La mPGES-1 : elle nous rend malades !

Staphylococcus aureus increases Prostaglandin E2 secretion in cow neutrophils by activating TLR2, TLR4, and NLRP3 inflammasome signaling pathways

“…Within minutes of bacterial invasion, neutrophils are drawn to the infection site in response to soluble substances such as chemokines and cytokines, where they ingest the pathogens and kill them (Guerra et al, 2017). PGE 2 is one of the prostaglandins most closely associated with various inflammatory diseases (Pecchi et al, 2009) and induces inflammatory cytokines that mediate tissue harm at some stages in bacterial invasion (Tingting et al, 2018(Tingting et al, , 2019. Microbial membrane components of bacteria are generally identified by using TLRs, along with TLR2 and TLR4, which are activated through LPS and lipoproteins and are imperative factors for initiating innate immune responses such as inflammation (Langmann, 2015).…”

“…In particular, PGE 2 is present in higher concentrations during inflammation compared to other PG S , and it is involved in all responses leading to the typical symptoms of inflammation, including fever, edema, and pain (Wan et al, 2018). PGE 2 production and biosynthesis, through inflammation, are exceptionally regulated by COX-2 and microsomal PGE synthase (mPGES)-1 and are induced by a variety of pro-inflammatory factors, which include interleukin-6 (IL-6), tumor necrosis factorα (TNF-α), and interleukin-1β (IL-1β) (Pecchi et al, 2009). Preliminary laboratory discovery shows that the use of TLR2, TLR4, and NLRP3-deficient mice in tests revealed that these proteins are involved in macrophage PGE 2 secretion in response to S. aureus (Wu et al, 2020).…”