کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5674062 | 1593683 | 2017 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
TGF-β1 promotes Staphylococcus aureus adhesion to and invasion into bovine mammary fibroblasts via the ERK pathway
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موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
میکروب شناسی
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چکیده انگلیسی
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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Microbial Pathogenesis - Volume 106, May 2017, Pages 25-29
Journal: Microbial Pathogenesis - Volume 106, May 2017, Pages 25-29
نویسندگان
Shuang Zhao, Yuanyuan Gao, Xiaojing Xia, Yanyi Che, Yuping Wang, Hongtao Liu, Yingying Sun, Wenbo Ren, Wenyu Han, Junling Yang, Liancheng Lei,