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MAVS deficiency induces gut dysbiotic microbiota conferring a proallergic phenotype
- Source :
- 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, 2018, 115 (41), pp.10404-10409. ⟨10.1073/pnas.1722372115⟩, 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⟩
- Publication Year :
- 2018
- Publisher :
- HAL CCSD, 2018.
-
Abstract
- 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.
- Subjects :
- 0301 basic medicine
MESH: Signal Transduction
RIG-like receptors
MESH: Intestines/immunology
MESH: Skin Diseases, Bacterial/pathology
Gut flora
MESH: Skin Diseases, Bacterial/metabolism
MESH: Mice, Knockout
[SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity
Mice
0302 clinical medicine
MESH: Animals
MESH: Hypersensitivity/metabolism
[SDV.IMM.ALL]Life Sciences [q-bio]/Immunology/Allergology
Sensitization
Mice, Knockout
Multidisciplinary
integumentary system
dysbiosis
Biological Sciences
MAVS
Phenotype
3. Good health
Intestines
medicine.anatomical_structure
MESH: Intestines/pathology
030220 oncology & carcinogenesis
[SDV.IMM]Life Sciences [q-bio]/Immunology
Female
[SDV.IMM.ALL] Life Sciences [q-bio]/Immunology/Allergology
Signal Transduction
MESH: Intestines/microbiology
[SDV.IMM] Life Sciences [q-bio]/Immunology
MESH: Dysbiosis/complications
Biology
MESH: Gastrointestinal Microbiome/immunology
MESH: Phenotype
digestive system
03 medical and health sciences
MESH: Skin Diseases, Bacterial/etiology
MESH: Hypersensitivity/etiology
Immunity
MESH: Mice, Inbred C57BL
MESH: Homeodomain Proteins/metabolism
medicine
Hypersensitivity
allergic skin pathologies
MESH: Hypersensitivity/pathology
Animals
Colitis
Allergic contact dermatitis
[SDV.IMM.II] Life Sciences [q-bio]/Immunology/Innate immunity
MESH: Mice
Adaptor Proteins, Signal Transducing
Homeodomain Proteins
MESH: Adaptor Proteins, Signal Transducing/physiology
Intestinal permeability
Skin Diseases, Bacterial
medicine.disease
biology.organism_classification
Gastrointestinal Microbiome
Mice, Inbred C57BL
Disease Models, Animal
030104 developmental biology
Immunology
MESH: Homeodomain Proteins/genetics
MESH: Disease Models, Animal
Dysbiosis
MESH: Female
Subjects
Details
- Language :
- English
- ISSN :
- 00278424 and 10916490
- Database :
- OpenAIRE
- Journal :
- 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, 2018, 115 (41), pp.10404-10409. ⟨10.1073/pnas.1722372115⟩, 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⟩
- Accession number :
- edsair.doi.dedup.....2f72c638beb7102ea94a7542c3c80f63