Obesity And Asthma: Beyond T(h)2 Inflammation

dc.creatorLeiria
dc.creatorLuiz O. S.; Martins
dc.creatorMilton A.; Saad
dc.creatorMario J. A.
dc.date2015-FEB
dc.date2016-06-07T13:36:44Z
dc.date2016-06-07T13:36:44Z
dc.date.accessioned2018-03-29T01:52:00Z
dc.date.available2018-03-29T01:52:00Z
dc.identifier
dc.identifierObesity And Asthma: Beyond T(h)2 Inflammation. W B Saunders Co-elsevier Inc, v. 64, p. 172-181 FEB-2015.
dc.identifier0026-0495
dc.identifierWOS:000347590300004
dc.identifier10.1016/j.metabol.2014.10.002
dc.identifierhttp://www.sciencedirect.com/science/article/pii/S0026049514002959
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/244357
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1308055
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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 noninflammatory pathways. Furthermore, the endocrine regulation of the airway-related preganglionic 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. (C) 2015 Elsevier Inc. All rights reserved.
dc.description64
dc.description2
dc.description
dc.description172
dc.description181
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description
dc.description
dc.description
dc.languageen
dc.publisherW B SAUNDERS CO-ELSEVIER INC
dc.publisher
dc.publisherPHILADELPHIA
dc.relationMETABOLISM-CLINICAL AND EXPERIMENTAL
dc.rightsembargo
dc.sourceWOS
dc.subjectBody-mass Index
dc.subjectAdiponectin-deficient Mice
dc.subjectSmooth-muscle Contraction
dc.subjectInnate Lymphoid-cells
dc.subjectNitric-oxide Synthase
dc.subjectDiet-induced Obesity
dc.subjectInsulin-resistance
dc.subjectMetabolic Syndrome
dc.subjectLeptin Receptor
dc.subjectAirway Hyperresponsiveness
dc.titleObesity And Asthma: Beyond T(h)2 Inflammation
dc.typeArtículos de revistas
dc.typeResumo


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