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Fecal Microbiota Composition Differs Between Children With β-Cell Autoimmunity and Those Without

机译:患有β细胞自身免疫的儿童和没有β细胞自身免疫的儿童的粪便微生物组成不同

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摘要

The role of the intestinal microbiota as a regulator of autoimmune diabetes in animal models is well-established, but data on human type 1 diabetes are tentative and based on studies including only a few study subjects. To exclude secondary effects of diabetes and HLA risk genotype on gut microbiota, we compared the intestinal microbiota composition in children with at least two diabetes-associated autoantibodies (n = 18) with autoantibody-negative children matched for age, sex, early feeding history, and HLA risk genotype using pyrosequencing. Principal component analysis indicated that a low abundance of lactate-producing and butyrate-producing species was associated with β-cell autoimmunity. In addition, a dearth of the two most dominant Bifidobacterium species, Bifidobacterium adolescentis and Bifidobacterium pseudocatenulatum, and an increased abundance of the Bacteroides genus were observed in the children with β-cell autoimmunity. We did not find increased fecal calprotectin or IgA as marker of inflammation in children with β-cell autoimmunity. Functional studies related to the observed alterations in the gut microbiome are warranted because the low abundance of bifldobacteria and butyrate-producing species could adversely affect the intestinal epithelial barrier function and inflammation, whereas the apparent importance of the Bacteroides genus in development of type 1 diabetes is insufficiently understood.
机译:肠道菌群在动物模型中作为自身免疫性糖尿病调节剂的作用已广为人知,但有关人类1型糖尿病的数据尚属初步,且仅基于包括少数研究对象的研究。为了排除糖尿病和HLA风险基因型对肠道菌群的继发影响,我们比较了至少两个与糖尿病相关的自身抗体(n = 18)和自身抗体阴性的儿童的肠道微生物群组成,这些儿童的年龄,性别,早期喂养史,焦磷酸测序法检测HLA风险基因型。主成分分析表明,生产乳酸和生产丁酸盐的物种数量少与β细胞自身免疫有关。另外,在患有β细胞自身免疫的儿童中,观察到两种最主要的双歧杆菌种类缺乏,即青春双歧杆菌和假双歧双歧杆菌,而拟杆菌属的数量增加。我们没有发现粪便钙卫蛋白或IgA升高是β细胞自身免疫儿童炎症反应的标志。与肠道微生物组中观察到的变化有关的功能研究是必要的,因为双歧杆菌和产生丁酸的物种的低丰度可能会对肠道上皮屏障功能和炎症产生不利影响,而拟杆菌属在1型糖尿病的发展中的明显重要性是不够了解。

著录项

  • 来源
    《Diabetes》 |2013年第4期|1238-1244|共7页
  • 作者单位

    Department of Medical Microbiology, University Medical Center Groningen and University of Groningen, Groningen, the Netherlands;

    Immune Response Unit, Department of Vaccination and Immune Protec-tion, National Institute for Health and Welfare, Helsinki, Finland;

    Children's Hospital, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland ,Folkhalsan Research Center, Helsinki, Fin-land ,Department of Pediatrics, Tampere University Hospital, Tampere, Finland;

    Immunogenetics Laboratory, University of Turku, Turku, Finland ,Department of Clinical Immunology, University of Eastern Finland, Kuopio, Finland.;

    Immune Response Unit, Department of Vaccination and Immune Protec-tion, National Institute for Health and Welfare, Helsinki, Finland;

    Children's Hospital, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland;

    Immune Response Unit, Department of Vaccination and Immune Protec-tion, National Institute for Health and Welfare, Helsinki, Finland;

    Immune Response Unit, Department of Vaccination and Immune Protec-tion, National Institute for Health and Welfare, Helsinki, Finland;

    Department of Medical Microbiology, University Medical Center Groningen and University of Groningen, Groningen, the Netherlands;

    Department of Medical Microbiology, University Medical Center Groningen and University of Groningen, Groningen, the Netherlands;

    Immune Response Unit, Department of Vaccination and Immune Protec-tion, National Institute for Health and Welfare, Helsinki, Finland;

  • 收录信息 美国《科学引文索引》(SCI);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
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