title: Obesity and asthma: an inflammatory disease of adipose tissue not the airway.
abstract: BACKGROUND
  Obesity is a major risk factor for asthma; the reasons for this are poorly understood, although it is thought that inflammatory changes in adipose tissue in obesity could contribute to airway inflammation and airway reactivity in individuals who are obese.
  
  
  OBJECTIVE
  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 women with asthma and obese control women. We followed subjects with asthma for 12 months after bariatric surgery. We compared markers in adipose tissue and the airway from subjects with asthma and control subjects, and changes in subjects with asthma over time.
  
  
  RESULTS
  Subjects with asthma 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 body mass index. 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 cytokine production from alveolar macrophages were similar in subjects with asthma and control subjects 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 people with asthma; these patterns reverse with bariatric surgery. Leptin and other adipokines may be important mediators of airway disease in obesity through direct effects on the airway rather than by enhancing airway inflammation.
authors: Division of Pulmonary and Critical Care Medicine, 89 Beaumont Avenue, Burlington, VT 05405, USA.
authors: Olga
authors: O
authors: Sideleva
authors: Benjamin T
authors: BT
authors: Suratt
authors: Kendall E
authors: KE
authors: Black
authors: William G
authors: WG
authors: Tharp
authors: Richard E
authors: RE
authors: Pratley
authors: Patrick
authors: P
authors: Forgione
authors: Oliver
authors: O
authors: Dienz
authors: Charles G
authors: CG
authors: Irvin
authors: Anne E
authors: AE
authors: Dixon
mesh_terms: D054392:Adipokines / Q000378:metabolism; D000273:Adipose Tissue; D000328:Adult; D001249:Asthma / Q000209:etiology* / Q000378:metabolism / Q000473:pathology*; D050110:Bariatric Surgery; D015415:Biomarkers / Q000378:metabolism; D015992:Body Mass Index; D016022:Case-Control Studies; D015331:Cohort Studies; D005260:Female; D006801:Humans; D007249:Inflammation; D018836:Inflammation Mediators / Q000378:metabolism; D008875:Middle Aged; D009765:Obesity / Q000150:complications* / Q000378:metabolism / Q000473:pathology*; D012307:Risk Factors
chemical_list: D054392:Adipokines; D015415:Biomarkers; D018836:Inflammation Mediators