NF-κB signaling pathway mechanism in cow intertoe skin inflammation caused by .

Background: 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.

Aim: 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.

Methods: 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 .

Results: 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 .

Conclusion: 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.