PM Renzi, N Sebastiao, AS al Assaad, A Giaid and Q Hamid
Department of Medicine and Pathology, Meakins Christic Labs, Montreal, Quebec, Canada.

We have previously shown that inducible nitric oxide (iNO)-synthase immunoreactivity is expressed in bronchial epithelium and increased in asthma which suggests a possible role for NO in airway hyperresponsiveness. We tested the hypothesis that exposure of a sensitized animal to antigen could account for the increased expression of iNO-synthase in the airways. We examined the expression of iNO- synthase mRNA and immunoreactivity in the lungs of ovalbumin (OA) sensitized Brown Norway (BN) rats 8 h after antigen challenge by in situ hybridization and immunocytochemistry. Sensitized and unchallenged or bovine serum albumin (BSA) challenged rats, or unsensitized and OA challenged rats served as controls. With the use of an iNO-synthase probe we found a higher expression of iNO-synthase mRNA in BN rat airways after antigen challenge with OA but not after antigen challenge with BSA or in other controls. Most of the expression was in the epithelium of the airways with few cells positive in the subepithelial inflammatory infiltrate or in lung lavage. Very strong iNO-synthase immunoreactivity was observed in the airway epithelium of sensitized and OA challenged rats. No significant immunoreactivity was observed in the inflammatory infiltrate of the airways or in lung parenchyma. In conclusion, iNO-synthase increases in the airways of sensitized rats after exposure to antigen, the major source being from airway epithelial cells. NO may have a role in the development of the late airway response and bronchial hyperresponsiveness.

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