ArticleThe American journal of pathology2015
The epithelial danger signal IL-1α is a potent activator of fibroblasts and reactivator of intestinal inflammation.
Article in The American journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 68 citations in OpenAlex.
- Cellular crosstalk of fibroblast-myofibroblast transition in intestinal homeostasis and disease.Biomarker research · 2026Review
- Dysplastic Epithelial Repair Propagates Chronic Pathology Through the Paracrine Transformation of Pulmonary Fibroblasts.bioRxiv : the preprint server for biology · 2026Article
- A model for Crohn's disease post-ileal resection fibrosis development using human ileal enteroids and myofibroblasts.Frontiers in physiology · 2026Article
- Cellular senescence in Crohn's disease: a double-edged sword in intestinal fibrosis.Frontiers in immunology · 2026Review
- Article
- Unraveling the Converging Roles of ASC-Dependent Inflammasomes, Interleukin-1 Superfamily Members, Serum Amyloid A, and Non-Sterile Inflammation in Disease Pathology and Fibrosis in Inflammatory Bowel Disease and Primary Sclerosing Cholangitis.International journal of molecular sciences · 2025Review
- Fibrosis: cross-organ biology and pathways to development of innovative drugs.Nature reviews. Drug discovery · 2025Review
- Inflammatory Gene Panel Guiding the Study of Genetics in Inflammatory Bowel Disease.Molecular diagnosis & therapy · 2024Review
- Inflammation accelerating intestinal fibrosis: from mechanism to clinic.European journal of medical research · 2024Review
- Epithelial-neuronal-immune cell interactions: Implications for immunity, inflammation, and tissue homeostasis at mucosal sites.The Journal of allergy and clinical immunology · 2024Review
- Article
- Review
- A TNF-IL-1 circuit controls Yersinia within intestinal pyogranulomas.The Journal of experimental medicine · 2024Article
- Distinct fibroblast functions associated with fibrotic and immune-mediated inflammatory diseases and their implications for therapeutic development.F1000Research · 2024Review
- Cellular and Molecular Mechanisms of Intestinal Fibrosis.Gut and liver · 2023Review
- Role of the epithelial barrier in intestinal fibrosis associated with inflammatory bowel disease: relevance of the epithelial-to mesenchymal transition.Frontiers in cell and developmental biology · 2023Review
- Review
- Lactobacillus reuteri Releasing IL-22 (LR-IL-22) Facilitates Intestinal Radioprotection for Whole-Abdomen Irradiation (WAI) of Ovarian Cancer.Radiation research · 2022Article
- Development of antifibrotic therapy for stricturing Crohn's disease: lessons from randomized trials in other fibrotic diseases.Physiological reviews · 2022Review
- Contribution of the Gut Microbiota to Intestinal Fibrosis in Crohn's Disease.Frontiers in medicine · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Intestinal epithelial cell (IEC) death is typical of inflammatory bowel disease (IBD). We investigated: i) whether IEC-released necrotic cell products (proinflammatory mediators) amplify mucosal inflammation, ii) the capacity of necrotic cell lysates from HT29 cells or human IECs to induce human intestinal fibroblasts' (HIF) production of IL-6 and IL-8, and iii) whether IL-1α, released by injured colonocytes, exacerbated experimental IBD. Necrotic cell lysates potently induced HIF IL-6 and IL-8 production independent of Toll-like receptors 2 and 4, receptor for advanced glycation end-products, high-mobility group box 1, uric acid, IL-33, or inflammasome activation. IL-1α was the key IEC-derived necrotic cell product involved in HIF cytokine production. IL-1α-positive cells were identified in the epithelium in human IBD and dextran sulfate sodium (DSS)-induced colitis. IL-1α was detected in the stool of colitic mice before IL-1β. IL-1α enemas reactivated inflammation after DSS colitis recovery, induced IL-1 receptor expression in subepithelial fibroblasts, and activated de novo inflammation even in mice without overt colitis, after the administration of low-dose DSS. IL-1α amplifies gut inflammation by inducing cytokine production by mesenchymal cells. IL-1α-mediated IEC-fibroblast interaction may be involved in amplifying and perpetuating inflammation, even without obvious intestinal damage. IL-1α may be a target for treating early IBD or preventing the reactivation of IBD.
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Registered trials
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.