気管支喘息発作時および回復期におけるneutrophil elastase およびアラキドン酸代謝産物の寄与

概要

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We investigated the molecular pathogenesis of bronchial asthma focusing on the contribution of neutrophil elastase (NE) and arachidonic acid metabolites to asthma exacerbations and their recovery phase. Serum eosinophil cationic protein (ECP), plasma NE levels, and urinary leukotriene E4 (LTE4) concentrations significantly increased during exacerbations (n=118) as compared with the stable state (n=48). Serum soluble interleukin-2-receptor, and thromboxane A2 and prostaglandin I2 urinary metabolites were unchanged. Within the exacerbation group, plasma NE levels in a severe group (n=12) were significantly higher (p＜0.05) than those in a moderate group (n=42), which in turn, were significantly higher (p＜0.01) than those in a mild group (n=64). Urinary LTE4 levels in the severe group were significantly elevated (p＜0.05) compared to the mild group, but no difference existed between the moderate and mild groups. Seven days of steroid therapy inhibited the rises in serum ECP and urinary LTE4 but not that of NE. Plasma NE might be one of the good markers of asthma exacerbation severity which is not inhibited by current steroid therapy. NE inhibitor might be an effective therapy for moderate to severe acute asthma exacerbations when they are associated with high levels of plasma NE.
札幌医科大学の論文
2005-04-01