Abstract
Abstract Particulate matter (PM) aggravates airway and lung inflammatory response in allergic asthma by directly inducing Th17 cells to secrete Th17 cell-associated inflammatory factors and chemokines. IL-17A is a key Th17 cell secretion pro-inflammatory cytokine. In this study, we investigated the role of IL-17A in PM-induced allergic asthma in mice. 7–8 weeks old wild type (WT) mice, and similarly IL-17A knockout (KO) mice, were divided into four experimental groups (healthy control, PM only, OVA only, OVA+PM treatment groups) and treated accordingly. Inflammatory cell and eosinophil infiltration were increased in the PM-induced WT mice compared to WT healthy control, but were decreased in KO mice compared to PM-induced WT mice. Among toll-like receptors (TLRs) that play an important role in innate immune response, TLR2/4/7 expression was significantly increased in PM-induced WT mice, but was reduced in KO mice. Furthermore, we observed decrease in mRNA expression of IL-13, IL-17A, IL-22, and TGF-β among cytokines of Th2 and Th17 cells in KO mice. PM-induced WT mice facilitated the overt histopathological symptoms of allergic asthma such as mucus overproduction and goblet cell hyperplasia while KO mice showed mitigated such responses compared to PM-induced allergic asthma WT mice. These results prove that IL-17A plays a key role in pathogenesis of PM-induced allergic asthma. This research was funded by the Ministry of Education. This research was funded by the Ministry of Education
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