College of Animal Science and Veterinary Medicine, Heilongjiang Bayi Agricultural University, Daqing, China.
Front Cell Infect Microbiol. 2023 Apr 21;13:1156449. doi: 10.3389/fcimb.2023.1156449. eCollection 2023.
is the main pathogen inducing bovine foot rot. The infected site is often accompanied by a strong inflammatory response, but the specific inflammatory regulatory mechanism remains unclear.
A cow skin explants model was established to elucidate the mechanism of bacillus causing foot rot in cows, and to provide reference for future clinical practice.
Cow intertoe skin explants were cultured , and bacteria solution and nuclear factor-κB (NF-κB) inhibitor BAY 1-7082 were added to establish an infection model. Hematoxylin and eosin staining, terminal - deoxynucleotidyl transferase mediated nick end labeling, and immunohistochemistry were used to detect the pathological changes of the skin explants infected with , the degree of tissue cell apoptosis, and the expression of the apoptosis-related protein Caspase-3, respectively. RT-qPCR, Western blot, and ELISA were used to detect the activation of the NF-κB pathway and inflammatory cytokines by .
The intertoe skin structure of cows infected with changed with different degrees of inflammation, and the degree of tissue cell apoptosis was significantly increased ( < 0.01). In addition, infection with significantly increased the phosphorylation level of IκBα protein and up-regulated the expression level of NF-κB p65. The high expression and transcriptional activity of NF-κB p65 significantly increased the expression and concentration of the inflammatory cytokines TNF-α, IL-1β, and IL-8, thus inducing the occurrence of an inflammatory response. However, inhibition of NF-κB p65 activity significantly decreased the expression of inflammatory factors in the intertoe skin of cows infected with .
activates NF-κB signaling pathway by increasing the expression of TNF-α, IL-1β, IL-8 and other inflammatory factors, leading to foot rot in dairy cows.
是引起牛腐蹄病的主要病原体。感染部位常伴有强烈的炎症反应，但具体的炎症调控机制尚不清楚。
建立牛皮肤组织块培养模型，阐明 引起牛腐蹄病的机制，为今后的临床实践提供参考。
培养牛趾间皮肤组织块，加入 细菌溶液和核因子-κB（NF-κB）抑制剂 BAY 1-7082，建立 感染模型。采用苏木精-伊红染色、末端脱氧核苷酸转移酶介导的缺口末端标记法和免疫组织化学法检测 感染皮肤组织块的病理变化、组织细胞凋亡程度以及凋亡相关蛋白 Caspase-3 的表达。采用 RT-qPCR、Western blot 和 ELISA 检测 对 NF-κB 通路和炎症细胞因子的激活作用。
感染 的牛趾间皮肤结构发生不同程度的炎症改变，组织细胞凋亡程度显著增加（ < 0.01）。此外，感染 显著增加了 IκBα 蛋白的磷酸化水平，并上调了 NF-κB p65 的表达水平。NF-κB p65 的高表达和转录活性显著增加了促炎细胞因子 TNF-α、IL-1β 和 IL-8 的表达和浓度，从而诱导炎症反应的发生。然而，抑制 NF-κB p65 活性显著降低了感染 的牛趾间皮肤中炎症因子的表达。
通过增加 TNF-α、IL-1β、IL-8 等炎症因子的表达，激活 NF-κB 信号通路，导致奶牛腐蹄病的发生。
