Naturally occurring prostaglandin E
2 (PGE
2) influences cytokine production regulation in bovine neutrophils exposed to
Staphylococcus aureus Rosenbach. Here, we employed bovine neutrophils as the primary experimental system, and administered specific inhibitors targeting various receptors, which were subsequently exposed to
S.
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Naturally occurring prostaglandin E
2 (PGE
2) influences cytokine production regulation in bovine neutrophils exposed to
Staphylococcus aureus Rosenbach. Here, we employed bovine neutrophils as the primary experimental system, and administered specific inhibitors targeting various receptors, which were subsequently exposed to
S. aureus. Cytokine expression levels in dairy cow neutrophils induced by
S. aureus via the endogenous PGE
2-EP2/4 receptor pathway were investigated, and its effects on P38, extracellular signal-regulated kinase (ERK), P65 activation, and phagocytic function in
Staphylococcus aureus Rosenbach-induced dairy cow neutrophils, were examined. Blocking cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase-1 (mPGES-1) enzymes substantially decreased PGE
2 production and release in
S. aureus-exposed bovine neutrophils. Cytokine output showed significant reduction compared to that in
SA113-infected controls. Phosphorylation of P38, ERK, and P65 signaling molecules was depressed in the infected group. Pharmacological interference with EP2/EP4 receptors similarly diminished cytokine secretion and phosphorylation patterns of P38, ERK, and P65, with preserved cellular phagocytic function. During
S. aureus infection of bovine neutrophils, COX-2 and mPGES-1 participated in controlling PGE
2 biosynthesis, and internally produced PGE
2 molecules triggered NF-κB and MAPK inflammatory pathways via EP2/EP4 receptor activation, later adjusting the equilibrium between cytokine types that promote or suppress inflammation. This signaling mechanism coordinated inflammatory phases through receptor-mediated processes.
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