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

Abstract

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.

Detection of R576 interleukin-4 receptor αn allele gene, serum interleukin-4, and eosinophilic cationic protein in atopic dermatitis patients

“…Similar results were obtained by Di Lorenzo et al , Kandil et al , Joseph-Bowen et al, and Higashi et al [33–36] Eosinophils[3738] contain abundant quantities of cationic granule proteins including major basic protein, ECP, eosinophil-derived neurotoxin, and eosinophil peroxidase. All can cause injurious microbial and tissue effects, and deposition has been demonstrated in AD lesions.…”

Airway hyperresponsiveness and acute chest syndrome in children with sickle cell anemia

“…17 A significant association between asthma and ACS has been reported. [4][5][6] Such an association could be explained by the inflammatory mediators and oxidant species produced during an asthma exacerbation 18,19 increasing the expression of adhesion molecules 20 and hence adhesion of the erythrocytes to the vascular endothelium [21][22][23] resulting in a vaso-occlusive crisis. In addition, the hypoxemia associated with an asthma exacerbation could promote sickling in the pulmonary vessels and hence an ACS episode.…”

Impact of acute chest syndrome on lung function of children with sickle cell disease

“…The relationship could be explained by the increased release of inflammatory mediators and vascular leak occurring during an ACS episode, 20 increasing AHR and hence asthma. Alternatively, inflammatory mediators and oxidant species produced during an asthma exacerbation 21,22 might increase the expression of adhesion molecules 23 and hence facilitate the adhesion of erythrocytes to the vascular endothelium, 24,25 resulting in a vaso-occlusive crisis. In addition, the hypoxemia associated with an asthma exacerbation could promote sickling in the pulmonary vessels and hence trigger an ACS episode.…”