BACKGROUND: Bronchial asthma is characterized by airway hyperresponsiveness (BHR) and airway (delete) inflammation. The cyclooxygenase(COX) seems (is believed ) to be one of the important enzyme (enzymes) in these inflammatory reaction (reactions). Recently, the COX was divided into two isoforms, COX1 and COX2. COX2 is induced by lipopolysaccharide and some cytokines at the site of inflammation (inflammation site). Prostaglandin E2 (PGE2), which is (delete) produced from COX2, may affect on (delete) airway inflammation. The purpose of this study was (is) to evaluate the effect of COX2 inhibitor on COX2 expression, plasma PGE2 and(,)airway resistance and histologic finding in (an) animal asthma model. METHODS : Sprague-Dawley rats were divided into 3 groups. Normal control didn't (The normal control group did not) receive any treatment. Asthma (,but the asthma) control group was sensitized by ovalbumin but not treated with (the) COX2 inhibitor(nimesulide, Mesulid ). Treatment (The treatment) group was sensitized and treated with nimesulide. We examined specific airway resistance (sRaw) before and after nimesulide ingestion (was investigated) . Also, we examined (The) PGE2 level in (the) plasma was examined and performed COX2 immunogold-silver stain on lung tissue (was performed). RESULTS: sRaw and eosionophilic infiltration on airway were,( which) increased in the asthma control group which was (, was) compared to normal control(p=0.014). But there However, there was no difference in eosinophilic infiltration between asthma control and treatment group (groups)(p=0.408). There was (and) no difference in COX2 expression on bronchiolar epithelium among (the) three groups. Plasma PGE2 levels were no statistically significant difference (were not statically different) among (the) three groups. CONCLUSION: We conclude that the role (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 on (of) allergic asthma.