Streptococcus Pneumoniae Invasion Mechanism Of Alveolar Type ¢ò Epithelial Cells - Streptococcus Pneumoniae In Vitro Trigger Alveolar Type ¢ò Epithelial Cells Of The F-actin Cytoskeleton Rearrangement

Streptococcus pneumoniae(S.pn) invasion of host cells plays an important role in its pathogenesis,but the mechanism of invasion is poorly understood.The research investigated whether S.pn can provoke filamentous actin(F-actin) rearrangements in vitro through signaling pathways. In this study, we still identified S.pn subcomponents and signaling pathways, which can lead to above the events. Method: Labelled F-actin with FITC-phalloidin,we observed F-actin rearrangements by S.pn adhesion of type II pneumocytes(A549). S.pn invasion of A549 cells was determined by pretreating A549 cells with Cytochalasin D .To investigate whether F-actin rearrangements can be blocked by TPK,PLC,Ca2 inhibitors,A549 cells were pretreated with TPK inhibitors geneistein and PLC inhibitors U73 122 and Ca2 inhibitors datrollene respectively. The effects of S.pn subcomponents, surface proteins and choline on F-actin rearrangements were characterized. A549 cells were loaded with Fura-2/AM to determine the concentration of cytosolic free calcium by S.pn adhesion of A549 cells after 30,60,90 minutes respectively. Result: Intact S.pn can promote F-actin rearrangements. Cytochalasin D is able to prevent S.pn invasion of A549 cells.Three subsets of inhit f TPK,PLC and Ca2 signal transduction molecules block F-actin rearrangeuients dose dependently.Surface proteins and choline of S.pn didn't affect F-actin rearrangements of A,49 cells.S.pn adhesion of A,49 cells increased cytosolic free calcium after 3 0,60,90 minuts. Conclusion : S.pn can provoke F-actin rearrangements through TPK,PLC and Ca2 signaling pathways, which will further lead to S.pn invasion of A,49 cells.