Am J Respir Crit Care Med. 2012 Jul 26. [Epub ahead of print]
Obesity and Asthma: An Inflammatory Disease of Adipose Tissue Not the Airway.
Source
University of Vermont, Burlington, Vermont, United States.
Abstract
RATIONALE:
Obesity is a major risk factor for asthma; the reasons for this are poorly understood, though it is thought that inflammatory changes in adipose tissue in obesity could contribute to airway inflammation and airway reactivity in obese individuals.
OBJECTIVES:
The purpose of the current study was to determine if inflammation in adipose tissue in obesity is related to late-onset asthma, and associated with increased markers of airway inflammation and reactivity.
METHODS:
We recruited a cohort of obese asthmatic and obese control women. We followed asthmatics for 12 months after bariatric surgery. We compared markers in adipose tissue and the airway from asthmatics and controls, and changes in asthmatics over time.
MEASUREMENTS AND MAIN RESULTS:
Asthmatics had increased macrophage infiltration of visceral adipose tissue (p< 0.01), with increased expression of leptin (p< 0.01) and decreased adiponectin (p< 0.001) when controlled for BMI. Similar trends were observed in subcutaneous adipose tissue. Airway epithelial cells expressed receptors for leptin and adiponectin, and airway reactivity was significantly related to visceral fat leptin expression (rho=-0.8, p< 0.01). Bronchoalveolar lavage cytokines, and cytokines production from alveolar macrophages were similar in asthmatics and controls at baseline, and tended to increase 12 months after surgery.
CONCLUSIONS:
Obesity is associated with increased markers of inflammation in serum and adipose tissue, and yet decreased airway inflammation in obese asthmatics; these patterns reverse with bariatric surgery. Leptin and other adipokines may be important mediators of airway disease inobesity through direct effects on the airway rather than by enhancing airway inflammation.
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