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. 2020 Sep;585(7823):102-106.
doi: 10.1038/s41586-020-2634-9. Epub 2020 Aug 26.

Gut microorganisms act together to exacerbate inflammation in spinal cords

Eiji Miyauchi  1 , Seok-Won Kim  1 , Wataru Suda  1 , Masami Kawasumi  1 , Satoshi Onawa  1 , Naoko Taguchi-Atarashi  1 , Hidetoshi Morita  2 , Todd D Taylor  1 , Masahira Hattori  1   3 , Hiroshi Ohno  4   5   6
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Gut microorganisms act together to exacerbate inflammation in spinal cords

"V体育官网" Eiji Miyauchi et al. Nature. 2020 Sep.

VSports手机版 - Abstract

Accumulating evidence indicates that gut microorganisms have a pathogenic role in autoimmune diseases, including in multiple sclerosis1. Studies of experimental autoimmune encephalomyelitis (an animal model of multiple sclerosis)2,3, as well as human studies4-6, 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 of Lactobacillus reuteri that possesses peptides that potentially mimic MOG VSports手机版. 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. .

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References

    1. Cosorich, I. et al. High frequency of intestinal TH17 cells correlates with microbiota alterations and disease activity in multiple sclerosis. Sci. Adv. 3, e1700492 (2017). - "V体育平台登录" DOI
    1. Yokote, H. et al. NKT cell-dependent amelioration of a mouse model of multiple sclerosis by altering gut flora. Am. J. Pathol. 173, 1714–1723 (2008). - DOI
    1. Berer, K. et al. Commensal microbiota and myelin autoantigen cooperate to trigger autoimmune demyelination. Nature 479, 538–541 (2011). - DOI
    1. Miyake, S. et al. Dysbiosis in the gut microbiota of patients with multiple sclerosis, with a striking depletion of species belonging to Clostridia XIVa and IV clusters. PLoS ONE 10, e0137429 (2015). - DOI
    1. Jangi, S. et al. Alterations of the human gut microbiome in multiple sclerosis. Nat. Commun. 7, 12015 (2016). - VSports app下载 - DOI

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