Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/202309
Type: Artigo de periódico
Title: Obesity And Asthma: Beyond T(h)2 Inflammation.
Author: Leiria, Luiz O S
Martins, Milton A
Saad, Mário J A
Abstract: Obesity 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.
Subject: Adiponectin
Adipose Tissue
Adiposity
Airway Resistance
Animals
Asthma
Humans
Leptin
Models, Biological
Obesity
Th2 Cells
Adiponectin
Airway Hyperreactivity
Insulin
Leptin
Citation: Metabolism: Clinical And Experimental. v. 64, n. 2, p. 172-81, 2015-Feb.
Rights: fechado
Identifier DOI: 10.1016/j.metabol.2014.10.002
Address: http://www.ncbi.nlm.nih.gov/pubmed/25458831
Date Issue: 2015
Appears in Collections:Unicamp - Artigos e Outros Documentos

Files in This Item:
File SizeFormat 
pmed_25458831.pdf544.53 kBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.