Persistent airway T-lymphocyte activation in chronic corticosteroid-treated symptomatic asthma

Background: A small proportion of patients with asthma have persistent symp toms despite regular treatment with high-dose inhaled and/or oral corticost eroids. There is little information regarding immunopathology in such patie nts. Objective: To compare airway inflammatory changes in subjects with chronic corticosteroid-dependent symptomatic asthma (n = 5) and subjects with asthm a that was clinically well controlled on inhaled corticosteroid therapy (n = 9). Subjects in the corticosteroid-dependent group were receiving long-te rm treatment with oral prednisolone and high-dose inhaled corticosteroids. Methods: Subjects underwent fiberoptic bronchoscopy with bronchoalveolar la vage (BAL) and bronchial biopsy. T-lymphocytes subsets and activation marke rs in BAL fluid and peripheral blood were determined by FAGS analysis. Bron chial biopsies were stained immunohistochemically, and numbers of inflammat ory cells quantitated. Inflammatory mediators in BAL fluid were measured by immunoassay. Results: There was significantly greater expression of CD25 (P =.02) and HL A-DR (P =.04) by BAL fluid T-lymphocytes in corticosteroid-treated symptoma tic asthmatics. In bronchial biopsies there were no significant differences between the two groups in the numbers of AA1(+) cells (mast cells), EG2(+) cells (eosinophils) or MT1(+) T-lymphocytes. Levels of albumin, histamine, tryptase, and eosinophil cationic protein in BAL fluid did not differ sign ificantly between groups. Conclusions: Chronic corticosteroid-treated symptomatic asthma is associate d with persistent airway T-lymphocyte activation. This, however, is not nec essarily accompanied by the recruitment and activation of inflammatory cell s within the airways.