Toxic Shock Syndrome Toxin 1 Induces Immune Response via the Activation of NLRP3 Inflammasome.

摘要: Staphylococcus aureus is a Gram-positive opportunistic pathogen which causes infections in variety of vertebrates. Virulence factors are the main pathogenesis S. as pathogen, induce host's innate and adaptive immune responses. Toxic shock syndrome toxin 1 (TSST-1) one most important virulence aureus. However, role nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) TSST-1-induced response still unclear. Here, purified recombinant TSST-1 (rTSST-1) was prepared used to stimulate mouse peritoneal macrophages. The results showed that under action adenosine-triphosphate (ATP), rTSST-1 significantly induced interleukin-1β (IL-1β) tumor necrosis factor-α (TNF-α) production macrophages dose-dependent. In addition, rTSST-1+ATP-stimulated cytokine macrophage depends on activation toll like 4 (TLR4), but not TLR2 cells. Furthermore, NLRP3-/- mice stimulated with rTSST-1+ATP low levels IL-1β compared wild-type mice. These demonstrated can expression inflammatory cytokines via TLR4 NLRP3 signaling pathways. Our study provides new information about mechanism TSST-1-inducing