TGF-β1 promotes Staphylococcus aureus adhesion to and invasion into bovine mammary fibroblasts via the ERK pathway

• DOI: 10.1016/j.micpath.2017.01.044
• Publication Date: 2017-01-25T14:00:31Z
• Authors: Shuang Zhao; Yuanyuan Gao; Xiaojing Xia; Yanyi Che; Yuping Wang; Hongtao Liu; Yingying Sun; Wenbo Ren; Wenyu Han; Junling Yang; Liancheng Lei
• Keywords: Staphylococcus aureus; 0303 health sciences; Time Factors; MAP Kinase Signaling System; Cell Culture Techniques; Cattle Diseases; Fibroblasts; Staphylococcal Infections; Fibrosis; Actins; Bacterial Adhesion; Collagen Type I; 3. Good health; 03 medical and health sciences; Mammary Glands, Animal; Gene Expression Regulation; Host-Pathogen Interactions; Animals; Lactation; Cattle; Female; RNA, Messenger; Mastitis, Bovine

Fibroblasts are the structural base of mammary breast tissues. TGF-β1 can regulate the fibrotic process; however, it remains unclear whether TGF-β1 influences the susceptibility of fibroblasts to bacteria. Staphylococcus aureus (S. aureus) is a major bacterium in both chronic and subclinical mastitis in lactating cows that acts by invading host cells. To better understand the function of TGF-β1 in bovine mammary fibroblasts' (BMFBs) susceptibility to bacteria as well as the mechanisms involved, a primary BMFB model was established by treating cells with TGF-β1 followed by infection with S. aureus. The results revealed that the adhesion and invasion of S. aureus into BMFBs was significantly increased after cells were treated with 5 ng/ml TGF-β1 for 12 h. Moreover, TGF-β1 can increase Collagen I and α-SMA expression via activation of ERK signaling. However, the increased adhesion and invasion of S. aureus can be blocked by specific antibodies against either Collagen I or α-SMA, indicating that the increased adhesion and invasion are dependent on TGF-β1-induced upregulation of both Collagen I and α-SMA. Using PD98059, an ERK inhibitor, could also decrease the adhesion and invasion of S. aureus. These results indicate that TGF-β1 could promote S. aureus adhesion to and invasion into BMFBs by increasing Collagen I and α-SMA expression and may provide a novel target for controlling bovine mastitis.