title: Obesity lowers the threshold of allergic sensitization and augments airway eosinophilia in a mouse model of asthma.
abstract: BACKGROUND
  Clinical and epidemiological studies show a close association between obesity and the risk of asthma development. The underlying cause-effect relationship between metabolism, innate and adaptive immunity, and inflammation remains to be elucidated.
  
  
  METHODS
  We developed an animal model to study the interaction between metabolic abnormalities and experimentally induced asthma. Obesity-susceptible AKR mice were fed with high-fat diet (HFD) or normal low-fat diet (LFD) and subjected to a protocol of ovalbumin (OVA) sensitization and airway allergen challenges followed by assessment of inflammation and lung function.
  
  
  RESULTS
  AKR mice developed obesity and a prestage of metabolic syndrome following HFD. This phenotype was associated with an increase in proinflammatory macrophages (CD11b+/CD11c+) together with higher serum levels of interleukin 6. Obese mice showed increased susceptibility to allergic sensitization as compared to LFD animals. Anti-ovalbumin IgE antibody titers correlated positively and anti-OVA IgG2a antibodies titers correlated negatively with body weight. Airway eosinophilia showed a positive correlation with body weight, whereas mucus production did not change with obesity.
  
  
  CONCLUSIONS
  This obesity model demonstrates that HFD-induced obesity lowers the sensitization threshold in a model of asthma. This finding helps to understand why, particularly during childhood, obesity is a risk factor for the development of allergic asthma.
authors.affiliation: Institute of Laboratory Medicine and Pathobiochemistry, Molecular Diagnostics, University Hospital Giessen and Marburg, Marburg, Germany.
authors.forename: J
authors.initials: J
authors.lastname: Dietze
authors.forename: C
authors.initials: C
authors.lastname: Böcking
authors.forename: J T
authors.initials: JT
authors.lastname: Heverhagen
authors.forename: M N
authors.initials: MN
authors.lastname: Voelker
authors.forename: H
authors.initials: H
authors.lastname: Renz
mesh_terms: D000818:Animals; D001249:Asthma / Q000150:complications / Q000276:immunology* / Q000378:metabolism; D059305:Diet, High-Fat; D004195:Disease Models, Animal; D004198:Disease Susceptibility / Q000276:immunology; D005260:Female; D007249:Inflammation / Q000150:complications / Q000276:immunology / Q000378:metabolism; D008168:Lung / Q000276:immunology / Q000503:physiopathology; D051379:Mice; D009765:Obesity / Q000150:complications / Q000276:immunology* / Q000378:metabolism; D011657:Pulmonary Eosinophilia / Q000276:immunology*; D020545:Respiratory Mucosa / Q000276:immunology / Q000378:metabolism