Gut microorganisms act together to exacerbate inflammation in spinal cords

Eiji Miyauchi, Seok-Won Kim, Wataru Suda, Masami Kawasumi, Satoshi Onawa, Naoko Taguchi-Atarashi, Hidetoshi Morita, Todd D. Taylor, Masahira Hattori and Hiroshi Ohno ()
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Eiji Miyauchi: RIKEN Center for Integrative Medical Sciences
Seok-Won Kim: RIKEN Center for Integrative Medical Sciences
Wataru Suda: RIKEN Center for Integrative Medical Sciences
Masami Kawasumi: RIKEN Center for Integrative Medical Sciences
Satoshi Onawa: RIKEN Center for Integrative Medical Sciences
Naoko Taguchi-Atarashi: RIKEN Center for Integrative Medical Sciences
Hidetoshi Morita: Okayama University
Todd D. Taylor: RIKEN Center for Integrative Medical Sciences
Masahira Hattori: RIKEN Center for Integrative Medical Sciences
Hiroshi Ohno: RIKEN Center for Integrative Medical Sciences

Nature, 2020, vol. 585, issue 7823, 102-106

Abstract: 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. 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.

Date: 2020
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DOI: 10.1038/s41586-020-2634-9

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