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AIRWAY HYPERRESPONSIVENESS IN MICE FOLLOWING ANTIGEN AND PARTICULATE MATTER EXPOSURE IS VAGALLY MEDIATED
Citation:
McAlexander, M. A., N HaykalCoates, AND S H. Gavett. AIRWAY HYPERRESPONSIVENESS IN MICE FOLLOWING ANTIGEN AND PARTICULATE MATTER EXPOSURE IS VAGALLY MEDIATED. Presented at American Thoracic Society Meeting, San Francisco, CA, May 18-23, 2001.
Description:
Sensory nerves within the airways can initiate a variety of protective reflexes. We hypothesized that insults such as exposure to antigen and particulate matter (PM) might dysregulate airway sensory nerve function, thereby contributing to enhanced airway inflammation and hyperresponsiveness to contractile agonists. Vagal contributions to airway responses in mice were examined following exposure to ovalbumin (OVA) antigen and the emission source particulate residual oil fly ash (ROFA). Baseline resistance in control Balb/C mice was 1.73 ? 0.07 cm H2O.s/L. This value was decreased (23.4 ? 3.7 %) by pretreatment with atropine, suggesting the existence of baseline cholinergic tone in the mouse airway. Baseline resistance, was, however, unaltered in mice following exposure to ROFA and/or sensitization and challenge with OVA. Methacholine (Mch), but not capsaicin, bradykinin or histamine, caused dose-dependent increases in lung resistance in Balb/C mice. Airway responsiveness to Mch, as well as inflammatory cell counts in the BAL fluid, were increased following OVA challenge, and further increased in mice treated with both OVA and ROFA. The increases in airway reactivity to Mch were abolished by bilateral vagotomy (resistance following 316 ug/kg Mch prevagotomy = 63.7 ? 24.5 cm H2O.s/L ; postvagotomy = 6.9 ? 3.1 cm H2O.s/L; P < 0.01) . These results indicate that PM and antigen can dysregulate airway nerve function in Balb/C mice and suggest that some PM-induced health effects may be dependent upon vagal reflexes. This abstract does not reflect EPA policy)