Purified Streptococcus pneumoniae Endopeptidase O (PepO) Enhances Particle Uptake by Macrophages in a Toll-Like Receptor 2- and miR-155-Dependent Manner.

摘要: ABSTRACT Insights into the host-microbial virulence factor interaction, especially immune signaling mechanisms, could provide novel prevention and treatment options for pneumococcal diseases. Streptococcus pneumoniae endopeptidase O (PepO) is a newly discovered ubiquitously expressed protein. A PepO-mutant strain showed impaired adherence to invasion of host cells compared with isogenic wild-type strain. It still unknown whether PepO involved in defense response infection. Here, we demonstrated that enhance phagocytosis Staphylococcus aureus by peritoneal exudate macrophages (PEMs). Further studies stimulation upregulated expression microRNA-155 (miR-155) PEMs time- dose-dependent manner. PepO-induced enhanced was decreased transfected an inhibitor miR-155, while it increased mimic miR-155. We also revealed upregulation miR-155 mediated Toll-like receptor 2 (TLR2)–NF-κB downregulated SHIP1. Taken together, these results indicate induces PEMs, contributing pneumococci aureus.