Guo Zhiyun, Chai Tongjie, Yu Luna, Liu Kuihao, Qu Zhengxiu, Zhang Zhaopeng, Liu Meiling, Qiu Jianhua, Wang Gang, Li Ning
College of Veterinary Medicine, Shandong Agricultural University, 7 Panhe Street, Tai'an City, 271000, Shandong Province, PR China; Shandong Provincial Key Laboratory of Zoonoses, Shandong Agricultural University, 7 Panhe Street, Tai'an City, 271018, Shandong Province, PR China; Sino-German Cooperative Research Centre for Zoonosis of Animal Origin Shandong Province, Shandong Agricultural University, 61 Daizong Street, Tai'an City, 271018, Shandong Province, PR China.
College of Veterinary Medicine, Shandong Agricultural University, 7 Panhe Street, Tai'an City, 271000, Shandong Province, PR China; Shandong Provincial Key Laboratory of Zoonoses, Shandong Agricultural University, 7 Panhe Street, Tai'an City, 271018, Shandong Province, PR China.
Poult Sci. 2025 Apr 16;104(8):105169. doi: 10.1016/j.psj.2025.105169.
The particulate matter (PM) generated during poultry farming is characterized by its complex composition and substantial emission levels. However, researches on the respiratory damage caused by poultry house PM and the underlying mechanisms remain limited. In this study, inhalable PM collected from duck houses was administered to experimental mice through inhalation exposure. After 10 days of short-term exposure and 30 days of long-term exposure, mice samples were collected for lung histopathological analysis and inflammatory cytokines detection. The results showed that inhalation of duck house PM induced pulmonary and systemic inflammatory responses in both groups of mice, with significant upregulation of IL-6 and CXCL2. Compared to short-term exposure, long-term exposure resulted in more severe microscopic lesions in the lungs. In addition, the concentrations of malondialdehyde (MDA) and glutathione (GSH) increased in mice, indicating that duck house PM could trigger oxidative stress in lungs, we also found duck house PM induced ferroptosis in mice. Furthermore, it was confirmed that duck house PM caused cell damage and increased intracellular iron levels in MLE-12 cells, and PM reduced GSH in a dose-dependent manner. Notably, ferroptosis inhibitor treatment effectively alleviated PM-induced cell damage. These findings indicated that duck house PM can induce ferroptosis in both mice and cells, and ferroptosis plays a critical role in duck house PM-induced lung damage. These results laid a solid foundation for further exploring the mechanism of PM-induced lung injury, and providing a new insight for targeting ferroptosis to treat such damage.
家禽养殖过程中产生的颗粒物（PM）具有成分复杂、排放量大的特点。然而，关于禽舍PM对呼吸道造成的损害及其潜在机制的研究仍然有限。在本研究中，将从鸭舍收集的可吸入PM通过吸入暴露的方式给予实验小鼠。经过10天的短期暴露和30天的长期暴露后，采集小鼠样本进行肺组织病理学分析和炎症细胞因子检测。结果表明，吸入鸭舍PM可在两组小鼠中诱导肺部和全身炎症反应，IL-6和CXCL2显著上调。与短期暴露相比，长期暴露导致肺部微观病变更严重。此外，小鼠体内丙二醛（MDA）和谷胱甘肽（GSH）的浓度升高，表明鸭舍PM可引发肺部氧化应激，我们还发现鸭舍PM可诱导小鼠铁死亡。此外，证实鸭舍PM可导致MLE-12细胞损伤并增加细胞内铁水平，且PM以剂量依赖的方式降低GSH。值得注意的是，铁死亡抑制剂治疗可有效减轻PM诱导的细胞损伤。这些发现表明，鸭舍PM可在小鼠和细胞中诱导铁死亡，且铁死亡在鸭舍PM诱导的肺损伤中起关键作用。这些结果为进一步探索PM诱导肺损伤的机制奠定了坚实基础，并为靶向铁死亡治疗此类损伤提供了新的见解。
