BLV-miR-B1-5p Promotes Staphylococcus aureus Adhesion to Mammary Epithelial Cells by Targeting MUC1.

Simple Summary: Bovine leukemia virus (BLV) is a retrovirus found in cattle, which reduces the lifespan of infected cows and is significantly associated with the occurrence of mastitis in dairy herds. A thorough understanding of the impacts and mechanisms of BLV on the antimicrobial defense function of mammary epithelial cells in dairy cows is essential for preventing and managing bovine mastitis. BLV-encoded microRNAs (BLV-miRNAs) represent functional components that contribute to oncogenesis. This study aimed to examine how BLV-miR-B1-5p promotes Staphylococcus aureus (S. aureus) adhesion to bovine mammary epithelial (MAC-T) cells via miRNA target gene prediction and validation. The results indicate that BLV-miR-B1-5p promotes S. aureus adhesion to bovine mammary epithelial cells by targeting mucin 1 (MUC1). Bovine leukemia virus (BLV) is widely prevalent worldwide and can persistently infect mammary epithelial cells in dairy cows, leading to reduced cellular antimicrobial capacity. BLV-encoded microRNAs (BLV-miRNAs) can modify host genes and promote BLV replication. We previously showed that BLV-miR-B1-5p significantly promoted Staphylococcus aureus (S. aureus) adhesion to bovine mammary epithelial (MAC-T) cells; however, the pathway responsible for this effect remained unclear. This study aims to examine how BLV-miR-B1-5p promotes S. aureus adhesion to MAC-T cells via miRNA target gene prediction and validation. Target site prediction showed that BLV-miR-B1-5p could target the mucin family gene mucin 1 (MUC1). Real-time polymerase chain reaction, immunofluorescence, and dual luciferase reporter assay further confirmed that BLV-miR-B1-5p could target and inhibit the expression of MUC1 in bovine MAC-T cells while interfering with the expression of MUC1 promoted S. aureus adhesion to MAC-T cells. These results indicate that BLV-miR-B1-5p promotes S. aureus adhesion to mammary epithelial cells by targeting MUC1. [ABSTRACT FROM AUTHOR]