Integration of Transcriptomics and Mammary Epithelial Cell Models Reveals the Regulatory Mechanism of CXCR1 in E. Coli-Induced Bovine Mastitis.

Abstract

Escherichia coli (E. coli) types bovine mastitis is an inflammatory disease triggered by E. coli infection, with its pathogenesis closely linked to the hyperactivation of host immune regulatory networks. In this study, we established an E. coli-induced bovine mastitis model and systematically screened differentially expressed mRNAs using high-throughput sequencing. We first revealed the significantly upregulated expression of the C-X-C chemokine receptor 1 (CXCR1) gene in E. coli-infected mammary tissues. In vitro experiments confirmed that lipopolysaccharide (LPS) stimulation markedly upregulated CXCR1 expression in bovine mammary epithelial cells (bMECs). To further elucidate the functional role of CXCR1 in bMEC inflammation, knockdown experiments were performed. Results demonstrated that CXCR1 gene silencing significantly suppressed the secretion of key pro-inflammatory cytokines (IL-6, IL-8, and IL-1β), enhanced bMECs viability and proliferation, and effectively inhibited apoptosis. Mechanistic investigations suggested that CXCR1 likely mediates inflammatory responses through the TLR4/MyD88/NF-κB signaling pathway. This study systematically elucidates the critical regulatory role of CXCR1 in E. coli-induced bovine mastitis, providing a theoretical foundation for the development of targeted therapeutic strategies.