黏着斑激酶信号通路在细菌侵入非吞噬细胞中的作用

摘要

细菌对宿主细胞的黏附和侵袭是引发传染病的重要步骤。细菌在黏附的过程中，其表面结构或特殊黏附分子和宿主细胞表面受体相互作用激活黏着斑激酶（focal adhesion kinase，FAK），通过 FAK/Src-Cortactin-Arp2/3通路和 FAK/PI3K-Rac 通路调控细胞骨架重排，促进细菌侵入非吞噬细胞。为了深入探讨细菌侵入非吞噬细胞的整个过程及调控机制，就细菌对非吞噬细胞的黏附、侵入以及细胞 FAK 信号通路在此过程中的调节作用进行综述。%The adhesion and invasion into eukaryotic cells are major steps in bacterial pathogenesis. In order to further study the entire process and molecular mechanisms of bacteria invading non-phagocytic cells,we reviewed the bacterial adhesion and invasion of non-phagocytic cells and the regulatory mechanisms of focal adhesion kinase(FAK)in this process. During the adhesion process,the interaction of surface adhesive molecules and special structures of bacteria with receptors of host cells activates the FAK to regulate the cytoskeletal rearrangement through FAK/Src-Cortactin-Arp2/3 and FAK/PI3K-Rac pathways,which promotes the bacterial invasion of non-phagocytic cells.