Obesity And Asthma: Beyond T(h)2 Inflammation.

dc.creatorLeiria, Luiz O S
dc.creatorMartins, Milton A
dc.creatorSaad, Mário J A
dc.date2015-Feb
dc.date2015-11-27T13:46:43Z
dc.date2015-11-27T13:46:43Z
dc.date.accessioned2018-03-29T01:24:14Z
dc.date.available2018-03-29T01:24:14Z
dc.identifierMetabolism: Clinical And Experimental. v. 64, n. 2, p. 172-81, 2015-Feb.
dc.identifier1532-8600
dc.identifier10.1016/j.metabol.2014.10.002
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/25458831
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/202309
dc.identifier25458831
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1302542
dc.descriptionObesity is a major risk factor for asthma. Likewise, obesity is known to increase disease severity in asthmatic subjects and also to impair the efficacy of first-line treatment medications for asthma, worsening asthma control in obese patients. This concept is in agreement with the current understanding that some asthma phenotypes are not accompanied by detectable inflammation, and may not be ameliorated by classical anti-inflammatory therapy. There are growing evidences suggesting that the obesity-related asthma phenotype does not necessarily involve the classical T(H)2-dependent inflammatory process. Hormones involved in glucose homeostasis and in the pathogeneses of obesity likely directly or indirectly link obesity and asthma through inflammatory and non-inflammatory pathways. Furthermore, the endocrine regulation of the airway-related pre-ganglionic nerves likely contributes to airway hyperreactivity (AHR) in obese states. In this review, we focused our efforts on understanding the mechanism underlying obesity-related asthma by exploring the T(H)2-independent mechanisms leading to this disease.
dc.description64
dc.description172-81
dc.languageeng
dc.relationMetabolism: Clinical And Experimental
dc.relationMetab. Clin. Exp.
dc.rightsfechado
dc.rightsCopyright © 2015 Elsevier Inc. All rights reserved.
dc.sourcePubMed
dc.subjectAdiponectin
dc.subjectAdipose Tissue
dc.subjectAdiposity
dc.subjectAirway Resistance
dc.subjectAnimals
dc.subjectAsthma
dc.subjectHumans
dc.subjectLeptin
dc.subjectModels, Biological
dc.subjectObesity
dc.subjectTh2 Cells
dc.subjectAdiponectin
dc.subjectAirway Hyperreactivity
dc.subjectInsulin
dc.subjectLeptin
dc.titleObesity And Asthma: Beyond T(h)2 Inflammation.
dc.typeArtículos de revistas


Este ítem pertenece a la siguiente institución