Résumé
Lymphocytes are prominent among the inflammatory cells infiltrating the asthmatic airways and T-cell activation appears to be a characteristic feature of acute asthma. In patients with acute asthma who respond well to bronchodilator therapy, the main mechanism of airflow obstruction is smooth muscle contraction, while in patients with poor response the main mechanism is airway inflammation. This study was conducted on 60 children with acute exacerbation of bronchial asthma. They were divided into three groups [mild, moderate and severe] according to the severity of the acute attack, utilizing a clinical scoring system and through measuring Peak Expiratory Flow Rate [PEFR], and oxygen saturation. Serum level of sIL-2R was measured using enzyme-linked immunosorbent assay both in the studied cases and in 20 healthy controls. The mean serum level of sIL-2R in the studied cases [5207.5 +/- 2084.9 pg/ml] was significantly higher than its mean level in controls [1742.5 +/- 801.9 pg/ml] [t=9.37, P=0.000]. Its mean level in severe exacerbation [8090.8 +/- 1222.6 pg/ml] was significantly higher than its mean level in moderate exacerbation [5255.0 +/- 1112.8 pg/ml], that was significantly higher than its mean level in mild exacerbation [3164.6 +/- 990.8 pg/ml] [F= 77.36, P=0.000]. There was a significant negative correlation between the levels of sIL-2R and both the baseline PEFR [r = -0.710, P=0.000] and oxygen saturation [r = -0.521, P=0.000]. After receiving bronchodilator therapy, the mean level of sIL-2R in cases with no or partial response [6486.8 +/- 1900.4 pg/ml] was significantly higher than its mean level in cases with complete response [4088.1 +/- 1534.9 pg/ml] [t=5.406, P=0.000]. A higher level of sIL-2R at acute asthma exacerbation was associated not only with more severe exacerbation but also with a lower degree of bronchodilator responsiveness