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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Autores principales: Michal Werbner, Yiftah Barsheshet, Nir Werbner, Mor Zigdon, Itamar Averbuch, Oren Ziv, Boris Brant, Evan Elliott, Shachaf Gelberg, Moran Titelbaum, Omry Koren, Orly Avni
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Publicado: American Society for Microbiology 2019
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spelling 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)
institution DOAJ
collection DOAJ
language EN
topic microbiome
autoimmunity
stress
Microbiology
QR1-502
spellingShingle 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
description 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
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