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Gut microorganisms act together to exacerbate inflammation in spinal cords

机译：肠道微生物在一起加剧脊髓中的炎症

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Germ-free mice co-colonized with two bacterial strains from the small intestinal flora showed increased susceptibility to experimental autoimmune encephalomyelitis, implicating the synergistic effects of these microorganisms in this mouse model of multiple sclerosis.Accumulating evidence indicates that gut microorganisms have a pathogenic role in autoimmune diseases, including in multiple sclerosis(1). Studies of experimental autoimmune encephalomyelitis (an animal model of multiple sclerosis)(2,3), as well as human studies(4-6), have implicated gut microorganisms in the development or severity of multiple sclerosis. However, it remains unclear how gut microorganisms act on the inflammation of extra-intestinal tissues such as the spinal cord. Here we show that two distinct signals from gut microorganisms coordinately activate autoreactive T cells in the small intestine that respond specifically to myelin oligodendrocyte glycoprotein (MOG). After induction of experimental autoimmune encephalomyelitis in mice, MOG-specific CD4(+)T cells are observed in the small intestine. Experiments using germ-free mice that were monocolonized with microorganisms from the small intestine demonstrated that a newly isolated strain in the family Erysipelotrichaceae acts similarly to an adjuvant to enhance the responses of T helper 17 cells. Shotgun sequencing of the contents of the small intestine revealed a strain ofLactobacillus reuterithat possesses peptides that potentially mimic MOG. Mice that were co-colonized with these two strains showed experimental autoimmune encephalomyelitis symptoms that were more severe than those of germ-free or monocolonized mice. These data suggest that the synergistic effects that result from the presence of these microorganisms should be considered in the pathogenicity of multiple sclerosis, and that further study of these microorganisms may lead to preventive strategies for this disease.
机译：与来自小肠菌群的两种细菌菌株共殖的无菌小鼠表现出对实验性自身免疫性脑髓炎的敏感性增加，这意味着这些微生物在多发性硬化症的小鼠模型中的协同作用。陷入困境的证据表明肠道微生物具有致病作用自身免疫疾病，包括多发性硬化症（1）。实验性自身免疫性脑脊髓炎（多发性硬化症的动物模型）（2,3）以及人类研究（4-6），在多发性硬化症的发育或严重程度中具有暗示的肠道微生物。然而，它仍然尚不清楚肠道微生物对脊髓外肠组织的炎症作用。在这里，我们表明来自肠道微生物的两个不同的信号在小肠中坐标激活特异性对髓鞘寡核细胞糖蛋白（MOG）的小肠中的自动反应性T细胞。在诱导小鼠中的实验性自身免疫脑髓炎后，在小肠中观察到萌芽的CD4（+）T细胞。使用来自小肠的微生物的无菌小鼠的实验证明了家庭红细胞的新分离菌株与佐剂类似，以增强T辅助17细胞的反应。小肠内容物的霰弹枪序列显示出杆状菌毛茛属ruterithat的菌株具有潜在模仿沼泽的肽。用这两个菌株共殖的小鼠表明了实验性自身免疫性脑脊髓炎，比无菌或单殖民化小鼠更严重。这些数据表明，由于存在这些微生物的存在而导致的协同效应应该在多发性硬化症的致病性中考虑，并且对这些微生物的进一步研究可能导致这种疾病的预防策略。

著录项

  • 来源
    《Nature》 |2020年第7823期|102-106|共5页
  • 作者

    Miyauchi Eiji; Kim Seok-Won; Suda Wataru; Kawasumi Masami; Onawa Satoshi; Taguchi-Atarashi Naoko; Morita Hidetoshi; Taylor Todd D.; Hattori Masahira; Ohno Hiroshi;

  • 作者单位

    RIKEN Ctr Integrat Med Sci Yokohama Kanagawa Japan;

    RIKEN Ctr Integrat Med Sci Yokohama Kanagawa Japan;

    RIKEN Ctr Integrat Med Sci Yokohama Kanagawa Japan;

    RIKEN Ctr Integrat Med Sci Yokohama Kanagawa Japan;

    RIKEN Ctr Integrat Med Sci Yokohama Kanagawa Japan;

    RIKEN Ctr Integrat Med Sci Yokohama Kanagawa Japan;

    Okayama Univ Grad Sch Environm & Life Sci Okayama Japan;

    RIKEN Ctr Integrat Med Sci Yokohama Kanagawa Japan;

    RIKEN Ctr Integrat Med Sci Yokohama Kanagawa Japan|Waseda Univ Grad Sch Adv Sci & Engn Tokyo Japan;

    RIKEN Ctr Integrat Med Sci Yokohama Kanagawa Japan|Yokohama City Univ Grad Sch Med Life Sci Dept Med Life Sci Immunobiol Lab Yokohama Kanagawa Japan|Kanagawa Inst Ind Sci & Technol Ebina Kanagawa Japan;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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