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Abstract
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 delayedtype 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 bymodulating 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.
Keywords
INTESTINAL PERMEABILITY, ATOPIC ECZEMA, CONTACT HYPERSENSITIVITY, COMMENSAL BACTERIA, CALIBRATE, RESPONSES, IMMUNITY, COLITIS, PROTEIN, MICE, RIG-like receptors, MAVS, dysbiosis, allergic skin pathologies

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Citation

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MLA
Plantamura, Emilie et al. “MAVS Deficiency Induces Gut Dysbiotic Microbiota Conferring a Proallergic Phenotype.” PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 115.41 (2018): 10404–10409. Print.
APA
Plantamura, E., Dzutsev, A., Chamaillard, M., Djebali, S., Moudombi, L., Boucinha, L., Grau, M., et al. (2018). MAVS deficiency induces gut dysbiotic microbiota conferring a proallergic phenotype. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 115(41), 10404–10409.
Chicago author-date
Plantamura, Emilie, Amiran Dzutsev, Mathias Chamaillard, Sophia Djebali, Lyvia Moudombi, Lilia Boucinha, Morgan Grau, et al. 2018. “MAVS Deficiency Induces Gut Dysbiotic Microbiota Conferring a Proallergic Phenotype.” Proceedings of the National Academy of Sciences of the United States of America 115 (41): 10404–10409.
Chicago author-date (all authors)
Plantamura, Emilie, Amiran Dzutsev, Mathias Chamaillard, Sophia Djebali, Lyvia Moudombi, Lilia Boucinha, Morgan Grau, Claire Macari, David Bauche, Oana Dumitrescu, Jean-Philippe Rasigade, Saskia Lippens, Michelina Plateroti, Elsa Kress, Annabelle Cesaro, Clovis Bondu, Ulrike Rothermel, Mathias Heikenwaelder, Gerard Lina, Azzak Bentaher-Belaaouaj, Julien C Marie, Christophe Caux, Giorgio Trinchieri, Jacqueline Marvel, and Marie-Cecile Michallet. 2018. “MAVS Deficiency Induces Gut Dysbiotic Microbiota Conferring a Proallergic Phenotype.” Proceedings of the National Academy of Sciences of the United States of America 115 (41): 10404–10409.
Vancouver
1.
Plantamura E, Dzutsev A, Chamaillard M, Djebali S, Moudombi L, Boucinha L, et al. MAVS deficiency induces gut dysbiotic microbiota conferring a proallergic phenotype. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 2018;115(41):10404–9.
IEEE
[1]
E. Plantamura et al., “MAVS deficiency induces gut dysbiotic microbiota conferring a proallergic phenotype,” PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, vol. 115, no. 41, pp. 10404–10409, 2018.
@article{8599240,
  abstract     = {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 delayedtype 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 bymodulating 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.},
  author       = {Plantamura, Emilie and Dzutsev, Amiran and Chamaillard, Mathias and Djebali, Sophia and Moudombi, Lyvia and Boucinha, Lilia and Grau, Morgan and Macari, Claire and Bauche, David and Dumitrescu, Oana and Rasigade, Jean-Philippe and Lippens, Saskia and Plateroti, Michelina and Kress, Elsa and Cesaro, Annabelle and Bondu, Clovis and Rothermel, Ulrike and Heikenwaelder, Mathias and Lina, Gerard and Bentaher-Belaaouaj, Azzak and Marie, Julien C and Caux, Christophe and Trinchieri, Giorgio and Marvel, Jacqueline and Michallet, Marie-Cecile},
  issn         = {0027-8424},
  journal      = {PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA},
  keywords     = {INTESTINAL PERMEABILITY,ATOPIC ECZEMA,CONTACT HYPERSENSITIVITY,COMMENSAL BACTERIA,CALIBRATE,RESPONSES,IMMUNITY,COLITIS,PROTEIN,MICE,RIG-like receptors,MAVS,dysbiosis,allergic skin pathologies},
  language     = {eng},
  number       = {41},
  pages        = {10404--10409},
  title        = {MAVS deficiency induces gut dysbiotic microbiota conferring a proallergic phenotype},
  url          = {http://dx.doi.org/10.1073/pnas.1722372115},
  volume       = {115},
  year         = {2018},
}

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