The role of endothelial microparticles in children with asthma: Does it promote atherosclerosis progress?

Abstract

Background:Asthma is a chronic inflammatory airway disease that has been linked to enhanced risks for atherosclerosis. The impact of asthma on cardiovascular disease risk in children is less well established. Asthma is defined by a history of respiratory symptoms and accompanied by airflow limitation, with heterogeneous clinical manifestations, and variability in the intensity of airway inflammation and remodeling. Endothelial microparticles (EMP) are biomarkers of endothelial dysfunction in several chronic diseases. Endothelial microparticles initiate an event of atherosclerotic plaque formation. Our study aimed to evaluate the role of endothelial microparticles in children with asthma.Methods:A cross-sectional study was performed on a total of 50 children with asthma aged seven‒17 years. Children with asthma exacerbations, infections, and steroid use were excluded. Endothelial microparticles were measured with beads, and the fluorescence signal was measured using a flow cytometer. Pro-inflammatory cytokines were measured by enzyme-linked immunosorbent assay (ELISA) method.Results:Based on the results from 50 asthmatic children, it was found that most children had a normal nutritional status, intermittent, and allergic asthma. The results of this study also showed that the circulation of asthmatic children found that the mean levels (µL) of CD31+/CD62E+, CD31+/CD62E-, and CD62E+/CD31- were 2,392.99 ± 7,787.94; 922.14 ± 1,554.03; 198.97 ± 387.68, with the average ratio of CD31+/CD62E+, which was ≤1.0 and identifies apoptosis. Path analysis results found that IL-6, TNF-α, and CD31+/CD62E- EMP played a role in peak expiratory flow rate (%PEFR, p = 0.02; p = 0.003; p = 0.04) in children with allergic asthma.Conclusions:Endothelial microparticles play a role on peak expiratory flow rate (PEFR) in children with allergic asthma. Further study is needed to investigate the role of these biomarkers and their correlation with pro-inflammatory cytokines in the mechanism of atherosclerosis progression.