IFN- γ Activates the TLR4-CCL5 Signaling Through Reducing Arginine Level, Leading to Enhanced Susceptibility of Bovine Mammary Epithelial Cells to Staphylococcus aureus

In this study, we utilized thein vitro bovine mammary epithelial cells (BMECs) model to explore the molecular mechanismvia transcriptome sequencing technology, immunofluorescence, and Western blotting. It was found that IFN- γ promoted the adhesion and invasion ofStaphylococcus aureus to BMECs through increasing the expression of TLR4-mediated CCL5 in BMECs. IFN- γ increased the activity of arginase II and reduced the level of arginine in cells, while the addition of arginine inhibited the expression of TLR4 and CCL5. An invasion experiment in mice further validated that IFN-γ treatment significantly increased the bacterial load in mammary glands and blood . However, the colonization and diffusion ofS. aureus were interestingly decreased after Arg supplement. These data reveal that increased IFN- γ reduces arginine levels and activates TLR4-CCL5 signaling, leading to enhanced susceptibility of BMECs toS. aureus. Our findings are helpful to understand the pathogenesis of dairy cow mastitis and provide a theoretical basis for improvement of mastitis resistance in dairy cows.
Source: Inflammation - Category: Allergy & Immunology Source Type: research