Gut microbiota promotes pain chronicity in Myosin1A deficient male mice.

Chronic pain DRG macrophages Dysbiosis Gut microbiota Myo1a Sex-gene-environmental interactions Sexual dimorphism

Journal

Brain, behavior, and immunity
ISSN: 1090-2139
Titre abrégé: Brain Behav Immun
Pays: Netherlands
ID NLM: 8800478

Informations de publication

Date de publication:
04 May 2024
Historique:
received: 11 08 2023
revised: 23 04 2024
accepted: 03 05 2024
medline: 7 5 2024
pubmed: 7 5 2024
entrez: 6 5 2024
Statut: aheadofprint

Résumé

Chronic pain is a heavily debilitating condition and a huge socio-economic burden, with no efficient treatment. Over the past decade, the gut microbiota has emerged as an important regulator of nervous system's health and disease states. Yet, its contribution to the pathogenesis of chronic somatic pain remains poorly documented. Here, we report that male but not female mice lacking Myosin1a (KO) raised under single genotype housing conditions (KO-SGH) are predisposed to develop chronic pain in response to a peripheral tissue injury. We further underscore the potential of MYO1A loss-of-function to alter the composition of the gut microbiota and uncover a functional connection between the vulnerability to chronic pain and the dysbiotic gut microbiota of KO-SGH males. As such, parental antibiotic treatment modifies gut microbiota composition and completely rescues the injury-induced pain chronicity in male KO-SGH offspring. Furthermore, in KO-SGH males, this dysbiosis is accompanied by a transcriptomic activation signature in the dorsal root ganglia (DRG) macrophage compartment, in response to tissue injury. We identify CD206

Identifiants

pubmed: 38710336
pii: S0889-1591(24)00397-0
doi: 10.1016/j.bbi.2024.05.010
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Ana Reynders (A)

Aix-Marseille-Université, CNRS, Institut de Biologie du Développement de Marseille, Marseille, France. Electronic address: ana.reynders@univ-amu.fr.

Z Anissa Jhumka (Z)

Aix-Marseille-Université, CNRS, Institut de Biologie du Développement de Marseille, Marseille, France.

Stéphane Gaillard (S)

Phenotype Expertise, Marseille, France.

Annabelle Mantilleri (A)

Aix-Marseille-Université, CNRS, Institut de Biologie du Développement de Marseille, Marseille, France.

Pascale Malapert (P)

Aix-Marseille-Université, CNRS, Institut de Biologie du Développement de Marseille, Marseille, France.

Karine Magalon (K)

Aix-Marseille-Université, CNRS, Institut de Biologie du Développement de Marseille, Marseille, France.

Anders Etzerodt (A)

Department of Biomedicine, Aarhus University, Aarhus, Denmark.

Chiara Salio (C)

Department of Veterinary Sciences, University of Turin, Grugliasco, TO, Italy.

Sophie Ugolini (S)

Aix-Marseille-Université, CNRS, INSER, Centre d'Immunologie de Marseille-Luminy, Marseille, France.

Francis Castets (F)

Aix-Marseille-Université, CNRS, Institut de Biologie du Développement de Marseille, Marseille, France.

Andrew J Saurin (AJ)

Aix-Marseille-Université, CNRS, Institut de Biologie du Développement de Marseille, Marseille, France.

Matteo Serino (M)

Institut de Recherche en Santé Digestive, Université de Toulouse-Paul Sabatier, INSERM, INRAe, ENVT, UPS, Toulouse, France.

Guillaume Hoeffel (G)

Aix-Marseille-Université, CNRS, INSER, Centre d'Immunologie de Marseille-Luminy, Marseille, France.

Aziz Moqrich (A)

Aix-Marseille-Université, CNRS, Institut de Biologie du Développement de Marseille, Marseille, France. Electronic address: aziz.moqrich@univ-amu.fr.

Classifications MeSH