The anti-inflammatory and protective role of interleukin-38 in inflammatory bowel disease
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- Ohno Masashi
- Department of Medicine, Shiga University of Medical Science
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- Imai Takayuki
- Department of Medicine, Shiga University of Medical Science
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- Chatani Motoharu
- Department of Medicine, Shiga University of Medical Science
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- Nishida Atsushi
- Department of Medicine, Shiga University of Medical Science
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- Inatomi Osamu
- Department of Medicine, Shiga University of Medical Science
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- Kawahara Masahiro
- Department of Medicine, Shiga University of Medical Science
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- Hoshino Tomoaki
- Division of Respirology, Neurology and Rheumatology, Kurume University School of Medicine
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- Andoh Akira
- Department of Medicine, Shiga University of Medical Science
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Abstract
<p>Interleukin (IL)-38 exerts an anti-inflammatory function by binding to several cytokine receptors, including the IL-36 receptor. In this study, we evaluated IL-38 expression in the inflamed mucosa of patients with inflammatory bowel disease (IBD) and investigated its functions. IL-38 mRNA expression in endoscopic biopsy samples was evaluated using quantitative PCR. IL-38 protein expression was analyzed using immunohistochemical technique. Dextran sulfate sodium-induced colitis was induced in C57BL/6 background IL-38KO mice. The IL-38 mRNA and protein expression were enhanced in the active mucosa of ulcerative colitis, but not in Crohn’s disease. The ratio of IL-36γ to IL-38 mRNA expression was significantly elevated in the active mucosa of UC patients. Immunofluorescence staining revealed that B cells are the major cellular source of IL-38 in the colonic mucosa. IL-38 dose-dependently suppressed the IL-36γ-induced mRNA expression of CXC chemokines (CXCL1, CXCL2, and CXCL8) in HT-29 and T84 cells. IL-38 inhibited the IL-36γ-induced activation of nuclear-factor kappa B (NF-κB) and mitogen-activated protein kinases in HT-29 cells. DSS-colitis was significantly exacerbated in IL-38KO mice compared to wild type mice. In conclusion, IL-38 may play an anti-inflammatory and protective role in the pathophysiology of IBD, in particular ulcerative colitis, through the suppression of IL-36-induced inflammatory responses.</p>
Journal
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- Journal of Clinical Biochemistry and Nutrition
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Journal of Clinical Biochemistry and Nutrition 70 (1), 64-71, 2022
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Details 詳細情報について
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- CRID
- 1390853567321102464
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- NII Article ID
- 130008139087
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- ISSN
- 18805086
- 09120009
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- Text Lang
- en
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- Data Source
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- JaLC
- IRDB
- Crossref
- CiNii Articles
- KAKEN
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- Abstract License Flag
- Disallowed