کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5584370 | 1567915 | 2017 | 30 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Regulation of autoimmune myocarditis by host responses to the microbiome
ترجمه فارسی عنوان
مقررات مایوکاردیت اتوایمیون با پاسخ میزبان به میکروبیوم
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کلمات کلیدی
ILCγcAMOVASFBEAM - POMSegmented filamentous bacteria - باکتری های رشته ای جداسازی شدهAutoimmune disease - بیماری خودایمنیanalysis of molecular variance - تجزیه و تحلیل واریانس مولکولیCommon gamma chain - زنجیره گامای مشترکinnate lymphoid cell - سلول لنفاوی ذاتیTh17 cells - سلول های Th17Innate lymphoid cells - سلولهای لنفی عظیمMyocarditis - میوکاردیتexperimental autoimmune myocarditis - میوکاردیت خود ایمنی تجربیMicrobiome - میکروبیومChemokines - کرموین ها
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیوشیمی بالینی
چکیده انگلیسی
The extensive, diverse communities that constitute the microbiome are increasingly appreciated as important regulators of human health and disease through inflammatory, immune, and metabolic pathways. We sought to elucidate pathways by which microbiota contribute to inflammatory, autoimmune cardiac disease. We employed an animal model of experimental autoimmune myocarditis (EAM), which results in inflammatory and autoimmune pathophysiology and subsequent maladaptive cardiac remodeling and heart failure. Antibiotic dysbiosis protected mice from EAM and fibrotic cardiac dysfunction. Additionally, mice derived from different sources with different microbiome colonization profiles demonstrated variable susceptibility to disease. Unexpectedly, it did not track with segmented filamentous bacteria (SFB)-driven Th17 programming of CD4+ T cells in the steady-state gut. Instead, we found disease susceptibility to track with presence of type 3 innate lymphoid cells (ILC3s). Ablating ILCs by antibody depletion or genetic tools in adoptive transfer variants of the EAM model demonstrated that ILCs and microbiome profiles contributed to the induction of CCL20/CCR6-mediated inflammatory chemotaxis to the diseased heart. From these data, we conclude that sensing of the microbiome by ILCs is an important checkpoint in the development of inflammatory cardiac disease processes through their ability to elicit cardiotropic chemotaxis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental and Molecular Pathology - Volume 103, Issue 2, October 2017, Pages 141-152
Journal: Experimental and Molecular Pathology - Volume 103, Issue 2, October 2017, Pages 141-152
نویسندگان
Jobert G. Barin, Monica V. Talor, Nicola L. Diny, SuFey Ong, Julie A. Schaub, Elizabeth Gebremariam, Djahida Bedja, Guobao Chen, Hee Sun Choi, Xuezhou Hou, Lei Wu, Ashley B. Cardamone, Daniel A. Peterson, Noel R. Rose, Daniela Äiháková,