Apoptosis induced by Staphylococcus aureus in human monocytic U937 cells involves Akt and mitogen-activated protein (MAPK) phosphorylation

摘要

Staphylococcus aureus?(S. aureus) is a leading etiologic agent of nosocomial and community-acquired infectious diseases. Numerous studies have shown that,?S. aureus?could promote apoptosis in host cells. Unfortunately, the cellular and molecular mechanisms responsible for this phenomenon are still poorly understood. The present study aims to elucidate the signaling mechanisms involved in?S. aureus-induced U937 cells apoptosis by investigating the role of phosphatidylinositol 3-kinase/Akt (PI3K/Akt), mitogen-activated protein (MAPK) and caspases.?Our?results showed that,?S. aureus?decreased the expression of phosphorylation-Akt. In contrast,?S. aureus?increased phosphorylation-JNK1/2, phosphorylation-ERK1/2 and phosphorylation-p38 MAPK. Treatment of U937 cells with?S. aureus?resulted in?the?activation of caspase-3 and -9. Furthermore, caspases inhibitors, SP600125 (JNK inhibitor), SB203580 (p38MAPK inhibitor) and PD98059 (ERK inhibitor) decreased apoptosis in U937 cells.?However, LY294002 (Akt inhibitor) increased U937 cells apoptosis.?Taken together,?our?study for the first time suggest that?S. aureus?is able to enhance?apoptosis of U937 cells through inhibition of PI3K/Akt and activation of MAPK signaling pathways.