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ABSTRACT Background Eosinophil activation is associated with asthma. Whether air pollution affects the activation of blood eosinophils in patients with asthma remains unknown. In this study, we investigated the correlation between transcriptional activity in eosinophils and air pollutant exposure in patients receiving different levels of Global Initiative for Asthma (GINA) treatment. Methods We evaluated the expression levels of activation‐ and function‐related genes in eosinophils from patients with GINA 4 or 5 (n = 20), those with GINA 3 (n = 12), and normal individuals (n = 7); the eosinophils were activated with interleukin (IL)−5 or IL‐17. A land use regression model was used to estimate air pollutant exposure. The correlations between mRNA expression, lung function, and air pollutant exposure were investigated. Results The expression levels of TGFB1, IL7R, and TLR3 were significantly higher for patients with GINA 4 or 5 than for those with GINA 3 or normal individuals. The expression of certain genes, particularly in IL‐17‐activated eosinophils, was correlated with lung function decline in patients with GINA 4 or 5. For patients with GINA 4 or 5, NO2 exposure was correlated with upregulated TGFB1 expression in IL‐5‐activated eosinophils. For patients with GINA 3, O3 exposure was correlated with upregulated CCR5, IL5RA, IL7R, and TGFB1 expression in IL‐17‐activated eosinophils and upregulated IL7R expression in IL‐5‐activated eosinophils. Conclusion Patients with GINA 4 or 5 may exhibit elevated transcriptional activity in eosinophils; this elevation is correlated with lung function decline. Air pollution may affect eosinophil mRNA expression in patients with asthma.

Abstract Background Toll‐like receptor (TLR)‐7‐associated rhinovirus (RV) activation is involved in the pathogenesis of asthma. Plasmacytoid dendritic cells (pDCs) are the main interferon‐α‐producing cells against viruses. Objective To determine whether asthmatic patients and control subjects differ in terms of interferon‐α expression in pDCs under TLR‐7 or RV stimulation. Methods pDCs were identified in BDCA‐2+ and HLA‐DR+ peripheral blood mononuclear cells. Interferon‐α expression of pDCs was analyzed after TLR‐7 stimulation with or without interleukin 4 (IL‐4)/IL‐13 pretreatment. Interferon‐α expression was also analyzed after RV stimulation over periods of 24, 48, or 96 h with or without IL‐4 pretreatment. RV detection and molecular typing were assayed from throat swabs. Results Following TLR‐7 stimulation, the expression of intracellular interferon‐α was higher in the pDCs of normal subjects than those of asthmatic patients; however, pretreatment with IL‐4 was shown to reduce this effect. After 48‐ and 96‐h RV stimulation, we observed a notable increase in the production of interferon‐α of pDCs in normal subjects but not in asthmatic patients. Baseline interferon‐α expression in pDCs and the incidence of asthma exacerbation to emergency was higher among the 13% of patients identified as rhinovirus+ than among their RV counterparts. Conclusion Our study discovered the response to TLR‐7 stimulation in pDCs was compromised and the sustainability of interferon‐α expression to RV stimulation was reduced in pDCs of asthmatic patients, which provide further evidence of defective innate response and subspeciality to RV infection in asthma. The high exacerbation history founded in RV+ patients agrees with these findings. Further research is required for the modulatory effect of IL‐4 on TLR‐7 stimulated pDCs.