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IL-17 producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity

Obesity is associated with the development of asthma and considerable asthma-related healthcare utilization. To understand the immunological pathways that lead to obesity-associated asthma, we fed mice a high fat diet for 12 weeks, which resulted in obesity and the development of airway hyperreactiv...

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Autores principales: Kim, Hye Young, Lee, Hyun Jun, Chang, Ya-Jen, Pichavant, Muriel, Shore, Stephanie A., Fitzgerald, Katherine A., Iwakura, Yoichiro, Israel, Elliot, Bolger, Kenneth, Faul, John, DeKruyff, Rosemarie H., Umetsu, Dale T.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3912313/
https://www.ncbi.nlm.nih.gov/pubmed/24336249
http://dx.doi.org/10.1038/nm.3423
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author Kim, Hye Young
Lee, Hyun Jun
Chang, Ya-Jen
Pichavant, Muriel
Shore, Stephanie A.
Fitzgerald, Katherine A.
Iwakura, Yoichiro
Israel, Elliot
Bolger, Kenneth
Faul, John
DeKruyff, Rosemarie H.
Umetsu, Dale T.
author_facet Kim, Hye Young
Lee, Hyun Jun
Chang, Ya-Jen
Pichavant, Muriel
Shore, Stephanie A.
Fitzgerald, Katherine A.
Iwakura, Yoichiro
Israel, Elliot
Bolger, Kenneth
Faul, John
DeKruyff, Rosemarie H.
Umetsu, Dale T.
author_sort Kim, Hye Young
collection PubMed
description Obesity is associated with the development of asthma and considerable asthma-related healthcare utilization. To understand the immunological pathways that lead to obesity-associated asthma, we fed mice a high fat diet for 12 weeks, which resulted in obesity and the development of airway hyperreactivity (AHR), a cardinal feature of asthma. This AHR depended on innate immunity, since it occurred in obese Rag(−/−) mice, and on IL-17A and the NLRP3 inflammasome, since it did not develop in obese Il17(−/−) or Nlrp3(−/−) mice. The AHR was also associated with the presence in the lungs of CCR6(+) innate lymphoid cells producing IL-17A (ILC3 cells), which could by themselves mediate AHR when adoptively transferred into Rag2(−/−) Il2rγ(−/−) mice. IL-1β played an important role by expanding the ILC3 cells, and treatment to block the function of IL-1β abolished obesity-induced AHR. Since we found ILC3-like cells in the bronchoalveolar lavage fluid of human patients with asthma, we suggest that obesity-associated asthma is facilitated by inflammation mediated by NLRP3, IL-1β and ILC3 cells.
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spelling pubmed-39123132014-07-01 IL-17 producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity Kim, Hye Young Lee, Hyun Jun Chang, Ya-Jen Pichavant, Muriel Shore, Stephanie A. Fitzgerald, Katherine A. Iwakura, Yoichiro Israel, Elliot Bolger, Kenneth Faul, John DeKruyff, Rosemarie H. Umetsu, Dale T. Nat Med Article Obesity is associated with the development of asthma and considerable asthma-related healthcare utilization. To understand the immunological pathways that lead to obesity-associated asthma, we fed mice a high fat diet for 12 weeks, which resulted in obesity and the development of airway hyperreactivity (AHR), a cardinal feature of asthma. This AHR depended on innate immunity, since it occurred in obese Rag(−/−) mice, and on IL-17A and the NLRP3 inflammasome, since it did not develop in obese Il17(−/−) or Nlrp3(−/−) mice. The AHR was also associated with the presence in the lungs of CCR6(+) innate lymphoid cells producing IL-17A (ILC3 cells), which could by themselves mediate AHR when adoptively transferred into Rag2(−/−) Il2rγ(−/−) mice. IL-1β played an important role by expanding the ILC3 cells, and treatment to block the function of IL-1β abolished obesity-induced AHR. Since we found ILC3-like cells in the bronchoalveolar lavage fluid of human patients with asthma, we suggest that obesity-associated asthma is facilitated by inflammation mediated by NLRP3, IL-1β and ILC3 cells. 2013-12-15 2014-01 /pmc/articles/PMC3912313/ /pubmed/24336249 http://dx.doi.org/10.1038/nm.3423 Text en Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms
spellingShingle Article
Kim, Hye Young
Lee, Hyun Jun
Chang, Ya-Jen
Pichavant, Muriel
Shore, Stephanie A.
Fitzgerald, Katherine A.
Iwakura, Yoichiro
Israel, Elliot
Bolger, Kenneth
Faul, John
DeKruyff, Rosemarie H.
Umetsu, Dale T.
IL-17 producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity
title IL-17 producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity
title_full IL-17 producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity
title_fullStr IL-17 producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity
title_full_unstemmed IL-17 producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity
title_short IL-17 producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity
title_sort il-17 producing innate lymphoid cells and the nlrp3 inflammasome facilitate obesity-associated airway hyperreactivity
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3912313/
https://www.ncbi.nlm.nih.gov/pubmed/24336249
http://dx.doi.org/10.1038/nm.3423
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