Yue Yang, Zhang Anchi, Liu Meng, Ge Yansong, Xu Enshuang, Zheng Jiasan
College of Animal Science and Veterinary Medicine, Heilongjiang Bayi Agricultural University, Daqing, China.
College of Animal Science and Veterinary Medicine, Heilongjiang Bayi Agricultural University, Daqing, China.
Vet Microbiol. 2025 May;304:110483. doi: 10.1016/j.vetmic.2025.110483. Epub 2025 Mar 17.
Foot rot is a contagious disease caused by F.necrophorum. It is responsible for economic losses in dairy farming. Studies on foot rot in dairy cows are focused on the isolation and identification of pathogens and treatment methods. Few studies have reported inflammatory changes in tissues and regulatory mechanisms following infection. Here, the effects of F.necrophorum infection on the skin explants and skin fibroblasts between the toes of cattle were analyzed using histopathology and other techniques. F.necrophorum infection increased the epidermal thickness and number of hair follicles and sebaceous glands. Other skin appendages exhibited varying degrees of necrosis, and a significant infiltration of inflammatory cells was noted in the interdigital skin explants. The expressions of pro-inflammatory cytokines (IL-1β and TNF-α) and key genes in the inflammatory signalling pathway (TNFR1 and NF-κB p65) were elevated. Treatment with the TNFR1 inhibitor CAY10500 reduced inflammatory cell infiltration and alleviated TNFR1 and p65 expression. An inflammatory cell model was established using different proportions of F.necrophorum to infect BDF cells. F.necrophorum infection significantly inhibited the proliferation and viability of BDF cells and enhanced the expression of TRADD, TRAF2, TNF-α, and IL-18. CAY10500 reduced the F.necrophorum infection-induced inflammatory response and induced inflammatory responses in interdigital skin explants and BDF cells by inhibiting the TNF-α/TNFR1/NF-κB signaling pathway. In summary, these findings provide new insights into the mechanism of inflammatory responses in dairy cows with foot rot.
腐蹄病是由坏死梭杆菌引起的一种传染性疾病。它会给奶牛养殖带来经济损失。关于奶牛腐蹄病的研究主要集中在病原体的分离鉴定和治疗方法上。很少有研究报道感染后组织中的炎症变化和调控机制。在此，利用组织病理学和其他技术分析了坏死梭杆菌感染对牛脚趾间皮肤外植体和皮肤成纤维细胞的影响。坏死梭杆菌感染增加了表皮厚度以及毛囊和皮脂腺的数量。其他皮肤附属器呈现出不同程度的坏死，并且在指间皮肤外植体中观察到炎症细胞的显著浸润。促炎细胞因子（IL-1β和TNF-α）以及炎症信号通路中的关键基因（TNFR1和NF-κB p65）的表达升高。用TNFR1抑制剂CAY10500进行治疗可减少炎症细胞浸润，并减轻TNFR1和p65的表达。使用不同比例的坏死梭杆菌感染BDF细胞建立了炎症细胞模型。坏死梭杆菌感染显著抑制了BDF细胞的增殖和活力，并增强了TRADD、TRAF2、TNF-α和IL-18的表达。CAY10500通过抑制TNF-α/TNFR1/NF-κB信号通路，减轻了坏死梭杆菌感染诱导的炎症反应，并在指间皮肤外植体和BDF细胞中诱导了炎症反应。总之，这些发现为奶牛腐蹄病炎症反应的机制提供了新的见解。
