[Inhibitory effects of oral glucocorticoid therapy on T-lymphocyte infiltration in the bronchial mucosa of asthmatic subjects].

Although one of the mechanisms of glucocorticoid action in asthma is thought to be suppression of bronchial inflammation, there is little evidence to support this view. In the present study we have attempted to clarify the effect of oral glucocorticoid therapy on lymphocyte infiltration in the bronchial mucosa. Bronchial biopsies were obtained from 9 patients with asthma who had been taking oral prednisolone for at least the previous 18 days. They were stained immunohistochemically with a panel of monoclonal antibodies against: T cell subsets (CD3, CD4, CD8, CD57), and interleukin-2 receptor (CD25). The numbers of positive staining cells were counted for each antibody and compared with those in 11 patients with asthma who were symptomatic but had not been receiving glucocorticoid therapy for at least the previous one month. There was a significant decrease in the numbers of CD3- CD4-, CD8- and CD57-positive cells in glucocorticoid treated asthmatics compared with those of symptomatic asthmatics. Moreover, when one patient who showed glucocorticoid resistance was excluded from the analysis, there was a significant inverse correlation between the dose of prednisolone expressed as the total dose for the previous 2 weeks and the numbers of CD3- and CD4-positive cells. The number of CD25-positive cells (interleukin-2 receptor-bearing cells, presumed activated T-lymphocytes) also showed a tendency to decrease but the difference was not statistically significant. These results suggest that oral glucocorticoids exert an inhibitory effect on T-lymphocyte infiltration in the bronchial mucosa, which could be a mechanism of their beneficial action in asthma.