Is there a link between obesity and asthma?

Abstract

Increasing epidemiological data identify a link between obesity and asthma incidence and severity. Based on experimental data, it is possible that shared inflammatory mechanisms play a role in determining this linkage. Although controversial, the role of adipokines may be central to this association and the maintenance of the asthma phenotype. While leptin and adiponectin have a causal link to experimental asthma in mice, data in humans are less conclusive. Recent studies demonstrate that adipokines can regulate the survival and function of eosinophils and that these factors can affect eosinophil trafficking from the bone marrow to the airways. In addition, efferocytosis, the clearance of dead cells, by airway macrophages or blood monocytes appears impaired in obese asthmatics and is inversely correlated with glucocorticoid responsiveness. This review examines the potential mechanisms linking obesity to asthma.

Keywords: Obesity; adipokines; adipose tissue; asthma; eosinophils; macrophages.

Figure

Schematic representation of links between obesity and asthma. (A) Adipokines (leptin and adiponectin) can regulate survival, chemotaxis, and adhesion of eosinophils and modulate activation of macrophages in tissue. (B) Migration of eosinophils from adipose tissue to the lungs of obese subjects is suggested by findings of decreased eosinophil numbers in adipose tissue and increases in lung tissue. Adipokines may result in delayed transit to the airway lumen, resulting in the selective accumulation of eosinophils in peribronchial lung tissue. (C) Immunological changes in activated macrophages of obese individuals may play an important role in systemic and airway inflammation, perhaps explaining the association and even the cause of a glucocorticoid-insensitive asthma phenotype. AAM, alternatively activated macrophages; CAM, classically activated macrophages; AHR, airway hyperreactivity.