Effects Of PM2.5 On Expression Of TLR2/4 And MTOR Signaling Pathway In Allergic Rhinitis Nasal Epithelium Of Rat

Background:Numerous epidemiological studies have shown that air pollution can increase the risk of allergic rhinitis and asthma.In conjunction with allergens,air pollutant can act as an adjuvant to enhance Ig E responses,inducing expression of cytokines/chemokines and adhesion molecules,and leading to immune and inflammatory response dysfunction.However,the impact of PM2.5 exposure on the incidence of allergic rhinitis in rat models is rare,and its corresponding mechanism of action is not entirely clear.Objective:This study was designed to investigate whether PM2.5 can promote the imbalance of Th1 / Th2 immune response in OVA-induced allergic rhinitis in rats and its effect on expression of TLR2/4 and m TOR signaling pathway in nasal epithelium.Methods:To perform a statistics of the number of outpatients with allergic rhinitis in the Second Hospital of Jilin University in 2014;sampling and traceability analysis of PM2.5 in filter-based samplers.Wistar rats were injected intraperitoneally with OVA basal sensitization,and then instilled nasal instillation of allergic rhinitis animal model.Automated blood cell analyzer counts the percentage of eosinophils(EOS)in peripheral blood.Severity of inflammatory infiltration in rat nasal mucosa were observed by morphologic observation and HE stain.Ig E and cytokines such as interleukin(IL)-4,IL-5,IL-6,TGF-?,IL-1?,TNF-?,IL-10,IFN-?,IL-12 in serum and nasal lavage fluid were assessed by enzymelinked immunosorbent assay(ELISA)kit.TLR2/4 and m TOR,e IF4 E,4EBP,HIF-1? in nasal mucosa epithelial tissue of allergic rhinitis rats were detected by immunohistochemistry.Results:Exposure of rat to PM2.5 resulted in increased AR symptoms ? EOS% in peripheral blood and levels of Ig E in serum and nasal lavage fluid.It also can drivea Th2-biased immune response in rat model,and up-regulate expression of TLR2/4and m TOR signaling pathway in nasal epithelium of rat.Conclusion:PM2.5 can regulate the inflammatory response of AR by activating TLR2 / 4 and m TOR signaling pathway in nasal epithelium of rat.