Obesity, airway hyperresponsiveness, and inflammation

J Appl Physiol (1985). 2010 Mar;108(3):735-43. doi: 10.1152/japplphysiol.00749.2009. Epub 2009 Oct 29.

Abstract

Epidemiological data indicate that obesity is a risk factor for asthma, but the mechanistic basis for this relationship is not established. Here we review data from human subjects and animal models investigating the relationship between obesity and airway hyperresponsiveness, a characteristic feature of asthma. We discuss obesity as a state of chronic systemic inflammation resulting from interactions between adipocytes and adipose tissue macrophages that are recruited to obese adipose tissue. Finally, we focus on the possibility that aspects of this inflammation, particularly obesity-related changes in TNF-alpha, leptin, and adiponectin, may contribute to airway hyperresponsiveness in obesity. Determining how obesity promotes asthma may uncover novel therapeutic strategies that are effective in the obese asthmatic subject.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Adiponectin / metabolism
  • Adipose Tissue / immunology
  • Adult
  • Animals
  • Asthma / etiology*
  • Asthma / immunology
  • Asthma / physiopathology
  • Bronchial Hyperreactivity / etiology*
  • Bronchial Hyperreactivity / immunology
  • Bronchial Hyperreactivity / physiopathology
  • Child
  • Female
  • Humans
  • Inflammation / etiology*
  • Inflammation / immunology
  • Inflammation / physiopathology
  • Inflammation Mediators / metabolism
  • Leptin / metabolism
  • Male
  • Obesity / complications*
  • Obesity / immunology
  • Obesity / physiopathology
  • Risk Factors
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Adiponectin
  • Inflammation Mediators
  • Leptin
  • Tumor Necrosis Factor-alpha