article
- Based on G-Series Mouse TH17 Array Study the Effect of Fluoride on C2C12 Cells Cytokines Expression.Biological trace element research · 2021Article
- Novel mechanisms and clinical trial endpoints in intestinal fibrosis.Immunological reviews · 2021Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe level of interleukin (IL)-17 is commonly increased in serum and intestinal mucosa of patients with inflammatory bowel disease, especially Crohn's disease with intestinal stricture. However, the role of IL-17 in the pathogenesis of intestinal fibrosis and the effect of anti-IL-17 treatment on intestinal fibrosis remain unclear; these issues are studied in vivo in this study.
methodA total of 24 wild female Balb/c mice (18-22 g) were randomly divided into three groups: (1) control group, (2) 2,4,6-trinitrobenzenesulfonic acid (TNBS) + immunoglobulin G (IgG) group, and (3) TNBS + anti-IL-17 group. The levels of IL-17, IL-1β, transforming growth factor (TGF)-β1, and tumor necrosis factor (TNF)-α in blood and of collagen 3 and IL-17 in gut were measured by enzyme-linked immunosorbent assay (ELISA). The messenger RNA (mRNA) levels of collagen 3, IL-17, TNF-α, tissue inhibitor of metalloproteinase (TIMP)-1, and matrix metalloproteinase (MMP)-2 in gut were measured by reverse-transcription polymerase chain reaction. The protein expression of IL-17, collagen 3, TNF-α, TIMP-1, and MMP-2 were measured by immunoblot analysis. Collagen deposition was evaluated by standard hematoxylin and eosin and Masson's trichrome staining.
resultsThe profibrogenic cytokines IL-17, IL-1β, TGF-β1, and TNF-α in serum, mRNA levels of collagen 3, IL-17, TNF-α, TIMP-1, and MMP-2, and protein levels of IL-17, collagen 3, TNF-α, TIMP-1, and MMP-2 in gut were upregulated in TNBS-induced intestinal fibrosis mice. Treatment with anti-IL-17 antibody significantly alleviated intestinal fibrosis and reduced both mRNA and protein levels of collagen 3, TNF-α, TIMP-1, and MMP-2. The levels of profibrogenic cytokines IL-1β, TGF-β1, and TNF-α were also decreased in mice treated with anti-IL-17 antibody.
conclusionsIL-17 contributes to the pathogenesis of intestinal fibrosis, and anti-IL-17 therapy may weaken this effect by downregulating expression of profibrogenic cytokines and disturbing the MMP/TIMPs balance.
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