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

Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology

PubMedID: 11152173

Redington AE, Wilson JW, Walls AF, Madden J, Djukanovic R, Holgate ST, Howarth PH. Persistent airway T-lymphocyte activation in chronic corticosteroid-treated symptomatic asthma. Ann Allergy Asthma Immunol. 2000;85(6 Pt 1):501-7.
BACKGROUND
A small proportion of patients with asthma have persistent symptoms despite regular treatment with high-dose inhaled and/or oral corticosteroids. There is little information regarding immunopathology in such patients.

OBJECTIVE
To compare airway inflammatory changes in subjects with chronic corticosteroid-dependent symptomatic asthma (n = 5) and subjects with asthma that was clinically well controlled on inhaled corticosteroid therapy (n = 9). Subjects in the corticosteroid-dependent group were receiving long-term treatment with oral prednisolone and high-dose inhaled corticosteroids.

METHODS
Subjects underwent fiberoptic bronchoscopy with bronchoalveolar lavage (BAL) and bronchial biopsy. T-lymphocytes subsets and activation markers in BAL fluid and peripheral blood were determined by FACS analysis. Bronchial biopsies were stained immunohistochemically, and numbers of inflammatory cells quantitated. Inflammatory mediators in BAL fluid were measured by immunoassay.

RESULTS
There was significantly greater expression of CD25 (P = .02) and HLA-DR (P = .04) by BAL fluid T-lymphocytes in corticosteroid-treated symptomatic 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 significantly between groups.

CONCLUSIONS
Chronic corticosteroid-treated symptomatic asthma is associated with persistent airway T-lymphocyte activation. This, however, is not necessarily accompanied by the recruitment and activation of inflammatory cells within the airways.