본문 바로가기
HOME> 논문 > 논문 검색상세

논문 상세정보

Experimental and molecular pathology v.103 no.2, 2017년, pp.141 - 152   SCIE SCOPUS
본 등재정보는 저널의 등재정보를 참고하여 보여주는 베타서비스로 정확한 논문의 등재여부는 등재기관에 확인하시기 바랍니다.

Regulation of autoimmune myocarditis by host responses to the microbiome

Barin, Jobert G.    (The Johns Hopkins University School of Medicine, Dept. of Pathology, Div. of Immunology, Baltimore, MD 21205, United States   ); Talor, Monica V.    (The Johns Hopkins University School of Medicine, Dept. of Pathology, Div. of Immunology, Baltimore, MD 21205, United States   ); Diny, Nicola L.    (The Johns Hopkins Bloomberg School of Public Health, The W. Harry Feinstone Dept. of Molecular Microbiology & Immunology, United States   ); Ong, SuFey    (The Johns Hopkins Bloomberg School of Public Health, The W. Harry Feinstone Dept. of Molecular Microbiology & Immunology, United States   ); Schaub, Julie A.    (The Johns Hopkins University School of Medicine, Dept. of Pathology, Div. of Immunology, Baltimore, MD 21205, United States   ); Gebremariam, Elizabeth    (The Johns Hopkins University School of Medicine, Dept. of Pathology, Div. of Immunology, Baltimore, MD 21205, United States   ); Bedja, Djahida    (The Johns Hopkins University School of Medicine, Dept. of Cardiology, United States   ); Chen, Guobao    (The Johns Hopkins University School of Medicine, Dept. of Pathology, Div. of Immunology, Baltimore, MD 21205, United States   ); Choi, Hee Sun    (The John  ); Hou, Xuezhou   Wu, Lei   Cardamone, Ashley B.   Peterson, Daniel A.   Rose, Noel R.   Čiháková, Daniela  

  • 초록  

    Abstract 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.


  • 주제어

    Microbiome .   Th17 cells .   Autoimmune disease .   Myocarditis .   Segmented filamentous bacteria .   Innate lymphoid cells .   Chemokines.  

 활용도 분석

  • 상세보기

    amChart 영역

  • 원문보기

    amChart 영역

원문보기

무료다운로드
  • 원문이 없습니다.
유료다운로드

유료 다운로드의 경우 해당 사이트의 정책에 따라 신규 회원가입, 로그인, 유료 구매 등이 필요할 수 있습니다. 해당 사이트에서 발생하는 귀하의 모든 정보활동은 NDSL의 서비스 정책과 무관합니다.

원문복사신청을 하시면, 일부 해외 인쇄학술지의 경우 외국학술지지원센터(FRIC)에서
무료 원문복사 서비스를 제공합니다.

NDSL에서는 해당 원문을 복사서비스하고 있습니다. 위의 원문복사신청 또는 장바구니 담기를 통하여 원문복사서비스 이용이 가능합니다.

이 논문과 함께 출판된 논문 + 더보기