Background: T lymphocytes play a central role in the regulation of airway inflammation in asthma, and T cell activation appears to be a characteristic feature of acute asthma. It is not clear, however, whether this is proportional to the severity of acute asthma and is directly related to airway inflammation relevant to airflow obstruction during acute asthma. It is presumed that the extent to which bronchoconstriction or inflammation contributes to airflow obstruction in acute asthma may determine responsiveness to bronchodilator therapy. Methods: Fifty asthmatic children who visited the emergency room due to acute exacerbation were studied. Serum levels of soluble interleukin–2 receptor (sIL–2R), a marker of T cell activation, were measured at the time of acute exacerbation and of clinical remission. At acute exacerbation, FEV1 was assessed before and after the administration of aerosolized salbutamol. Results: The mean (±SD) serum level of sIL–2R at acute exacerbation (854±248 U/ml) was significantly higher (p<0.01) than at clinical remission (676±211 U/ml). It correlated positively with the severity of exacerbation (r = 0.47, p<0.01), but showed no significant relationship with bronchodilator response (r = –0.17, p = 0.20). Conclusion: A higher serum level of sIL–2R at acute exacerbation was associated with more severe exacerbation but not with lower bronchodilator response. These findings suggest that in the context of acute asthma, T cell activation is proportional to disease activity, but its relationship to airway inflammation relevant to the genesis of airflow obstruction remains obscure.

Keywords:
Soluble interleukin–2 receptor, T lymphocyte, Acute exacerbation, Clinical remission, Bronchodilator response, Bronchial asthma
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1999
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