Relationship of Adipokines with Immune Response and Lung Function in Obese Asthmatic and Non-Asthmatic Women

Abstract

Background. Obesity is a risk factor for asthma. Studies in mice suggest that the adipokines leptin and adiponectin affect asthmatic responses. The purpose of this study was to determine if adipokines associated with obesity are (1) altered in obese women with asthma compared to controls and (2) associated with increased cytokines and chemokines involved in allergic inflammation. Methods. We performed a cross-sectional study of asthmatic and non-asthmatic obese premenopausal women. Participants answered questionnaires and performed lung function tests. Serum and peripheral blood mononuclear cells (PBMCs) were collected for analysis of cytokines and adipokines. Results. A total of 22 asthmatic (mean body mass index 40.0 ± 5.1 kg/m²) and 20 non-asthmatic women (mean body mass index 41.3 ± 5.6 kg/m²) participated. We found no difference in serum adipokine concentrations between asthmatics and non-asthmatics. Serum adiponectin correlated positively with PBMC eotaxin (r_s = 0.55, p = .0003) and RANTES (regulated upon activation, normal T-cell expressed, and secreted) (r_s = 0.36, p = .03), whereas serum leptin correlated negatively with PBMC eotaxin (r_s = −0.34, p = .04). There was a negative correlation between serum adiponectin and PBMC interferon-γ (r_s = −0.41, p = .01). Conclusions. Perturbations of adipokines that occur in obesity were correlated with decreased cytokine production typically associated with allergic responses in PBMC of obese premenopausal women. This study suggests that although obese asthmatics may have elements of Th2-mediated inflammation, adipokine derangements in obesity are associated with Th1 rather than Th2 bias. Obesity has complex effects on allergic inflammation and is likely to be important modifier of the pathogenesis of airway disease in asthma.

• asthma
• inflammation
• obesity
• Th1/Th2

Acknowledgements

Contribution to Authorship. Dr. A. E. Dixon was involved in all phases of study design, participant recruitment, data collection, data analysis, and writing of manuscript. Dr. S. E. Johnson was involved with data collection, data analysis, and writing of the manuscript. Ms. L. V. Griffes recruited all participants at the University of Vermont, was involved with data collection, and assisted with writing manuscript. Ms. D. M. Raymond performed all the laboratory-based assays. Ms. R. Ramdeo recruited participants at Long Island Jewish, collected data, and assisted with writing manuscript. Ms. A. Soloveichik assisted with recruitment of participants at Long Island Jewish, collected data, and assisted with writing manuscript. Dr. B. T. Suratt assisted with design of laboratory-based assays, data interpretation, and writing of manuscript. Dr. R. I. Cohen was involved in all phases of study design, participant recruitment, data collection, data analysis, and writing of manuscript.

Declaration of Interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.