Shen Dan, Wang Kai, Guo Zhendong, Huang Kai, Li Yansen, Li Chunmei
Research Centre for Livestock Environmental Control and Smart Production, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.
Changchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, State Key Laboratory of Pathogen and Biosecurity, Key Laboratory of Jilin Province for Zoonosis Prevention and Control, 573 Tulip Street, Changchun 130122, Jilin, China.
Poult Sci. 2025 Jun 2;104(9):105388. doi: 10.1016/j.psj.2025.105388.
Airborne particulate matter (PM) generated by intensive broiler production poses significant risks to poultry respiratory health, yet the molecular mechanisms underlying pulmonary injury remain poorly defined. In this study, PM was collected from a commercial broiler house. Fourteen-day-old AA broilers were exposed to fresh air (control, 0.47 mg·m³), or 4 and 8 mg·m³ total suspended particulates (TSP) for 7 days. iTRAQ-based proteomic profiling identified 4,605 proteins, with 64 differentially expressed (16 upregulated, 48 downregulated) in the high-dose group (8 mg·m³). Enrichment analysis revealed involvement of metabolic pathways, phosphatidylinositol signaling, ATP-binding cassette (ABC) transporters, autophagy, and phagosome-related processes. Key hub proteins-PIK3CD, PIK3C2α, SGK3, and MAP3K20-were highlighted by protein-protein interaction networks and validated by ELISA. Their expression levels correlated significantly with cytokine responses, microbial community shifts, and lung metabolites. RT-qPCR confirmed activation of the MyD88-dependent TLR4/NF-κB and MAPK signaling cascades, along with oxidative stress and apoptotic markers. These findings uncover a PI3K/Akt-centered inflammatory pathway in PM-induced broiler lung injury, offering novel targets for improving poultry respiratory health.
集约化肉鸡生产产生的空气传播颗粒物（PM）对家禽呼吸道健康构成重大风险，但肺部损伤的分子机制仍不清楚。在本研究中，从一家商业肉鸡舍收集了PM。将14日龄的AA肉鸡暴露于新鲜空气（对照组，0.47毫克·立方米）、或4毫克·立方米和8毫克·立方米的总悬浮颗粒物（TSP）中7天。基于iTRAQ的蛋白质组学分析鉴定出4605种蛋白质，高剂量组（8毫克·立方米）中有64种差异表达（16种上调，48种下调）。富集分析显示代谢途径、磷脂酰肌醇信号传导、ATP结合盒（ABC）转运蛋白、自噬和吞噬体相关过程参与其中。蛋白质-蛋白质相互作用网络突出了关键枢纽蛋白PIK3CD、PIK3C2α、SGK3和MAP3K20，并通过ELISA进行了验证。它们的表达水平与细胞因子反应、微生物群落变化和肺代谢产物显著相关。RT-qPCR证实了MyD88依赖的TLR4/NF-κB和MAPK信号级联的激活，以及氧化应激和凋亡标志物。这些发现揭示了PM诱导的肉鸡肺损伤中以PI3K/Akt为中心的炎症途径，为改善家禽呼吸道健康提供了新的靶点。
