Stress enhances airway reactivity and airway XXXX in an animal model of allergic @entity565 .

@entity32 @entity10328 @entity59 @entity19 @entity565 @entity60 @entity58 @entity1224
OBJECTIVE: Despite the long-standing clinical assumption that stress and @entity565 morbidity are associated, convincing experimental evidence on mechanisms has been unavailable. A wide range of immunological, endocrinological, and neuronal pathways are known to mediate and modulate a systemic stress response. Interestingly, most of these mediators play a crucial role in initiating and perpetuating symptoms associated with @entity565 . To explore potential mechanisms linking stress to @entity565 exacerbation we developed an animal model that combines allergic airway @entity32 and exposure to stress. METHODS: CBA/J @entity19 were sensitized by intraperitoneal injection of @entity10328 (OVA) and challenged with OVA aerosol via the airways. Additionally, some @entity19 were stressed by exposure to an ultrasonic stressor. @entity1224 ( @entity1224 ) was measured in vitro by electric field stimulation (EFS) of tracheal smooth muscle elements. Bronchoalveolar lavage fluid (BAL) was obtained and cell numbers determined. Cytokine levels of @entity58 , @entity59 , and @entity60 in BAL were determined by ELISA. RESULTS: Our findings demonstrate that exogenously applied stress dramatically enhances airway reactivity in OVA-sensitized and challenged @entity19 . Further, stress significantly increases allergen-induced airway @entity32 identified by increased leukocyte (ie, eosinophil) numbers in bronchoalveolar lavage fluids. CONCLUSIONS: We found further evidence that stress can indeed exacerbate @entity1224 and airway @entity32 in an animal model of allergic @entity565 and now introduce a novel @entity19 model to identify stress-triggered pathways, including mediators as neurohormones, neuropeptides, and markers of @entity32 .
