BioModels offers a mouse model of ovalbumin (OVA) induced allergic asthma. In the acute model, mice are sensitized with an intraperitoneal (IP) injection of OVA and adjuvant and then challenged with intranasal delivery of OVA followed by collections on day 16. Chronic versions of this model run from 4-12 weeks. The OVA model recapitulates many of the hallmarks of allergic asthma in humans, including elevated IgE and Th2 related cytokines, mucus hypersecretion, airway inflammation, goblet cell hyperplasia, epithelial hypertrophy, and airway hyperreactivity. Endpoints in this model include total and differential cell counts and inflammatory mediator content in the broncho-alveolar lavage fluid, airway hyperreactivity and detailed lung mechanics, as well as histopathology and immunohistochemistry.
BALB/c mice are sensitized with an IP injection of OVA with adjuvant on days 0 and 7. Mice are then challenged with OVA intranasally on days 13, 14, and 15 and endpoints are assessed on day 16. Reference treatment animals receive 3 mg/kg dexamethasone 1 hour prior to the challenges.
Total cells and eosinophils recover in broncho-alveolar lavage fluid on day 16 of an OVA-induced acute allergic asthma model. Mice demonstrate a dose responsive increase in total cells and eosinophils. Dexamethasone lower total inflammatory cell counts and eosinophils in the BAL fluid.
Lung Resistance and Elastance is measured on day 16 of an OVA-induced acute allergic asthma model, following exposure to increasing doses of methacholine. Animals that are sensitized and challenged with OVA displayed increased lung resistance and elastance parameters in comparison to Naïve animals. 3 mg/kg Dexamethasone treatment reduced airway hyperreactivity in diseased animals.
H&E-stained lung sections from naïve mice and mice from an OVA-induced acute allergic asthma model with and without 3 mg/kg dexamethasone treatment. The infiltration of mixed inflammatory cells observed in diseased animals is decreased in animals treated with 3 mg/kg dexamethasone.