دورية أكاديمية
Candida albicans extracellular vesicles trigger type I IFN signalling via cGAS and STING.
| العنوان: | Candida albicans extracellular vesicles trigger type I IFN signalling via cGAS and STING. |
|---|---|
| المؤلفون: | Brown Harding H; Division of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA.; Department of Medicine, Harvard Medical School, Boston, MA, USA., Kwaku GN; Division of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA., Reardon CM; Division of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA., Khan NS; Division of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA., Zamith-Miranda D; Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA.; Division of Infectious Diseases, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, USA., Zarnowski R; Department of Medicine, University of Wisconsin-Madison, Madison, WI, USA.; Department of Microbiology and Immunology, University of Wisconsin Madison, Madison, WI, USA., Tam JM; Wyss Institute for Biologically Inspired Engineering, Harvard University, Boston, MA, USA., Bohaen CK; Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, the Netherlands., Richey L; Tufts Comparative Medicine Services, Tufts University, Boston, MA, USA., Mosallanejad K; Division of Gastroenterology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA., Crossen AJ; Division of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA., Reedy JL; Division of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA.; Department of Medicine, Harvard Medical School, Boston, MA, USA., Ward RA; Division of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA., Vargas-Blanco DA; Division of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA.; Department of Medicine, Harvard Medical School, Boston, MA, USA., Basham KJ; Division of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA., Bhattacharyya RP; Division of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA.; Department of Medicine, Harvard Medical School, Boston, MA, USA.; Broad Institute of MIT and Harvard, Cambridge, MA, USA., Nett JE; Department of Medicine, University of Wisconsin-Madison, Madison, WI, USA.; Department of Microbiology and Immunology, University of Wisconsin Madison, Madison, WI, USA., Mansour MK; Division of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA.; Department of Medicine, Harvard Medical School, Boston, MA, USA., van de Veerdonk FL; Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, the Netherlands., Kumar V; Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, the Netherlands.; University Medical Center Groningen, Department of Genetics, University of Groningen, Groningen, the Netherlands.; Nitte University Centre for Science Education and Research, Medical Sciences Complex, Mangaluru, India., Kagan JC; Division of Gastroenterology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA., Andes DR; Department of Medicine, University of Wisconsin-Madison, Madison, WI, USA.; Department of Microbiology and Immunology, University of Wisconsin Madison, Madison, WI, USA., Nosanchuk JD; Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA.; Division of Infectious Diseases, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, USA., Vyas JM; Division of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA. jvyas@mgh.harvard.edu.; Department of Medicine, Harvard Medical School, Boston, MA, USA. jvyas@mgh.harvard.edu.; Broad Institute of MIT and Harvard, Cambridge, MA, USA. jvyas@mgh.harvard.edu. |
| المصدر: | Nature microbiology [Nat Microbiol] 2024 Jan; Vol. 9 (1), pp. 95-107. Date of Electronic Publication: 2024 Jan 02. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Nature Publishing Group Country of Publication: England NLM ID: 101674869 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2058-5276 (Electronic) Linking ISSN: 20585276 NLM ISO Abbreviation: Nat Microbiol Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: [London] : Nature Publishing Group, [2016]- |
| مواضيع طبية MeSH: | Interferon Type I*/metabolism , Candidiasis*/metabolism , Candidiasis*/pathology, Animals ; Mice ; Candida albicans/pathogenicity ; CARD Signaling Adaptor Proteins/metabolism ; Immunity, Innate ; Nucleotidyltransferases/genetics ; Nucleotidyltransferases/metabolism ; Signal Transduction |
| مستخلص: | The host type I interferon (IFN) pathway is a major signature of inflammation induced by the human fungal pathogen, Candida albicans. However, the molecular mechanism for activating this pathway in the host defence against C. albicans remains unknown. Here we reveal that mice lacking cyclic GMP-AMP synthase (cGAS)-stimulator of IFN genes (STING) pathway components had improved survival following an intravenous challenge by C. albicans. Biofilm-associated C. albicans DNA packaged in extracellular vesicles triggers the cGAS-STING pathway as determined by induction of interferon-stimulated genes, IFNβ production, and phosphorylation of IFN regulatory factor 3 and TANK-binding kinase 1. Extracellular vesicle-induced activation of type I IFNs was independent of the Dectin-1/Card9 pathway and did not require toll-like receptor 9. Single nucleotide polymorphisms in cGAS and STING potently altered inflammatory cytokine production in human monocytes challenged by C. albicans. These studies provide insights into the early innate immune response induced by a clinically significant fungal pathogen. (© 2024. The Author(s), under exclusive licence to Springer Nature Limited.) |
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| معلومات مُعتمدة: | K08 AI141755 United States AI NIAID NIH HHS; R37 AI116550 United States AI NIAID NIH HHS; R01 AI136529 United States AI NIAID NIH HHS; R01 AI150181 United States AI NIAID NIH HHS; R21 AI152499 United States AI NIAID NIH HHS; R01 AI145939 United States AI NIAID NIH HHS; R01 AI153405 United States AI NIAID NIH HHS; R01 AI167993 United States AI NIAID NIH HHS; R01 AI073289 United States AI NIAID NIH HHS; R21 AI156104 United States AI NIAID NIH HHS; R21 AI109303 United States AI NIAID NIH HHS; R21 AI159583 United States AI NIAID NIH HHS; R01 AI092084 United States AI NIAID NIH HHS |
| المشرفين على المادة: | 0 (CARD Signaling Adaptor Proteins) 0 (Card9 protein, mouse) 0 (Interferon Type I) EC 2.7.7.- (Nucleotidyltransferases) EC 2.7.7.- (cGAS protein, mouse) 0 (Sting1 protein, mouse) |
| تواريخ الأحداث: | Date Created: 20240103 Date Completed: 20240130 Latest Revision: 20240323 |
| رمز التحديث: | 20240323 |
| مُعرف محوري في PubMed: | PMC10959075 |
| DOI: | 10.1038/s41564-023-01546-0 |
| PMID: | 38168615 |
| قاعدة البيانات: | MEDLINE |
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