Type II pneumocytes filamentous actin rearrangements induced by Streptococcus pneumoniae in vitro

Objective Streptococcus pneumoniae (S.pn) invasion to host cells plays an important role in its pathogenesis, but the mechanism of invasion is poorly understood. The research was to find if S.pn can provoked filamentous actin (F-actin) rearrangements in vitro through signaling pathways. Methods With FITC-phalloidin, labelled F-actin, we observed F-actin rearrangements by S.pn adhesion of type Ⅱ pneumocytes (A 549 ). S.pn invasion of A 549 cells by pretreating A 549 cells with cytochalasin D. To find the possibility of F-actin rearrangements being blocked by TPK, PLC inhibitors, A 549 cells were pretreated with TPK inhibitors geneistein and PLC inhibitors U73122 respectively. Results Intact S.pn promoted F-actin rearrangements. Cytochalasin D was able to prevent S.pn from invasion into A 549 cells. Two subsets of inhibitors of TPK, PLC signal transduction molecules blocked F-actin rearrangements dose dependently. Conclusion S.pn provoked F-actin rearrangements through TPK, PLC signaling pathways, which further lead to S.pn invasion into A 549 cells. [