Social-Stress-Responsive Microbiota Induces Stimulation of Self-Reactive Effector T Helper Cells
ABSTRACT Stressful life events are considered a risk factor for autoimmune disorders, though the mechanisms are unclear. Here we demonstrate that chronic social stress induces virulence-associated transcriptional patterns in the murine gut microbiota. The stress-influenced microbiota increased the p...
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American Society for Microbiology
2019
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oai:doaj.org-article:9008a55ace5d435b970208b6ef0e29b02021-12-02T19:46:18ZSocial-Stress-Responsive Microbiota Induces Stimulation of Self-Reactive Effector T Helper Cells10.1128/mSystems.00292-182379-5077https://doaj.org/article/9008a55ace5d435b970208b6ef0e29b02019-08-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mSystems.00292-18https://doaj.org/toc/2379-5077ABSTRACT Stressful life events are considered a risk factor for autoimmune disorders, though the mechanisms are unclear. Here we demonstrate that chronic social stress induces virulence-associated transcriptional patterns in the murine gut microbiota. The stress-influenced microbiota increased the presence of effector T helper cells in the mesenteric lymph nodes, including myelin-autoreactive cells. Inhibition of the bacterial quorum sensor QseC, which is also responsive to norepinephrine, diminished the presence of effector T helper cells and bacteria such as Acinetobacter in the mesenteric lymph nodes, without remarkably affecting the gut microbial composition. Together, our results delineate a model in which the immune reaction to stress-responsive microbiota may compromise tolerance to self and therefore may increase the risk for autoimmune diseases in susceptible individuals. IMPORTANCE How do stressful life events increase the risk for autoimmune disorders? Here we show that chronic social stress in mice promotes the expression of virulent genes in the gut microbiota and alters the microbial translocation into the mesenteric lymph nodes. Our results also suggest that the consequent immune response to the stress-affected microbiota may endanger the tolerance for self. The presence of specific translocated bacteria and the immune response in the mesenteric lymph nodes can be diminished using an inhibitor of the bacterial communication system without drastically affecting the gut microbial composition as antibiotics do.Michal WerbnerYiftah BarsheshetNir WerbnerMor ZigdonItamar AverbuchOren ZivBoris BrantEvan ElliottShachaf GelbergMoran TitelbaumOmry KorenOrly AvniAmerican Society for MicrobiologyarticlemicrobiomeautoimmunitystressMicrobiologyQR1-502ENmSystems, Vol 4, Iss 4 (2019) |
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microbiome autoimmunity stress Microbiology QR1-502 |
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microbiome autoimmunity stress Microbiology QR1-502 Michal Werbner Yiftah Barsheshet Nir Werbner Mor Zigdon Itamar Averbuch Oren Ziv Boris Brant Evan Elliott Shachaf Gelberg Moran Titelbaum Omry Koren Orly Avni Social-Stress-Responsive Microbiota Induces Stimulation of Self-Reactive Effector T Helper Cells |
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ABSTRACT Stressful life events are considered a risk factor for autoimmune disorders, though the mechanisms are unclear. Here we demonstrate that chronic social stress induces virulence-associated transcriptional patterns in the murine gut microbiota. The stress-influenced microbiota increased the presence of effector T helper cells in the mesenteric lymph nodes, including myelin-autoreactive cells. Inhibition of the bacterial quorum sensor QseC, which is also responsive to norepinephrine, diminished the presence of effector T helper cells and bacteria such as Acinetobacter in the mesenteric lymph nodes, without remarkably affecting the gut microbial composition. Together, our results delineate a model in which the immune reaction to stress-responsive microbiota may compromise tolerance to self and therefore may increase the risk for autoimmune diseases in susceptible individuals. IMPORTANCE How do stressful life events increase the risk for autoimmune disorders? Here we show that chronic social stress in mice promotes the expression of virulent genes in the gut microbiota and alters the microbial translocation into the mesenteric lymph nodes. Our results also suggest that the consequent immune response to the stress-affected microbiota may endanger the tolerance for self. The presence of specific translocated bacteria and the immune response in the mesenteric lymph nodes can be diminished using an inhibitor of the bacterial communication system without drastically affecting the gut microbial composition as antibiotics do. |
format |
article |
author |
Michal Werbner Yiftah Barsheshet Nir Werbner Mor Zigdon Itamar Averbuch Oren Ziv Boris Brant Evan Elliott Shachaf Gelberg Moran Titelbaum Omry Koren Orly Avni |
author_facet |
Michal Werbner Yiftah Barsheshet Nir Werbner Mor Zigdon Itamar Averbuch Oren Ziv Boris Brant Evan Elliott Shachaf Gelberg Moran Titelbaum Omry Koren Orly Avni |
author_sort |
Michal Werbner |
title |
Social-Stress-Responsive Microbiota Induces Stimulation of Self-Reactive Effector T Helper Cells |
title_short |
Social-Stress-Responsive Microbiota Induces Stimulation of Self-Reactive Effector T Helper Cells |
title_full |
Social-Stress-Responsive Microbiota Induces Stimulation of Self-Reactive Effector T Helper Cells |
title_fullStr |
Social-Stress-Responsive Microbiota Induces Stimulation of Self-Reactive Effector T Helper Cells |
title_full_unstemmed |
Social-Stress-Responsive Microbiota Induces Stimulation of Self-Reactive Effector T Helper Cells |
title_sort |
social-stress-responsive microbiota induces stimulation of self-reactive effector t helper cells |
publisher |
American Society for Microbiology |
publishDate |
2019 |
url |
https://doaj.org/article/9008a55ace5d435b970208b6ef0e29b0 |
work_keys_str_mv |
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