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To evaluate the activation of T-lymphocytes in the airways of patients with asthma, we attempted to measure the concentration of soluble interleukin-2 receptor (sIL-2R) in sputum extracts from asthma patients with acute attacks or in remission. The large amount of alkaline phosphatase in the sputum extracts excluded the use of an ELISA kit. Measurement was attempted by radiolabeling the second antibody in the ELISA kit. sIL-2R was detectable in 10/23 (43%) of the sputum extracts from patients with acute asthma attacks, but not in those from patients in remission (n = 12, p < 0.02). These observations suggest that T-lymphocyte activation takes place in the airways of patients with acute asthma attacks.

Bronchial hyperresponsiveness (BHR) was evaluated before and after antigen challenge in 12 patients with bronchial asthma as allergic reaction to house dust mites. Six out of the 12 showed an increase in BHR 48 hours after antigen challenge. Although there was no difference in the decrease of FEV1.0 in IAR and LAR between patients with (group A) and without (group B) the increase of BHR after antigen challenge, patients in group A expectorated a significantly larger number of clumps of respiratory epithelial cells (Creola bodies, CrB) in their sputum in both IAR and LAR. In addition, the degree of the increase of BHR significantly correlated with the CrB score, which was determined from the number and the size of CrB. These results suggest that epithelial desquamation participates in the increase of BHR after antigen challenge. The concentration of the eosinophil cationic protein (ECP) in their sputum did not change significantly in IAR and LAR compared with that before antigen challenge. There was no difference in the concentration of ECP in their sputum between the two groups either. One antigen challenge seemed to be too mild to induce an elevation of the concentration of ECP in their sputum. Judging from the fact that CrB could be observed not only at LAR but also IAR, epithelial desquamation seemed to be dependent on the degree of damage before antigen challenge rather than on the activation of eosinophils after antigen challenge.