Published ahead of print on June 19, 2008, doi:10.1164/rccm.200802-301OC Am. J. Respir. Crit. Care Med., Volume 178, Number 5, September 2008, 469-475 A more recent version of this article appeared on September 1, 2008
Submitted on February 20, 2008 The Association Between Obesity and Asthma: Interactions Between Systemic and Airway InflammationTim J.T. Sutherland1,1 Respiratory Research Unit, Department of Medical and Surgical Sciences, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand, 2 Department of Medical Microbiology, Division of Health Sciences, University of Otago, Dunedin, New Zealand, 3 Department of Medical and Surgical Sciences, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand, 4 Department of Preventive and Social Medicine, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand * To whom correspondence should be addressed. E-mail: robin.taylor{at}stonebow.otago.ac.nz.
Rationale: Both obesity and asthma are common conditions, and both are characterised by the presence of inflammation. Animal studies suggest that the development of airway hyper-responsiveness with antigen challenge is exaggerated with obesity. However, clear evidence for either an additive or a synergistic pathological interaction between obesity and asthma is lacking in humans. Objectives: To identify whether an interaction between systemic and local inflammation occurs in obese subjects with asthma in a controlled observational study. Measurements and Main Results: We studied 79 women: obese asthmatics (n=20), normal weight asthmatics (n=19), obese non-asthmatics (n=20), and normal weight non-asthmatics (n=20). After corticosteroid withdrawal, between-group differences in spirometric values, lung volumes, exhaled nitric oxide, induced sputum cell counts, and biomarkers of inflammation in sputum supernatant and blood were measured, and interactions explored. Markers of systemic inflammation were increased with obesity, and TH-2 cytokines were increased with asthma, but no important interactions were identified. Obesity adversely affected lung function with increases in functional residual capacity and residual volume in obese but not normal weight asthmatics, with a significant obesity by asthma interaction. Conclusions: The link between obesity and asthma is unlikely to be explained by enhancement of the "classical" forms of airway inflammation resulting from the systemic inflammatory effects of obesity itself. Other mechanisms, possibly related to innate immunity, may explain the relationship between obesity and asthma. Key words: asthma, obesity, inflammation, interaction
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