Guo Jia, Cao Qinqin, Wang Zhihao, Wang Pengzi, Liu Kangjun, Guo Long, Dong Junsheng, Cui Luying, Li Jianji, Zhu Guoqiang, Meng Xia, Wang Heng
College of Veterinary Medicine, Yangzhou University, Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, Jiangsu, China; International Research Laboratory of Prevention and Control of Important Animal Infectious Diseases and Zoonotic Diseases of Jiangsu Higher Education Institutions, Yangzhou University, Yangzhou, China; Joint International Research Laboratory of Agriculture and Agri-product Safety of the Ministry of Education, Yangzhou, Jiangsu, China.
College of Veterinary Medicine, Yangzhou University, Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, Jiangsu, China; International Research Laboratory of Prevention and Control of Important Animal Infectious Diseases and Zoonotic Diseases of Jiangsu Higher Education Institutions, Yangzhou University, Yangzhou, China; Joint International Research Laboratory of Agriculture and Agri-product Safety of the Ministry of Education, Yangzhou, Jiangsu, China.
J Therm Biol. 2025 Apr;129:104114. doi: 10.1016/j.jtherbio.2025.104114. Epub 2025 Apr 25.
The incidence of bovine mastitis caused by K. pneumoniae increases during summer. This experiment aimed to clarify the connection between heat stress and K. pneumoniae-induced mastitis in terms of inflammatory responses and barrier function. From day 9-16 of the postpartum period, lactating rats were exposed to 35 °C in the daytime and 29 °C at night to establish a heat stress model. On day 8 of the heat stress treatment, the rat mastitis model was established by intramammary infection with K. pneumoniae through the milk ducts. At 12 h post-infection, the rectal temperature, serum biochemistry, K. pneumoniae burden, as well as histopathology, epithelium integrity, inflammatory response, and HSP70 expression of the mammary glands were detected. The results showed that heat-stressed rats with K. pneumoniae infection displayed higher rectal temperatures, more neutrophil infiltration, and more significant pathological damage to the acinar lumen. Heat stress promoted the disruption of the structural integrity of tight junction and the downregulation of relative protein expressions (ZO-1, Occludin, and Claudin-3) as a consequence of the increased production of inflammatory parameters (endotoxin, MPO, IL-1β, IL-6, and TNF-α) by accelerating NF-κB pathway activation and HSP70 expression after K. pneumoniae infection. Thus, heat stress disrupts mammary epithelium integrity, contributing to the pathogen invasion, and aggravates intramammary damage during K. pneumoniae mastitis by facilitating barrier disruption and inflammatory response, which could trigger more severe mastitis.
由肺炎克雷伯菌引起的牛乳腺炎发病率在夏季会升高。本实验旨在从炎症反应和屏障功能方面阐明热应激与肺炎克雷伯菌诱导的乳腺炎之间的联系。在产后第9至16天，将哺乳期大鼠白天置于35°C、夜间置于29°C环境中以建立热应激模型。在热应激处理的第8天，通过经乳腺导管接种肺炎克雷伯菌建立大鼠乳腺炎模型。感染后12小时，检测直肠温度、血清生化指标、肺炎克雷伯菌载量，以及乳腺的组织病理学、上皮完整性、炎症反应和热休克蛋白70（HSP70）表达。结果显示，感染肺炎克雷伯菌的热应激大鼠直肠温度更高，中性粒细胞浸润更多，腺泡腔的病理损伤更显著。热应激通过加速肺炎克雷伯菌感染后核因子κB（NF-κB）信号通路激活和HSP70表达，促进炎症参数（内毒素、髓过氧化物酶、白细胞介素-1β、白细胞介素-6和肿瘤坏死因子-α）生成增加，导致紧密连接结构完整性破坏以及相关蛋白表达（闭锁小带蛋白1、闭合蛋白和紧密连接蛋白3）下调。因此，热应激破坏乳腺上皮完整性，促使病原体入侵，并通过加剧屏障破坏和炎症反应加重肺炎克雷伯菌乳腺炎期间的乳腺内损伤，这可能引发更严重的乳腺炎。
