Zhang Jianlong, Liu Chong, Zhao Guangrong, Li Meng, Ma Di, Meng Qingguo, Tang Wenli, Huang Qingrong, Shi Peimin, Li Youzhi, Jiang Linlin, Yu Xin, Zhu Hongwei, Chen Guozhong, Zhang Xingxiao
School of Life Sciences, Ludong University, Yantai, China.
Shandong Provincial Key Laboratory of Quality Safty Monitoring and Risk Assessment for Animal Products, Ji'nan, China.
Front Pharmacol. 2022 Jun 21;13:924242. doi: 10.3389/fphar.2022.924242. eCollection 2022.
High concentrations of PM2.5 in enclosed broiler houses cause respiratory disorders in humans and animals. () is an opportunistic pathogen that can induce severe respiratory disease in animals under stress or with abnormal immune functions. Alveolar macrophages are lung-resident immune cells that play important roles in lung host defence and immune balance. In this study, the mechanism by which PM2.5 synergizes with . to damage alveolar macrophage function and induce inflammation was investigated. The results will provide a theoretical basis for improving the poultry breeding environment and preventing the recurrence of infection with . . Alveolar macrophages were stimulated by PM2.5 collected in an enclosed broiler house and . Phagocytosis was determined by the neutral red test. The apoptosis rate and cytoskeleton changes were observed by flow cytometry assays and laser scanning confocal microscopy. Protein levels related to autophagy and the mTOR pathway were detected by Western blotting. The results indicated that PM2.5 in combination with could decrease phagocytosis, inhibit autophagy, increase apoptosis, and destroy the cytoskeleton in alveolar macrophages. In addition, alveolar macrophages had significantly increased expression of mTOR pathway-related proteins in response to the synergistic stimulation of PM2.5 and . The above results confirmed that PM2.5 in poultry houses synergized with to impede alveolar macrophage function and caused more severe respiratory system injuries through a process closely related to the activation of the mTOR signalling pathway.
封闭肉鸡舍内高浓度的细颗粒物2.5（PM2.5）会导致人和动物出现呼吸系统疾病。（某病原体名称）是一种机会致病菌，可在应激或免疫功能异常的动物中诱发严重的呼吸系统疾病。肺泡巨噬细胞是驻留在肺部的免疫细胞，在肺部宿主防御和免疫平衡中发挥重要作用。在本研究中，探究了PM2.5与（某病原体名称）协同作用破坏肺泡巨噬细胞功能并诱导炎症的机制。研究结果将为改善家禽养殖环境和预防（某病原体名称）感染复发提供理论依据。用封闭肉鸡舍收集的PM2.5和（某病原体名称）刺激肺泡巨噬细胞。通过中性红试验测定吞噬作用。通过流式细胞术和激光扫描共聚焦显微镜观察细胞凋亡率和细胞骨架变化。通过蛋白质印迹法检测与自噬和mTOR途径相关的蛋白质水平。结果表明，PM2.5与（某病原体名称）联合作用可降低肺泡巨噬细胞的吞噬作用，抑制自噬，增加细胞凋亡，并破坏细胞骨架。此外，在PM2.5和（某病原体名称）的协同刺激下，肺泡巨噬细胞中mTOR途径相关蛋白的表达显著增加。上述结果证实，禽舍中的PM2.5与（某病原体名称）协同作用，通过与mTOR信号通路激活密切相关的过程阻碍肺泡巨噬细胞功能，并导致更严重的呼吸系统损伤。
