دورية أكاديمية

IL-36 and IL-1/IL-17 Drive Immunity to Oral Candidiasis via Parallel Mechanisms.

التفاصيل البيبلوغرافية
العنوان: IL-36 and IL-1/IL-17 Drive Immunity to Oral Candidiasis via Parallel Mechanisms.
المؤلفون: Verma AH; Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pittsburgh, PA 15261., Zafar H; Mucosal and Salivary Biology Division, King's College London Dental Institute, London SE1 1UL, United Kingdom.; Centre for Host-Microbiome Interactions, Mucosal and Salivary Biology Division, King's College London Dental Institute, London SE1 9RT, United Kingdom., Ponde NO; Mucosal and Salivary Biology Division, King's College London Dental Institute, London SE1 1UL, United Kingdom., Hepworth OW; Mucosal and Salivary Biology Division, King's College London Dental Institute, London SE1 1UL, United Kingdom.; Centre for Host-Microbiome Interactions, Mucosal and Salivary Biology Division, King's College London Dental Institute, London SE1 9RT, United Kingdom., Sihra D; Mucosal and Salivary Biology Division, King's College London Dental Institute, London SE1 1UL, United Kingdom., Aggor FEY; Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pittsburgh, PA 15261., Ainscough JS; Faculty of Biological Sciences, School of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT, United Kingdom., Ho J; Mucosal and Salivary Biology Division, King's College London Dental Institute, London SE1 1UL, United Kingdom., Richardson JP; Mucosal and Salivary Biology Division, King's College London Dental Institute, London SE1 1UL, United Kingdom., Coleman BM; Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pittsburgh, PA 15261., Hube B; Department of Microbial Pathogenicity Mechanisms, Leibniz Institute for Natural Product Research and Infection Biology-Hans Knoell Institute, D-07745 Jena, Germany.; Friedrich Schiller University, D-07737 Jena, Germany; and.; Center for Sepsis Control and Care, D-07747 Jena, Germany., Stacey M; Faculty of Biological Sciences, School of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT, United Kingdom., McGeachy MJ; Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pittsburgh, PA 15261., Naglik JR; Mucosal and Salivary Biology Division, King's College London Dental Institute, London SE1 1UL, United Kingdom., Gaffen SL; Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pittsburgh, PA 15261; david.moyes@kcl.ac.uk sarah.gaffen@pitt.edu., Moyes DL; Mucosal and Salivary Biology Division, King's College London Dental Institute, London SE1 1UL, United Kingdom; david.moyes@kcl.ac.uk sarah.gaffen@pitt.edu.; Centre for Host-Microbiome Interactions, Mucosal and Salivary Biology Division, King's College London Dental Institute, London SE1 9RT, United Kingdom.
المصدر: Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 2018 Jul 15; Vol. 201 (2), pp. 627-634. Date of Electronic Publication: 2018 Jun 11.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: American Association of Immunologists Country of Publication: United States NLM ID: 2985117R Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1550-6606 (Electronic) Linking ISSN: 00221767 NLM ISO Abbreviation: J Immunol Subsets: MEDLINE
أسماء مطبوعة: Publication: Bethesda, MD : American Association of Immunologists
Original Publication: Baltimore : Williams & Wilkins, c1950-
مواضيع طبية MeSH: Candida albicans/*immunology , Candidiasis/*immunology , Fungal Proteins/*metabolism , Interleukin-1/*metabolism , Interleukin-17/*metabolism , Mouth Mucosa/*physiology, Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Cell Line ; Gene Expression Regulation ; Immunity, Innate ; Interleukin-23/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mouth Mucosa/microbiology ; Receptors, Interleukin-1/genetics ; Signal Transduction ; p38 Mitogen-Activated Protein Kinases/metabolism
مستخلص: Protection against microbial infection by the induction of inflammation is a key function of the IL-1 superfamily, including both classical IL-1 and the new IL-36 cytokine families. Candida albicans is a frequent human fungal pathogen causing mucosal infections. Although the initiators and effectors important in protective host responses to C. albicans are well described, the key players in driving these responses remain poorly defined. Recent work has identified a central role played by IL-1 in inducing innate Type-17 immune responses to clear C. albicans infections. Despite this, lack of IL-1 signaling does not result in complete loss of immunity, indicating that there are other factors involved in mediating protection to this fungus. In this study, we identify IL-36 cytokines as a new player in these responses. We show that C. albicans infection of the oral mucosa induces the production of IL-36. As with IL-1α/β, induction of epithelial IL-36 depends on the hypha-associated peptide toxin Candidalysin. Epithelial IL-36 gene expression requires p38-MAPK/c-Fos, NF-κB, and PI3K signaling and is regulated by the MAPK phosphatase MKP1. Oral candidiasis in IL-36R -/- mice shows increased fungal burdens and reduced IL-23 gene expression, indicating a key role played by IL-36 and IL-23 in innate protective responses to this fungus. Strikingly, we observed no impact on gene expression of IL-17 or IL-17-dependent genes, indicating that this protection occurs via an alternative pathway to IL-1-driven immunity. Thus, IL-1 and IL-36 represent parallel epithelial cell-driven protective pathways in immunity to oral C. albicans infection.
(Copyright © 2018 by The American Association of Immunologists, Inc.)
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معلومات مُعتمدة: R01 DE022550 United States DE NIDCR NIH HHS; R37 DE022550 United States DE NIDCR NIH HHS; MR/J008303/1 United Kingdom MRC_ Medical Research Council; United Kingdom DH_ Department of Health; R01 DE023815 United States DE NIDCR NIH HHS; BB/N014677/1 United Kingdom BB_ Biotechnology and Biological Sciences Research Council; MR/M011372/1 United Kingdom MRC_ Medical Research Council
المشرفين على المادة: 0 (Adaptor Proteins, Signal Transducing)
0 (ECE1 protein, Candida albicans)
0 (Fungal Proteins)
0 (Interleukin-1)
0 (Interleukin-17)
0 (Interleukin-23)
0 (Receptors, Interleukin-1)
0 (Traf3ip2 protein, mouse)
0 (interleukin-36 receptor, mouse)
0 (interleukin-36, mouse)
EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
تواريخ الأحداث: Date Created: 20180613 Date Completed: 20190705 Latest Revision: 20230926
رمز التحديث: 20240829
مُعرف محوري في PubMed: PMC6039262
DOI: 10.4049/jimmunol.1800515
PMID: 29891557
قاعدة البيانات: MEDLINE
الوصف
تدمد:1550-6606
DOI:10.4049/jimmunol.1800515