Université Grenoble Alpes, CNRS ERL5261, CEA BIG-BCI, INSERM UMR1036, Grenoble 38054, France.
Toxins (Basel). 2018 Sep 25;10(10):387. doi: 10.3390/toxins10100387.
Bacterial pore-forming toxins induce a rapid and massive increase in cytosolic Ca concentration due to the formation of pores in the plasma membrane and/or activation of Ca-channels. As Ca is an essential messenger in cellular signaling, a sustained increase in Ca concentration has dramatic consequences on cellular behavior, eventually leading to cell death. However, host cells have adapted mechanisms to protect against Ca intoxication, such as Ca efflux and membrane repair. The final outcome depends upon the nature and concentration of the toxin and on the cell type. This review highlights the repercussions of Ca overload on the induction of cell death, repair mechanisms, cellular adhesive properties, and the inflammatory response.
细菌孔形成毒素通过在质膜中形成孔和/或激活钙通道,导致细胞质中钙离子浓度的快速和大量增加。由于钙是细胞信号传递中的重要信使,钙离子浓度的持续增加对细胞行为有巨大的影响,最终导致细胞死亡。然而,宿主细胞已经适应了保护机制来防止钙中毒,例如钙外排和膜修复。最终结果取决于毒素的性质和浓度以及细胞类型。本文综述了钙超载对细胞死亡诱导、修复机制、细胞黏附特性和炎症反应的影响。