Staphylococcus aureus is majorly involved in bovine mastitis; however, it weakly induces pro-inflammatory factors in mammary gland epithelial cells. We aimed to clarify the involvement of S. aureus in other inflammation types and its relationship with inflammatory factor secretion in bovine endometritis. We used live S. aureus (LSA)- and heat-killed S. aureus (HK-SA)-treated bovine endometrial tissue in vitro. The HK-SA-treated group showed significantly higher IL-6, IL-1β, TNF-α, CXCL1/2 and TLR2 expression than the LSA-infected group. Contrastingly, the LSA-infected group showed significantly higher PTGS2, mPGES-1, and EP4 expression than the HK-SA treated group. There was no significant between-group difference in hyaluronan-binding protein 1 expression, which suggested similar inflammatory responses. H&E results indicated that LSA and HK-SA induced shedding of endometrial gland epithelial cells. The LSA-infected group showed higher high-mobility group box 1 protein expression than the HK-SA treated groups, which indicated differences in signaling pathway activation. Further, the LSA-treated group had higher JNK and p38 MAPK levels while the HK-SA-treated group had higher IκB-α levels. There was no significant between-group difference in the ERK signaling pathway. Our findings indicate that the pathogen-associated molecular patterns (PAMPs) of S. aureus activate pro-inflammatory factor expression via the TLR2-ERK-NF-κB signaling pathway. Contrastingly, LSA induced PGE₂ accumulation via the TLR2/MAPKs signaling pathway. This is the first report that S. aureus and the PAMPs of S. aureus activate different signaling pathways and that LSA mainly induce PGE₂ accumulation rather than cytokine secretion.

金黄色葡萄球菌主要与牛乳腺炎有关；然而，它在乳腺上皮细胞中弱诱导促炎因子。我们旨在阐明金黄色葡萄球菌在其他炎症类型中的参与及其与牛子宫内膜炎炎症因子分泌的关系。我们在体外使用活的金黄色葡萄球菌(LSA) 和热灭活的金黄色葡萄球菌(HK-SA) 处理的牛子宫内膜组织. HK-SA 治疗组的 IL-6、IL-1β、TNF-α、CXCL1/2 和 TLR2 表达显着高于 LSA 感染组。相比之下，LSA 感染组的 PTGS2、mPGES-1 和 EP4 表达明显高于 HK-SA 治疗组。透明质酸结合蛋白 1 的表达没有显着的组间差异，这表明炎症反应相似。H&E 结果表明 LSA 和 HK-SA 诱导子宫内膜腺上皮细胞脱落。LSA 感染组显示出比 HK-SA 治疗组更高的高迁移率组框 1 蛋白表达，这表明信号通路激活存在差异。此外，LSA 治疗组具有更高的 JNK 和 p38 MAPK 水平，而 HK-SA 治疗组具有更高的 IκB-α 水平。ERK 信号通路没有显着的组间差异。我们的研究结果表明，病原体相关分子模式 (PAMP)金黄色葡萄球菌通过 TLR2-ERK-NF-κB 信号通路激活促炎因子表达。相比之下，LSA通过 TLR2/MAPKs 信号通路诱导 PGE ₂积累。这是首次报道金黄色葡萄球菌和的的PAMP金黄色葡萄球菌激活不同的信号传导途径和LSA主要诱导PGE ₂堆积而不是细胞因子分泌。