Stress-induced VIPergic activation mediates microbiota/Th17cell-dependent depressive-like behaviors

•VIPergic promotion of depressive-like behaviors is dependent on the microbiome.•VIPergic activation increases SFB and hippocampal Th17 cells.•VIPergic activation induces IL-17A-mediated increase of hippocampal microglia. Chronic stress often has deleterious effects leading to the development of psy...

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Veröffentlicht in:Brain, behavior, and immunity Jg. 123; S. 739 - 751
Hauptverfasser: Medina-Rodriguez, Eva M., Han, Dongmei, Zeltzer, Shanie E., Moraskie Alvarez-Tabío, Michael P., O’Connor, Gregory, Daunert, Sylvia, Beurel, Eléonore
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Netherlands Elsevier Inc 01.01.2025
Schlagworte:
Animals
Behavior, Animal - physiology
Brain-Gut Axis - physiology
Depression
Depression - immunology
Depression - metabolism
Gastrointestinal Microbiome - physiology
Hippocampus - metabolism
Interleukin-17 - metabolism
Male
Mice
Mice, Inbred C57BL
Microglia
Microglia - immunology
Microglia - metabolism
Stress, Psychological - immunology
Stress, Psychological - metabolism
Th17 cell
Th17 Cells - immunology
Th17 Cells - metabolism
Vasoactive Intestinal Peptide - metabolism
VIP
Depression
Th17 cell
VIP
Microglia
ISSN:0889-1591, 1090-2139, 1090-2139
Online-Zugang:Volltext
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Zusammenfassung:•VIPergic promotion of depressive-like behaviors is dependent on the microbiome.•VIPergic activation increases SFB and hippocampal Th17 cells.•VIPergic activation induces IL-17A-mediated increase of hippocampal microglia. Chronic stress often has deleterious effects leading to the development of psychiatric diseases. The gut-brain axis represents a novel avenue for stress research. The negative effects of stress on the gut physiology have been well-described, whereas the pathways whereby stress controls microbial composition to modulate behaviors remains mainly unknown. We discovered that vasoactive intestinal peptide (VIP) activation promoted stress-induced microbial changes leading to increased infiltration of T helper (Th) 17 cells and microglial activation in the hippocampus and depressive-like behaviors, uncovering a close crosstalk between intestinal VIPergic release and the gut microbiota during stress and providing a new interaction between the nervous system and the gut microbiome after stress. Neutralization of the signature cytokine of Th17 cells, interleukin (IL)-17A, was sufficient to block depressive-like behaviors, reduce neuronal VIPergic activation and microglia activation induced by VIPergic activation after stress, opening new potential therapeutic targets for depression.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
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EB planned the study. EB, EMMR and DH performed and analyzed the experiments. MPM, GO, and SD assisted with bacteria experiments and manuscript revisions. EB wrote the manuscript.
Author contributions
ISSN:0889-1591
1090-2139
1090-2139
DOI:10.1016/j.bbi.2024.10.016