Airways reversibility after prednisolone therapy in chronic asthma is associated with alterations in leukocyte function.

In 6 patients with chronic asthma, we studied the effects of orally administered prednisolone on monocyte and neutrophil membrane receptor expression for IgG (Fc) and complement, neutrophil locomotion, and calcium ionophore-induced leukotriene C4 production by granulocytes. Prior to treatment, monocyte IgG (Fc) and complement receptor expression, but not neutrophil IgG (Fc) or complement receptor expression, were increased when patients were compared with nonasthmatic control subjects (p less than 0.01 and p less than 0.01, respectively). After a 7-day course of orally administered prednisolone (30 mg/day daily), the increases in peak expiratory flow rate were accompanied by significant decreases from baseline in the percent of monocyte IgG (Fc) (Day 3, p less than 0.001; Day 7, p less than 0.001), monocyte complement (Day 3, p less than 0.001; Day 7, p less than 0.001), and neutrophil complement rosettes (Day 3, p less than 0.02; Day 7, p less than 0.02), but not neutrophil IgG (Fc) rosettes. Neutrophil locomotion in vitro, in response to casein, from the asthmatics was enhanced when compared with cells from control subjects, and was significantly depressed following prednisolone. Each of the 6 subjects had a peripheral blood eosinopenia in response to prednisolone that corresponded to a decrease in the amount of immunoreactive LTC4 generated from granulocyte suspensions challenged with the calcium ionophore A23187. These findings suggest that prednisolone suppresses monocyte and neutrophil activation in chronic asthma and that this is accompanied by an improvement in lung function.