The microbiota and autoimmunity: Their role in thyroid autoimmune diseases

被引:89
作者
Koehling, Hedda L. [1 ,2 ]
Plummer, Sue F. [2 ]
Marchesi, Julian R. [3 ,6 ]
Davidge, Kelly S. [4 ]
Ludgate, Marian [5 ]
机构
[1] Univ Hop Essen, Inst Med Microbiol, Essen, Germany
[2] Cultech Ltd, Baglan, Port Talbot, Wales
[3] Cardiff Univ, Sch Biosci, Cardiff, S Glam, Wales
[4] Kirkstall Ltd, Rotherham, S Yorkshire, England
[5] Cardiff Univ, Sch Med, Div Infect & Immun, Cardiff, S Glam, Wales
[6] Imperial Coll London, Ctr Digest & Gut Hlth, London W2 1NY, England
关键词
Bacteria; Graves' disease; Hashimotos's thyroiditis; YERSINIA-ENTEROCOLITICA INFECTION; HELICOBACTER-PYLORI INFECTION; INTESTINAL EPITHELIAL-CELLS; HUMAN GUT MICROBIOTA; REGULATORY T-CELLS; CHAIN FATTY-ACIDS; IN-VITRO MODEL; GRAVES-DISEASE; CELIAC-DISEASE; STAPHYLOCOCCUS-AUREUS;
D O I
10.1016/j.clim.2017.07.001
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Since the 1970s, the role of infectious diseases in the pathogenesis of Graves' disease (GD) has been an object of intensive research. The last decade has witnessed many studies on Yersinia enterocolitica, Helicobacter pylori and other bacterial organisms and their potential impact on GD. Retrospective, prospective and molecular binding studies have been performed with contrary outcomes. Until now it is not clear whether bacterial infections can trigger autoimmune thyroid disease. Common risk factors for GD (gender, smoking, stress, and pregnancy) reveal profound changes in the bacterial communities of the gut compared to that of healthy controls but a pathogenetic link between GD and dysbiosis has not yet been fully elucidated. Conventional bacterial culture, in vitro models, next generation and high-throughput DNA sequencing are applicable methods to assess the impact of bacteria in disease onset and development. Further studies on the involvement of bacteria in GD are needed and may contribute to the understanding of pathogenetic processes. This review will examine available evidence on the subject. (C) 2017 Elsevier Inc. All rights reserved.
引用
收藏
页码:63 / 74
页数:12
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