关键词: Bovine mammary epithelial cells Bovine mastitis Phagosome Rab11A Staphylococcus aureus

Mesh : Animals Cattle rab GTP-Binding Proteins / metabolism genetics Staphylococcus aureus / physiology Female Epithelial Cells / microbiology Phagocytosis Staphylococcal Infections / veterinary microbiology Mastitis, Bovine / microbiology Mammary Glands, Animal / microbiology Endosomes / metabolism microbiology Lysosomes / metabolism microbiology Cell Line Phagosomes / microbiology

来  源:   DOI:10.1016/j.vetmic.2024.110091

Abstract:
Mastitis in dairy cows is mainly caused by bacteria, in which Staphylococcus aureus appears frequently. Epithelial cells, as a major physical barrier of mammary gland, play an important role in preventing mastitis in dairy cows. Our previous study reported that Rab11fip4 (an effector of Rab11) was significantly changed in response to stimulation by S. aureus. So, in this study, the role of Rab11A in phagocytosis of bovine mammary epithelial cells (MAC-T) against S. aureus was evaluated. First, changes of Rab11A and Rab11fip4 were analyzed in response to S. aureus by immunofluorescence and western blotting. Subsequently, the effects of Rab11A and Rab11fip4 on proliferation of S. aureus, as well as formation and function of late endosomes (LEs) and lysosomes (LYSs) were investigated. The results showed that, after infection, Rab11A and Rab11fip4 were recruited to phagosomes containing S. aureus. Rab11A promoted bacterial clearance and rescues the destruction of LEs and LYSs by S. aureus, whereas Rab11fip4 did the opposite. These findings provide new insights into phagocytosis and control of S. aureus in host cells, thus lay the foundation to elucidate the pathogenesis of S. aureus in bovine mastitis.
摘要:
奶牛乳房炎主要由细菌引起,金黄色葡萄球菌经常出现。上皮细胞,作为乳腺的主要物理屏障,在预防奶牛乳房炎方面发挥重要作用。我们先前的研究报道Rab11fip4(Rab11的效应物)响应于金黄色葡萄球菌的刺激而显著改变。所以,在这项研究中,评估了Rab11A在奶牛乳腺上皮细胞(MAC-T)针对金黄色葡萄球菌的吞噬作用中的作用。首先,通过免疫荧光和蛋白质印迹分析了Rab11A和Rab11fip4对金黄色葡萄球菌的反应。随后,Rab11A和Rab11fip4对金黄色葡萄球菌增殖的影响,以及晚期内体(LEs)和溶酶体(LYSs)的形成和功能进行了研究。结果表明,感染后,Rab11A和Rab11fip4被招募到含有金黄色葡萄球菌的吞噬体。Rab11A促进细菌清除并挽救金黄色葡萄球菌对LE和LYSs的破坏,而Rab11fip4则相反。这些发现为宿主细胞中金黄色葡萄球菌的吞噬和控制提供了新的见解,从而为阐明金黄色葡萄球菌在奶牛乳腺炎中的发病机制奠定基础。
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