ArticleFrontiers in medicine2015
Interleukin(IL)-36α and IL-36γ Induce Proinflammatory Mediators from Human Colonic Subepithelial Myofibroblasts.
Article in Frontiers in medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Differential Expression of IL-36 Family Members and IL-38 by Immune and Nonimmune Cells in Patients with Active Inflammatory Bowel Disease.BioMed research international · 2018Trial
- Preliminary IL-1 Family Cytokine Signature for Crohn's Disease Onset in Pediatric Juvenile Idiopathic Arthritis.International journal of molecular sciences · 2026Article
- Bidirectional causal relationship between inflammatory cytokines and endometriosis at different sites.BMC women's health · 2025Article
- FloxedCells · 2024Article
- Sublingual Immunotherapy Decreased the Serum Levels of Interleukin-36Mediators of inflammation · 2024Article
- New insights on IL‑36 in intestinal inflammation and colorectal cancer (Review).Experimental and therapeutic medicine · 2023Review
- Interleukin-36γ is causative for liver damage upon infection with Rift Valley fever virus in type I interferon receptor-deficient mice.Frontiers in immunology · 2023Article
- Regulation of Interleukin-36γ/IL-36R Signaling Axis by PIN1 in Epithelial Cell Transformation and Breast Tumorigenesis.Cancers · 2022Article
- IL-36γ in enthesitis-related juvenile idiopathic arthritis and its association with disease activity.Clinical and experimental immunology · 2022Article
- The anti-inflammatory and protective role of interleukin-38 in inflammatory bowel disease.Journal of clinical biochemistry and nutrition · 2022Article
- IL-36α Enhances Host Defense againstJournal of immunology (Baltimore, Md. : 1950) · 2021Article
- IL-36 cytokines in inflammatory and malignant diseases: not the new kid on the block anymore.Cellular and molecular life sciences : CMLS · 2021Review
- IL-36 in chronic inflammation and fibrosis - bridging the gap?The Journal of clinical investigation · 2021Review
- Association of IL-36γ with tertiary lymphoid structures and inflammatory immune infiltrates in human colorectal cancer.Cancer immunology, immunotherapy : CII · 2019Article
- A cytokine network involving IL-36γ, IL-23, and IL-22 promotes antimicrobial defense and recovery from intestinal barrier damage.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Altered expression of IL36γ and IL36 receptor (IL1RL2) in the colon of patients with Hirschsprung's disease.Pediatric surgery international · 2017Article
- IL-36γ inhibits differentiation and induces inflammation of keratinocyte via Wnt signaling pathway in psoriasis.International journal of medical sciences · 2017Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInterleukin (IL)-36 cytokines are recently reported member of the IL-1 cytokine family. However, there is little information regarding the association between IL-36 cytokines and gut inflammation. In the present study, we investigated the biological activity of IL-36α and IL-36γ using human colonic subepithelial myofibroblasts (SEMFs).
methodsThe mRNA expression and the protein expression of target molecules in SEMFs were evaluated using real-time polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. The intracellular signaling of IL-36 cytokines was analyzed using Western blot analysis and small interfering RNAs (siRNAs) specific for MyD88 adaptor proteins (MyD88 and IRAK1) and NF-κB p65.
resultsIL-36α and IL-36γ significantly enhanced the secretion of IL-6 and CXC chemokines (CXCL1, CXCL2, and CXCL8) by SEMFs. The combination of IL-36α/γ and IL-17A or of IL-36α/γ and tumor necrosis factor-α showed a synergistic effect on the induction of IL-6 and CXC chemokines. The mRNA expression of proinflammatory mediators induced by IL-36α and/or IL-36γ was significantly suppressed by transfection of siRNA for MyD88 or IRAK1. Both inhibitors of mitogen activated protein kinases and siRNAs specific for NF-κBp65 significantly reduced the expression of IL-6 and CXC chemokines induced by IL-36α and/or IL-36γ.
conclusionThese results suggest that IL-36α and IL-36γ contribute to gut inflammation through the induction of proinflammatory mediators.
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