Regulatory Effect of PGE2-EP2/EP4 Receptor Pathway on Staphylococcus aureus-Induced Inflammatory Factors in Dairy Cow Neutrophils

文献类型： 外文期刊

第一作者： Zhao, Yi

作者： Zhao, Yi;Wang, Chao;Liu, Bo;Zhang, Shuangyi;Wang, Yongfei;Gong, Zhiguo;Zhao, Jiamin;Yang, Xiaolin;Bai, Yuting;Mao, Wei;Zhao, Yi;Wang, Chao;Liu, Bo;Zhang, Shuangyi;Gong, Zhiguo;Zhao, Jiamin;Yang, Xiaolin;Wang, Yongfei;Qian, Yinghong

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关键词： neutrophils of cows; Staphylococcus aureus Rosenbach; prostaglandin E-2; EP2/EP4 receptor pathway; anti-inflammatory therapy

期刊名称：BIOMOLECULES （ 影响因子：4.8； 五年影响因子：5.6 ）

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年卷期： 2025 年 15 卷 8 期

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收录情况： SCI

摘要： 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-kappa B 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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