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首页> 外文期刊>Biology of Reproduction: Offical Journal of the Society for the Study of Reproduction >PGE(2) increases inflammatory damage in Escherichia coli-infected bovine endometrial tissue in vitro via the EP4-PKA signaling pathway
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PGE(2) increases inflammatory damage in Escherichia coli-infected bovine endometrial tissue in vitro via the EP4-PKA signaling pathway

机译：PGE（2）通过EP4-PKA信号通路在体外增加大肠杆菌感染牛子宫内膜组织的炎症损伤

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摘要

Endometritis is the most common bovine uterine disease following parturition. The role of prostaglandin E-2 (PGE(2)) in the regulation of endometrial inflammation and repair is well understood. Excess PGE(2) is also generated in multiple inflammatory diseases, including endometritis. However, it remains unclear whether PGE(2) is associated with pathogen-induced inflammatory damage to the endometrium. To clarify the role of PGE(2) in pathogen-induced inflammatory damage, this study evaluated the production of PGE(2), inflammatory factors, and damage-associated molecular patterns (DAMPs) in cultured Escherichia coli-infected bovine endometrial tissue. PGE(2) production was significantly higher in E. coli-infected tissue, and in E. coli-infected tissue treated with 15-prostaglandin dehydrogenase (15-PGDH) inhibitors, as compared to uninfected tissue. Phospholipase A2 (PLA2), cyclooxygenase-2 (COX-2), and microsomal prostaglandin E synthase-1 (mPGES-1) were also upregulated in E. coli-infected tissue, while concentrations of arachidonic acid (AA), leukotrienes, DAMPs, and other proinflammatory factors increased. The accumulation of PGE(2) clearly damaged the cultured tissue. Treatment with the COX-2, mPGES-1, EP4, and protein kinase A (PKA) inhibitors decreased the production of PGE(2), inflammatory factors, and DAMPs, simultaneously alleviating the E. coli-induced endometrial tissue damage. Therefore, the PGE(2) that was generated by COX-2 and mPGES-1 accumulated, and this pathogenic PGE(2) increased inflammatory damage by upregulating inflammatory factors and DAMPs in E. coli-infected bovine endometrial tissue. This upregulation of inflammatory factors and DAMPs might be regulated by the EP4-PKA signaling pathway.
机译：子宫内膜炎是分娩后最常见的牛子宫疾病。前列腺素E-2的作用（PGE（2））在子宫内膜炎炎症和修复的调节中得到了很好的理解。过量的PGE（2）也在多种炎性疾病中产生，包括子宫内膜炎。然而，仍然不清楚PGE（2）是否与病原体诱导的子宫内膜造成的炎症损伤有关。为了阐明PGE（2）在病原体诱导的炎症损伤中的作用，本研究评估了培养的大肠杆菌感染牛子宫内膜组织中PGE（2），炎症因子和损伤相关分子模式（潮湿）的产生。与未感染的组织相比，在大肠杆菌感染组织中，在大肠杆菌感染组织中，在大肠杆菌感染的组织中，在大肠杆菌感染的组织中，在大肠杆菌感染组织中，与未感染的组织相比，用15-前列腺素脱氢酶（15-PGDH）抑制剂。磷脂酶A2（PLA2），环氧化酶-2（COX-2）和微粒体前列腺素E合酶-1（MPGES-1）也被上调在大肠杆菌感染的组织中，而花生素酸（AA），白三烯，潮湿的浓度而且其他促炎因子增加。 PGE（2）的积累显然受到培养的组织。用COX-2，MPGES-1，EP4和蛋白激酶A（PKA）抑制剂治疗降低了PGE（2），炎症因子和潮湿的产生，同时缓解了大肠杆菌诱导的子宫内膜组织损伤。因此，通过COX-2和MPGES-1产生的PGE（2）和该致病PGE（2）通过上调炎性因子和湿度在大肠杆菌感染的牛子宫内膜组织中增加炎症损伤。这种炎症因子和潮湿的上调可能由EP4-PKA信号通路调节。

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