Platelets inhibit the proliferation of Staphylococcus epidermidis by directly down-regulating G6PD

Beyond their seminal role in hemostasis and thrombosis, platelets (PLTs) are now acknowledged as having multiple roles in the host's defense against infection. PLTs are proven to exert antimicrobial functions in vitro, ex vivo, and in vivo. However, different species of bacteria interact with PLTs differentially. Data concerning the interaction between PLTs and Staphylococcus epidermidis (S. epidermidis), the major prevalent species of nosocomial pathogens, and their related mechanisms are limited. In this study, the direct effects of PLTs on the metabolism and proliferation of S. epidermidis were evaluated. The PLTs from peripheral blood were purified and washed. The PLTs were found to significantly inhibit the proliferation of S. epidermidis when they were cocultured in vitro. Moreover, qRT-PCR showed that the expression of G6PD of the bacteria, a key enzyme in the pentose phosphate pathway, had been down-regulated signally. When the products (GDL, IMP) of the phosphate pentose pathway (PPP) were added to the culture, the antibacterial effect of PLTs was alleviated. This study suggests that PLTs can directly inhibit the proliferation of S. epidermidis and regulate their glucose metabolism, which may play an important role in their direct antimicrobial functions.