Interleukin-13 status in children with bronchial asthma

Interleukin-13 [IL-13] is a newly described cytokine. The objective of this study is to evaluate the rote of IL-13 in the pathogenesis of bronchial asthma among children, studying the relation of IL-13 to disease state and other laboratory findings and studying the effect of steroid therapy on IL-13 expression. This study was conducted on 40 asthmatic children presented with acute exacerbation of bronchial asthma. Their ages ranged from 4-14 years [mean age 7.5 +/- 2.8 years] 22 patients [55%] were mates and 18 patients [45%] were females. The study included as well 15 healthy children as controls. Patients and controls were subjected to detailed history taking, complete physical examination, complete blood count, total serum IgE level estimation, and PEER measurement. Serum IL-13 was measured for all subjects using the ELISA technique, during acute attack and one week after treatment. Treatment included bronchodilators with or without steriod therapy. Serum IL-13 was higher in atopic asthmatics during acute attack compared to non-atopic patients and control subjects. There was a statistically highly significant decrease in the level of IL-13 one-week after treatment. There was a positive correlation between mean serum IL-13 and, both total serum IgE and absolute eosinophilic count. There was an inverse relationship between IL-13 mean level during acute attack and PEFR in all asthmatics

Endothelin-1 [ET-1] concentrations in plasma and bronchoalveolar lavage of some asthmatic patients

Endothelin-1 [ET-1] is a potent bronchoconstrictor which may have a role in the pathogenesis of asthma. To clarify the interrelation between ET-1 and bronchial asthma, the concentrations of ET-1 in plasma and BAL fluid were measured [by ELISA technique] in [10] healthy subjects, [10] patients with atopic asthma treated with bronchodilators alone [Group 1], and [10] patients with atopic ashma treated with inhaled an/or oral corticosteroids [Group II]. Pulmonary functions [FEV1% predicted and FEF25-75% predicated] and the provocation concentrations of methacholine required to reduce FEV1 by 20% of the prechallenge baseline [PD20 were also measured. There was no significant difference in the plasma ET-1 level among either the control group and group 1 [15.95 +/- 6.5 pg/ml versus 17.84 +/- 7.8 pg/ml][and group II [15.95 +/- 6.5 pg/ml versus 16.75 +/- 6.7 pg/ml] or group I and II [17.84 +/- 6.7 pg/ml]. There was a significant increase in BAL fluid ET-1 levels in both the non steroid treated patients with asthma [Group I] and the steroid treated patients [Group II] compared with the normal subjects [20.94 +/- 3.96 pg/ml versus 15.61 +/- 3.37 pg/ml][and [16.03 +/- 3.5 pg/ml] respectively. There was statistically significant difference in BAL ET-1 level between Group II and group I indicating that ET-1 level may be modulated by corticosteroid therapy. In group I and II there was a significant negative correlation between the BAL ET-1 concentrations and ventilatory functions [% predicated FEV1 and FEF25-75].No correlation between BAL fluid ET-1 concentrations and bronchial reactivity or plasma ET-1 level was found in either Group I and II. These findings indicate that the potent bronchoconstricitive substance, endotheline, may contribute to pathogenesis of airflow obstruction in asthma