This Article Full Text Full Text (PDF) Online Supplement All Versions of this Article: 200802-301OCv1 178/5/469    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sutherland, T. J. T. Articles by Taylor, D. R. Search for Related Content PubMed PubMed Citation Articles by Sutherland, T. J. T. Articles by Taylor, D. R.

The Association between Obesity and Asthma

Interactions between Systemic and Airway Inflammation

¹ Respiratory Research Unit, Department of Medical and Surgical Sciences, Dunedin School of Medicine; ² Department of Medical Microbiology, Division of Health Sciences; ³ Department of Medical and Surgical Sciences, Dunedin School of Medicine; and ⁴ Department of Preventive and Social Medicine, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand

Correspondence and requests for reprints should be addressed to Professor D. Robin Taylor, M.D., F.R.C.P.C., Dunedin School of Medicine, University of Otago, P.O. Box 913, Dunedin, New Zealand. E-mail: robin.taylor{at}stonebow.otago.ac.nz

Rationale: Both obesity and asthma are common conditions, and both are characterized by the presence of inflammation. Animal studies suggest that the development of airway hyperresponsiveness with antigen challenge is exaggerated with obesity. However, clear evidence for either an additive or a synergistic pathologic 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.

Methods: We studied 79 women: obese patients with asthma (n = 20), normal-weight patients with asthma (n = 19), obese patients without asthma (n = 20), and normal-weight patients without asthma (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.

Measurements and Main Results: Markers of systemic inflammation were increased with obesity, and Th2 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 patients with asthma, 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

AT A GLANCE COMMENTARY Scientific Knowledge on the Subject Epidemiologic and clinical evidence suggests an important link between obesity and asthma. The fact that both are "inflammatory" diseases raises the possibility of pathophysiologic interaction. What This Study Adds to the Field Although both systemic and airway inflammation were demonstrated with obesity and asthma, there was no clear evidence of an interaction between the two.

 

This article has been cited by other articles:

				R. Torchio, A. Gobbi, C. Gulotta, R. Dellaca, M. Tinivella, R. E. Hyatt, V. Brusasco, and R. Pellegrino Mechanical effects of obesity on airway responsiveness in otherwise healthy humans J Appl Physiol, August 1, 2009; 107(2): 408 - 416. [Abstract] [Full Text] [PDF]

				W. C. Moore Update in Asthma 2008 Am. J. Respir. Crit. Care Med., May 15, 2009; 179(10): 869 - 874. [Full Text] [PDF]

				L-P. Boulet Influence of comorbid conditions on asthma Eur. Respir. J., April 1, 2009; 33(4): 897 - 906. [Abstract] [Full Text] [PDF]

				A. Munitz, L. Seidu, E. T. Cole, R. Ahrens, S. P. Hogan, and M. E. Rothenberg Resistin-Like Molecule {alpha} Decreases Glucose Tolerance during Intestinal Inflammation J. Immunol., February 15, 2009; 182(4): 2357 - 2363. [Abstract] [Full Text] [PDF]