The effect of inhaled glucocorticosteroid on protein kinase Cα expression and interleukin-5 production in induced sputum inflammatory cells of asthma patients

Objective To investigate the expression of protein kinase Cα(PKCα) in inflammatory cells and the level of interleukin-5(IL-5) in induced sputum in asthma patients and the effect of inhaled glucocorticosteroid on them. Methods 29 asthma patients were classified into 2 groups; 14 patients were treated with fluticasone propionate for 2 weeks and the others were treated with fluticasone propionate for 4 weeks. Induced sputum with inhaled hypertonic saline (4%-5%) was collected. 13 healthy volunteers were included as controls. Lung ventilatory function and forced expiratory volume in one second (FEV 1) were measured in all patients. The expression of PKCα in the inflammatory cells was detected using immunocytochemistry and the positive percentage in different cells was counted. IL-5 in sputum supernatants was detected using enzyme-linked immunosorbent assay. Results The percentage of eosinophils (11.1±4.3)%, lymphocytes (4.3±2.6) %, PKCα positive cells (79.0±9.6) % and the concentration of IL-5 (64.9±46.0) ng/L in asthmatics were higher than the percentage of eosinophils (0.7±0.5)%, lymphocytes (1.1±0.5)%, PKCαpositive cells (10.5±2.3) % and the concentration of IL-5 (14.3±8.4) ng/L in the controls ( P 0.01). The percentage of PKCα positive cells and the concentration of IL-5 in the two groups of asthma were lower than that before fluticasone propionate treatment ( P 0.05), and the forced expiratory volume in first second was correlated to them (respectively, r =-0.423, P 0.05; n =29, r =-0.664, P 0.01).The concentration of IL-5 was correlated to the percentage of PKCα positive cells ( n =29, r =0.623, P 0.01). Conclusions PKCα in the inflammatory cells and IL-5 may play an important part in airway inflammation, and the signal transduction of the PKCα may be one of the mechanisms of the airway inflammation in asthma. Glucocorticosteroid could suppress the expression of PKCα in airway inflammatory cells and then decrease the production of IL-5 in asthmatic airways.