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MAVS deficiency induces gut dysbiotic microbiota conferring a proallergic phenotype

Emilie Plantamura1, Amiran Dzutsev2,3, Mathias Chamaillard4,5,6,7

  • 1Centre International de Recherche en Infectiologie, INSERM U1111-CNRS UMR5308, 69365 Lyon Cedex 07, France.

Proceedings of the National Academy of Sciences of the United States of America
|September 26, 2018
PubMed

Insights

Mice lacking mitochondrial antiviral signaling (MAVS) show altered gut bacteria, leading to allergic skin disease. This gut dysbiosis can be transferred, suggesting microbiota manipulation as a therapeutic target for human allergic skin pathologies.

Area of Science:

  • Immunology
  • Microbiology
  • Dermatology

Background:

  • Gut microbiota dysbiosis is linked to allergic disorders, but mechanisms are unclear.
  • Delayed-type hypersensitivity (DTH) models inform allergic contact dermatitis.
  • RIG-I-like receptor pathways are implicated in immune responses.

Purpose of the Study:

  • Investigate the role of mitochondrial antiviral signaling (MAVS) in DTH.
  • Determine how MAVS influences gut microbiota ecology.
  • Explore the link between MAVS, gut bacteria, and allergic skin disease.

Main Methods:

  • Utilized mouse models with altered MAVS expression (Mavs-/- mice).
  • Conducted cohousing and fecal transplantation experiments.
  • Assessed DTH responses, intestinal permeability, and bacterial translocation.

Main Results:

  • Mavs-/- mice exhibited a dysbiotic gut microbiota and a proallergic phenotype.
  • The proallergic phenotype and dysbiosis were transferable to wild-type mice via microbiota.
  • Increased intestinal permeability and bacterial translocation correlated with DTH severity.

Conclusions:

  • MAVS negatively regulates DTH by modulating gut bacterial ecology.
  • Dysbiosis driven by MAVS deficiency impacts allergic skin disease.
  • Targeting the gut microbiota offers potential therapeutic strategies for allergic skin pathologies.
Keywords:
MAVSRIG-like receptorsallergic skin pathologiesdysbiosis

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