Serum Levels of Soluble Interleukin-2 Receptor in Asthma Patients

The aim of this study was to assess the relevance of immunoinflammatory markers on the response to short acting β₂-agonist in acute asthma exacerbation. Thus, we measured serum eosinophil cationic protein (ECP) levels and sIL-2R at acute exacerbation in 52 adult patients with atopic asthma, and assessed forced expiratory volume in 1 s (FEV₁) before and after the administration of aerosolized salbutamol. After a cumulative dose of salbutamol causing a 10% improvement in FEV₁ from baseline [CD10, i.e. cumulative doses of salbutamol (800 µg) causing an improvement in FEV₁ from baseline to 10%] the patients were divided into two groups: group A with CD <10 and group B with CD >10. The bronchodilator response, as defined by a ΔFEV₁ (percentage of predictive value of FEV₁) of ≧10 predictive value, was shown by 40% of the patients. After 200, 400 and 800 µg of salbutamol, significant differences of FEV₁ with respect to baseline values were, respectively, p = 0.049, 0.0039 and 0.0014. In contrast, no significant difference of the means of FEV₁ between the doses of salbutamol was observed. Significant differences of ΔFEV₁ between 200 and 400 µg (p = 0.0002) and between 200 and 800 µg (p < 0.0001) were observed, but not between 400 and 800 µg of salbutamol. There were significant correlations between baseline values of predictive FEV₁ and serum ECP levels (rho = –0.60, p < 0.0001) and sIL-2R levels (rho = –0.35, p = 0.01) respectively. Besides, a correlation between ΔFEV₁ and serum ECP levels (rho = –0.53, p < 0.0001) was observed, whereas no correlation was found between ΔFEV₁ and sIL-2R. By analyzing differences between the two groups (A and B) for serum ECP levels, sIL-2R and blood eosinophil count, a significant difference was found for serum ECP levels. We conclude that subjects with acute exacerbation of asthma show high serum levels of ECP and sIL-2R and, more interestingly, that the response to brochodilator was higher in patients with lower serum ECP levels.

Section: Discussionmentioning

confidence: 99%

Measurement of Inflammatory Mediators of Eosinophils and Lymphocytes in Blood in Acute Asthma: Serum Levels of ECP Influence the Bronchodilator Response

Lorenzo¹,

Pacor

Morici³

et al. 2002

“…Several studies have demonstrated that serum levels of sIL–2R are elevated in patients with asthma [9, 16, 21]. It is not clear, however, whether the levels increase further during acute asthma [15, 16].…”

Section: Discussionmentioning

confidence: 99%

Serum Levels of Soluble Interleukin–2 Receptor at Acute Asthma Exacerbation: Relationship with Severity of Exacerbation and Bronchodilator Response

Kim

Koh

1998

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.

“…A significant inverse correla tion is found between pulmonary function and serum lev els of ECP or EPX [4][5][6]. T lymphocyte activation is also found in peripheral blood of asthma, which is dominant in symptomatic asthma [7,8], T lymphocyte-derived cytokines, such as interleukin-3 (IL-3), IL-5, and granulo cyte-macrophage colony-stimulating factor (GM-CSF) can activate eosinophils in vitro [1,2]. In the airways of asthmatics, a relation between these cytokines and eosino phil activation has been reported [9,10].…”

Section: Introductionmentioning

confidence: 99%

Serum Levels of Eosinophil Cationic Protein and IL-5 in Patients with Asthma without Systemic Corticosteroids

Motojima

Tateishi

Koseki

et al. 1997

Self Cite

We measured the serum levels of eosinophil cationic protein (ECP) and interleukin-5 (IL-5) in 39 patients with asthma (symptomatic 12, asymtomatic 27) without systemic corticosteroids and 49 healthy subjects. There were significant differences in serum levels in both ECP and IL-5 between symptomatic and asymptomatic asthma, and healthy subjects. A significant positive correlation was found between serum levels of ECP and IL-5. No significant correlation was found between %FEV₁ and serum level of ECP or IL-5, however, when the analysis was restricted to patients of less than 60 years of age, the correlations were significant. These results suggest that IL-5 is one of the factors that activate eosinophils even in peripheral blood, and that measurement of serum levels of ECP and IL-5 is useful for in vitro monitoring of asthma.