Effects of Diet-Induced Mild Obesity on Airway Hyperreactivity and Lung Inflammation in Mice.
10.3349/ymj.2013.54.6.1430
- Author:
Sun Hee JUNG
1
;
Jang Mi KWON
;
Jae Won SHIM
;
Deok Soo KIM
;
Hye Lim JUNG
;
Moon Soo PARK
;
Soo Hee PARK
;
Jinmi LEE
;
Won Young LEE
;
Jung Yeon SHIM
Author Information
1. Department of Pediatrics, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea. jy7.shim@samsung.com
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Adipokine;
asthma;
high fat;
vascular endothelial growth factor;
transforming growth factor beta;
tumor necrosis factor alpha;
obesity;
airway hyperresponsiveness
- MeSH:
Animals;
Asthma/physiopathology;
Bronchial Hyperreactivity/*physiopathology;
Bronchoalveolar Lavage Fluid/chemistry;
Dietary Fats/adverse effects;
Mice;
Obesity/*etiology/*physiopathology;
Pneumonia/*physiopathology;
Transforming Growth Factors/metabolism;
Tumor Necrosis Factor-alpha/metabolism;
Vascular Endothelial Growth Factor A/metabolism
- From:Yonsei Medical Journal
2013;54(6):1430-1437
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Obesity has been suggested to be linked to asthma. However, it is not yet known whether obesity directly leads to airway hyperreactivity (AHR) or obesity-induced airway inflammation associated with asthma. We investigated obesity-related changes in adipokines, AHR, and lung inflammation in a murine model of asthma and obesity. MATERIALS AND METHODS: We developed mouse models of chronic asthma via ovalbumin (OVA)-challenge and of obesity by feeding a high-fat diet, and then performed the methacholine bronchial provocation test, and real-time PCR for leptin, leptin receptor, adiponectin, adiponectin receptor (adipor1 and 2), vascular endothelial growth factor (VEGF), transforming growth factor (TGF) beta, and tumor necrosis factor (TNF) alpha in lung tissue. We also measured cell counts in bronchoalveolar lavage fluid. RESULTS: Both obese and lean mice chronically exposed to OVA developed eosinophilic lung inflammation and AHR to methacholine. However, obese mice without OVA challenge did not develop AHR or eosinophilic inflammation in lung tissue. In obese mice, lung mRNA expressions of leptin, leptin receptor, VEGF, TGF, and TNF were enhanced, and adipor1 and 2 expressions were decreased compared to mice in the control group. On the other hand, there were no differences between obese mice with or without OVA challenge. CONCLUSION: Diet-induced mild obesity may not augment AHR or eosinophilic lung inflammation in asthma.
