Over exposure to particulate matter (PM) could irritate respiratory tract infection; while, Pseudomonas aeruginosa (P. aeruginosa) is one of the main common pathogens. Our study aims are to define whether PM exposure enhances the invasion of P. aeruginosa into the airway epithelia and to characterize the underlying mechanisms. Human bronchial epithelial cells (BEAS-2B) or BEAS-2B transfected by PAFR siRNA were challenged with PM and pretreated with N-acetylcysteine (NAC), LY294002 (PI3K inhibitor), BAY 11-7082 (NF-κB inhibitor), or CV-3988 (PAFR antagonist). P. aeruginosa invasion was evaluated using colony-forming units assay and confocal microscopy. Real-time RT-PCR, immunofluorescence, flow cytometry and western blotting were used to detect the genes or proteins expression. PM exposure promoted P. aeruginosa invasion into BEAS-2B cells through ROS-mediated PI3K pathway which enhanced the expression of PAFR, which could be alleviated by treatment with NAC, LY294002, and BAY 11-7082. Furthermore, NAC and PAFR siRNA attenuated PM-stimulated activation of PI3K pathway. Treatment with PAFR antagonist and siRNA also alleviated PM exposure-induced P. aeruginosa invasion into BEAS-2B cells. Our results demonstrated that PM exposure increased the PAFR expression and activated the PI3K pathway in a ROS-dependent manner. Upregulated PAFR and activated PI3K pathway formed a positive regulatory loop and promoted the invasion of P. aeruginosa into airway epithelia. These mechanisms may provide a novel approach against P.aeruginosa invasion.

过度接触颗粒物 (PM) 会刺激呼吸道感染；而铜绿假单胞菌（P. aeruginosa）是主要的常见病原菌之一。我们的研究旨在确定 PM 暴露是否会增强铜绿假单胞菌侵入气道上皮细胞并描述其潜在机制。用 PM 攻击转染 PAFR siRNA 的人支气管上皮细胞 (BEAS-2B) 或 BEAS-2B，并用 N-乙酰半胱氨酸 (NAC)、LY294002（PI3K 抑制剂）、BAY 11-7082（NF-κB 抑制剂）或 CV 预处理-3988（PAFR 拮抗剂）。铜绿假单胞菌使用菌落形成单位测定和共聚焦显微镜评估入侵。实时RT-PCR、免疫荧光、流式细胞术和蛋白质印迹用于检测基因或蛋白质的表达。PM 暴露促进铜绿假单胞菌通过 ROS 介导的 PI3K 途径侵入 BEAS-2B 细胞，从而增强 PAFR 的表达，这可以通过用 NAC、LY294002 和 BAY 11-7082 处理来缓解。此外，NAC 和 PAFR siRNA 减弱 PM 刺激的 PI3K 通路激活。用 PAFR 拮抗剂和 siRNA 治疗也减轻了 PM 暴露诱导的铜绿假单胞菌侵入 BEAS-2B 细胞。我们的结果表明，PM 暴露增加了 PAFR 的表达并以 ROS 依赖的方式激活了 PI3K 通路。上调的 PAFR 和激活的 PI3K 通路形成正向调节环，促进铜绿假单胞菌侵入气道上皮细胞。这些机制可能提供一种对抗铜绿假单胞菌入侵的新方法。