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Tytuł pozycji:

MAVS deficiency induces gut dysbiotic microbiota conferring a proallergic phenotype

Tytuł :
MAVS deficiency induces gut dysbiotic microbiota conferring a proallergic phenotype
Autorzy :
Plantamura, Emilie
Dzutsev, Amiran
Chamaillard, Mathias
Djebali, Sophia
Moudombi, Lyvia
Boucinha, Lilia
Grau, Morgan
Macari, Claire
Bauché, David
Dumitrescu, Oana
Rasigade, Jean-Philippe
Lippens, Saskia
Plateroti, Michelina
Kress, Elsa
Cesaro, Annabelle
Bondu, Clovis
Rothermel, Ulrike
Heikenwalder, Mathias
Lina, Gérard
Bentaher-Belaaouaj, Azzak
Marie, Julien
Caux, Christophe
Trinchieri, Giorgio
Marvel, Jacqueline
Michallet, Marie-Cécile
Pokaż więcej
Temat :
allergic skin pathologies
[SDV.IMM.ALL]Life Sciences [q-bio]/Immunology/Allergology
MESH: Adaptor Proteins, Signal Transducing/physiology
MESH: Animals
MESH: Homeodomain Proteins/genetics
digestive system
MESH: Disease Models, Animal
[SDV.IMM]Life Sciences [q-bio]/Immunology
MESH: Dysbiosis/complications
MESH: Phenotype
MESH: Skin Diseases, Bacterial/metabolism
MESH: Skin Diseases, Bacterial/etiology
MESH: Mice, Inbred C57BL
MESH: Female
MESH: Homeodomain Proteins/metabolism
MESH: Hypersensitivity/pathology
MESH: Intestines/pathology
dysbiosis
MAVS
MESH: Skin Diseases, Bacterial/pathology
MESH: Hypersensitivity/etiology
RIG-like receptors
MESH: Hypersensitivity/metabolism
[SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity
MESH: Intestines/immunology
integumentary system
Biological Sciences
MESH: Intestines/microbiology
MESH: Mice
MESH: Gastrointestinal Microbiome/immunology
MESH: Mice, Knockout
MESH: Signal Transduction
Źródło :
Proceedings of the National Academy of Sciences of the United States of America
Proceedings of the National Academy of Sciences of the United States of America, National Academy of Sciences, 2018, 115 (41), pp.10404-10409. ⟨10.1073/pnas.1722372115⟩
Wydawca :
National Academy of Sciences, 2018.
Rok publikacji :
2018
Kolekcja :
Hyper_Article_en_Ligne_enriched
Hyper_Article_en_Ligne
Oryginalny identyfikator :
pmc: PMC6187193
pmid: 30249647
Język :
English
ISSN :
1091-6490
0027-8424
DOI :
10.1073/pnas.1722372115
International audience; Prominent changes in the gut microbiota (referred to as "dysbiosis") play a key role in the development of allergic disorders, but the underlying mechanisms remain unknown. Study of the delayed-type hypersensitivity (DTH) response in mice contributed to our knowledge of the pathophysiology of human allergic contact dermatitis. Here we report a negative regulatory role of the RIG-I-like receptor adaptor mitochondrial antiviral signaling (MAVS) on DTH by modulating gut bacterial ecology. Cohousing and fecal transplantation experiments revealed that the dysbiotic microbiota of Mavs -/- mice conferred a proallergic phenotype that is communicable to wild-type mice. DTH sensitization coincided with increased intestinal permeability and bacterial translocation within lymphoid organs that enhanced DTH severity. Collectively, we unveiled an unexpected impact of RIG-I-like signaling on the gut microbiota with consequences on allergic skin disease outcome. Primarily, these data indicate that manipulating the gut microbiota may help in the development of therapeutic strategies for the treatment of human allergic skin pathologies.

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