Staphylococcus aureus (S. aureus) is one of the most infamous and widespread bacterial pathogens, causing a hard-to-estimate number of uncomplicated skin
infections and probably hundreds of thousands to millions of more severe, invasive
infections globally per year. S. aureus may also be acquired from animals, especially in the livestock industry. The interaction mechanism of host and S. aureus has significance for finding ways to against S. aureus
infection and control inflammatory response of host, while the molecular biological activities after S. aureus
infection, particular in inflammatory and immune cells are not fully clear. The present study aimed to explore whether
pattern recognition receptors (
PRRs) mediate
prostaglandin D2 (
PGD2) synthesis and
PGD2 participates in the regulation of inflammatory response in macrophages during S. aureus
infection or synthetic bacterial
lipopeptide (
Pam2CSK4) stimulation.
PGD2 secretion level was enhanced by mice peritoneal macrophages infected with the S. aureus. The results indicated that
PGD2 secretion was impaired in S. aureus infected-macrophages from
toll-like receptors 2 (TLR2)-deficient and NLR pyrin domain-containing 3 (NLRP3)-deficient mice.
PGD2 synthetase (hematopoietic
PGD synthase, HPGDS) inhibitors could reduce the activation of macrophage
mitogen-activated protein kinase (MAPK)/nuclear factor-κ-gene binding (NF-κB) signaling pathways. HPGDS inhibition impaired
cytokines (TNF-α, IL-1β, IL-10 and
RANTES) secretion and macrophage phagocytosis during S. aureus
infection. In addition, inhibition of endogenous
PGD2 synthesis was unable to affect the TLR2 and NLRP3 expression in S. aureus-infected macrophages. Taken together, macrophage
PGD2 secretion after S. aureus
infection depended on receptors TLR2 and NLRP3, and the induced
PGD2 participated in the regulation of inflammatory response in S. aureus-infected macrophages. Interestingly, it was found that exogenous
PGD2 down-regulated the
cytokines secretion and had no effect on phagocytosis in the S. aureus-infected macrophages.