• Tuberculosis and Respiratory Diseases
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• v.48 no.2
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• pp.191-202
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• 2000

Background: Bronchial asthma is characterized by airway hyperresponsiveness(BHR) and inflammation. The cyclooxygenase(COX) is believed to be one of the important enzymes in these inflammatory reactions. Recently, the COX was divided into two isoforms, COX1 and COX2. COX2 is induced by lipopolysaccharide and some cytokines at the inflammation site. Prostaglandin E2(PGE2), produced from COX2, may affect airway inflammation. The purpose of this study is to evaluate the effect of COX2 inhibitor on COX2 expression, plasma PGE2, airway resistance and histologic finding in an animal asthma model. Methods : Sprague-Dawley rats were divided into 3 groups. The normal control group did not receive any treatment, but the asthma control group was sensitized by ovalbumin but not treated with the COX2 inhibitor(nimesulide, Mesulid$^{(R)}$). The treatment group was sensitized and treated with nimesulide. Specific airway resistance(sRaw) before and after nimesulide ingestion was investigated. The PGE2 level in the plasma was examined and COX2 immunogold-silver stain on lung tissue was performed. Results: sRaw and eosionophilic infiltration on airway, which increased in the asthma control group, was compared to normal control(p=0.014). However, there was no difference in eosinophilic infiltration between asthma control and treatment groups(p=0.408) and no difference in COX2 expression on bronchiolar epithelium among the three groups. Plasma PGE2 levels were not statically different among the three groups. Conclusion: The role of COX2 in the allergen-induced BHR was not significant The effect of nimesulide was not observed on BHR, COX2 expression, and plasma PGE2 level. Therefore, COX2 may not be a major substance of allergic asthma.