Fig. 8.

The relationship between PGE₂ and TLR2-, TLR4-, and ­NLRP3-mediated activation of macrophages after S. aureus infection. BLP in general of S. aureus is essential immunobiologically active compounds that activate mouse peritoneal macrophages via TLR2 and NLRP3 inflammasomes. This process can be optimized by TLR4 to ensure an effective immune response, which leads to the secretion of a series of inflammatory mediators inducing TNF-α, IL-1β, RANTES, and PGE₂ through MAPK, NF-κB, cAMP-PKA, and caspase-1 signaling (a). Meanwhile, BLP is required for S. aureus phagocytosis and their survival within peritoneal macrophages. These processes can be modified by exogenous PGE₂ treatment, but not endogenous PGE₂, which can decrease bacterial phagocytosis while also increasing intracellular killing, activation of TLR-mediated MAPK, and NF-κB signaling and can promote NLRP3 inflammasome priming and IL-1β secretion. The relationship between NLRP3-mediated IL-1β production and inhibition of intracellular invasion by S. aureus is unknown (b). The green arrows indicate activation, induction, or invasion; the pink arrows indicate recognition or interaction; the red arrows indicate modulation. COX-2, cyclooxygenases-2; TLR, toll-like receptors; PGE₂, prostaglandin E₂.