Allergy · 2012
Obesity lowers the threshold of allergic sensitization and augments airway eosinophilia in a mouse model of asthma.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Dietze J, Böcking C, Heverhagen J T, Voelker M N, Renz H
Аннотация
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.
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.