Abstract
Streptococcus agalactiae (S. agalactiae) is a contagious obligate parasite of the udder in dairy cows. Here, we examined S. agalactiae-host interactions in bovine mammary epithelial cells (BMECs) in vitro. We found that S. agalactiae infected BMECs through laminin β2 and integrin. Crk, Vps25, and RhoA were differentially expressed in S. agalactiae-infected cells. S. agalactiae infection activated FAK and Crk. FAK deficiency decreased the number of intracellular S. agalactiae and Crk activation. Knockdown of Crk or Vps25 increased the level of intracellular S. agalactiae, whereas its overexpression had the opposite effect. RhoA expression and actin cytoskeleton were altered in S. agalactiae-infected BMECs. Crk and Vps25 interact in cells, and invaded S. agalactiae also activates Crk, allowing it to cooperate with Vps25 to defend against intracellular infection by S. agalactiae. This study provides insights into the mechanism by which intracellular infection by S. agalactiae is regulated in BMECs.