Serum levels of soluble interleukin-2 receptor at acute asthma exacerbation: Relationship with severity of exacerbation and bronchodilator response

Citation
Jt. Kim et al., Serum levels of soluble interleukin-2 receptor at acute asthma exacerbation: Relationship with severity of exacerbation and bronchodilator response, INT A AL IM, 117(4), 1998, pp. 263-269
Citations number
31
Categorie Soggetti
Immunology
Journal title
INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY
ISSN journal
10182438 → ACNP
Volume
117
Issue
4
Year of publication
1998
Pages
263 - 269
Database
ISI
SICI code
1018-2438(199812)117:4<263:SLOSIR>2.0.ZU;2-V
Abstract
Background: T lymphocytes play a central role in the regulation of airway i nflammation in asthma, and T cell activation appears to be a characteristic feature of acute asthma. It is not clear, however, whether this is proport ional to the severity of acute asthma and is directly related to airway inf lammation relevant to airflow obstruction during acute asthma, It is presum ed that the extent to which bronchoconstriction or inflammation contributes to airflow obstruction in acute asthma may determine responsiveness to bro nchodilator therapy, Methods: Fifty asthmatic children who visited the emer gency room due to acute exacerbation were studied. Serum levels of soluble interleukin-2 receptor (sIL-2R), a marker of T cell activation, were measur ed at the time of acute exacerbation and of clinical remission, At acute ex acerbation, FEV1 was assessed before and after the administration of aeroso lized 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 cli nical remission (676+/-211 U/ml). It correlated positively with the severit y of exacerbation (r = 0.47, p<0.01), but showed no significant relationshi p 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 su ggest that in the context of acute asthma, T cell activation is proportiona l to disease activity, but its relationship to airway inflammation relevant to the genesis of airflow obstruction remains obscure.