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The underlying cause\u2013effect relationship between metabolism, innate and adaptive immunity, and inflammation remains to be elucidated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We developed an animal model to study the interaction between metabolic abnormalities and experimentally induced asthma. Obesity\u2010susceptible <jats:styled-content style=\"fixed-case\">AKR<\/jats:styled-content> mice were fed with high\u2010fat diet (<jats:styled-content style=\"fixed-case\">HFD<\/jats:styled-content>) or normal low\u2010fat diet (<jats:styled-content style=\"fixed-case\">LFD<\/jats:styled-content>) and subjected to a protocol of ovalbumin (<jats:styled-content style=\"fixed-case\">OVA<\/jats:styled-content>) sensitization and airway allergen challenges followed by assessment of inflammation and lung function.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">AKR<\/jats:styled-content> mice developed obesity and a prestage of metabolic syndrome following <jats:styled-content style=\"fixed-case\">HFD<\/jats:styled-content>. This phenotype was associated with an increase in proinflammatory macrophages (<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>11b+\/<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>11c+) together with higher serum levels of interleukin 6. Obese mice showed increased susceptibility to allergic sensitization as compared to <jats:styled-content style=\"fixed-case\">LFD<\/jats:styled-content> animals. Anti\u2010ovalbumin <jats:styled-content style=\"fixed-case\">I<\/jats:styled-content>g<jats:styled-content style=\"fixed-case\">E<\/jats:styled-content> antibody titers correlated positively and anti\u2010<jats:styled-content style=\"fixed-case\">OVA I<\/jats:styled-content>g<jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>2a antibodies titers correlated negatively with body weight. Airway eosinophilia showed a positive correlation with body weight, whereas mucus production did not change with obesity.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>This obesity model demonstrates that <jats:styled-content style=\"fixed-case\">HFD<\/jats:styled-content>\u2010induced 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.<\/jats:p><\/jats:sec>","DOI":"10.1111\/all.12031","type":"journal-article","created":{"date-parts":[[2012,9,25]],"date-time":"2012-09-25T17:35:00Z","timestamp":1348594500000},"page":"1519-1529","source":"Crossref","is-referenced-by-count":42,"title":["Obesity lowers the threshold of allergic sensitization and augments airway eosinophilia in a mouse model of asthma"],"prefix":"10.1111","volume":"67","author":[{"given":"J.","family":"Dietze","sequence":"first","affiliation":[{"name":"Institute of Laboratory Medicine and Pathobiochemistry, Molecular Diagnostics University Hospital Giessen and Marburg Marburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C.","family":"B\u00f6cking","sequence":"additional","affiliation":[{"name":"Institute of Laboratory Medicine and Pathobiochemistry, Molecular Diagnostics University Hospital Giessen and Marburg Marburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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