Obesity, smooth muscle, and airway hyperresponsiveness

J Allergy Clin Immunol. 2005 May;115(5):925-7. doi: 10.1016/j.jaci.2005.01.064.


Both asthma and obesity are large and growing public health issues. Mounting evidence now implicates obesity as a major risk factor for asthma, thus linking these 2 major epidemics. Moreover, both in human subjects and in mice, obesity appears to predispose toward airway hyperresponsiveness. This review describes potential mechanisms whereby obesity might modify airway smooth muscle function to explain these observations. These mechanisms include both static and dynamic mechanical factors attributable to decreases in functional residual capacity and decreases in tidal volume that are observed in the obese. They include also obesity-related changes in lung development, chronic systemic inflammation (including increased serum levels of inflammatory cytokines and chemokines), and adipocyte-derived factors, including leptin, adiponectin, and plasminogen activator inhibitor.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Adiponectin
  • Animals
  • Asthma / etiology
  • Asthma / physiopathology*
  • Cytokines / physiology
  • Functional Residual Capacity
  • Humans
  • Inflammation / physiopathology
  • Intercellular Signaling Peptides and Proteins / physiology
  • Leptin / physiology
  • Muscle, Smooth / physiopathology*
  • Obesity / complications
  • Obesity / physiopathology*
  • Plasminogen Activators / antagonists & inhibitors
  • Plasminogen Activators / physiology
  • Respiratory System / physiopathology


  • Adiponectin
  • Cytokines
  • Intercellular Signaling Peptides and Proteins
  • Leptin
  • Plasminogen Activators