Guo Zhixin, Ma Yuze, Jia Zhibo, Wang Liping, Lu Xinyue, Chen Yuhao, Wang Yanfeng, Hao Huifang, Yu Shuixing, Wang Zhigang
State Key Laboratory of Reproductive Regulation & Breeding of Grassland Livestock, School of Life Sciences, Inner Mongolia University, Hohhot 010021, China.
School of Fisheries and Life Science, Dalian Ocean University, Dalian 116023, China.
iScience. 2023 Sep 9;26(10):107884. doi: 10.1016/j.isci.2023.107884. eCollection 2023 Oct 20.
() is a contagious obligate parasite of the udder in dairy cows. Here, we examined -host interactions in bovine mammary epithelial cells (BMECs) . We found that infected BMECs through laminin β2 and integrin. Crk, Vps25, and RhoA were differentially expressed in -infected cells. infection activated FAK and Crk. FAK deficiency decreased the number of intracellular and Crk activation. Knockdown of or increased the level of intracellular , whereas its overexpression had the opposite effect. RhoA expression and actin cytoskeleton were altered in -infected BMECs. Crk and Vps25 interact in cells, and invaded also activates Crk, allowing it to cooperate with Vps25 to defend against intracellular infection by . This study provides insights into the mechanism by which intracellular infection by is regulated in BMECs.
()是奶牛乳房的一种传染性专性寄生虫。在此,我们研究了其与牛乳腺上皮细胞(BMECs)的宿主相互作用。我们发现其通过层粘连蛋白β2和整合素感染BMECs。Crk、Vps25和RhoA在其感染的细胞中差异表达。其感染激活了FAK和Crk。FAK缺陷减少了细胞内其的数量以及Crk的激活。敲低其或Vps25增加了细胞内其的水平,而其过表达则有相反的效果。RhoA表达和肌动蛋白细胞骨架在其感染的BMECs中发生改变。Crk和Vps25在细胞中相互作用,且入侵的其也激活Crk,使其能够与Vps25合作以抵御其的细胞内感染。本研究为BMECs中其细胞内感染的调控机制提供了见解。