In bovine placentomes, the inflammatory response is considered important for the detachment of the fetal membrane from the caruncle after parturition. Glucocorticoids, a trigger of the onset of parturition, facilitate functional maturation of placentomes via prostaglandin (PG) and estrogen production in cattle. This study investigated how exogeneous glucocorticoids, which exert immunosuppressive effects, affect placental inflammation at parturition. Placentomes were collected immediately after spontaneous or induced parturition. Parturition was conventionally induced using PGF2α or dexamethasone or with a combination of triamcinolone acetonide and high-dose betamethasone (TABET treatment). Polymerase chain reaction (PCR) array analysis indicated that 9/13 C–C motif chemokine ligands (CCLs) were upregulated > two-fold in spontaneous parturition, with CCL2 and CCL8 being highly expressed. The expressions of CCL2, CCL8, C–C motif chemokine receptor 1 (CCR1), and CCR5 in caruncles were significantly higher in spontaneous parturition than in induced parturition. Although the clinical dose of dexamethasone did not influence the expression of these CCLs and CCRs, TABET treatment increased CCR1 expression. CCL8, CCR1, CCR2, and CCR5 were localized in the caruncular epithelial cells. CCR2 was also localized in the epithelial cells of the cotyledonary villi. This study is the first report to reveal the disruption in CCL and CCR expression in bovine placentomes at induced parturition. Enhanced glucocorticoid exposure for the induction of parturition may upregulate CCR1 expression in placentomes, but the treatment does not adequately promote CCL expression. Additionally, immunohistochemistry suggested that the CCL–CCR system is involved in the functional regulation of maternal and fetal epithelial cells in placentomes at parturition.

中文翻译：

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C-C基序趋化因子及其受体在自然和诱导分娩牛胎盘中的表达

在牛胎盘中，炎症反应被认为对于分娩后胎膜从肉阜上的分离很重要。糖皮质激素是分娩开始的触发因素，通过前列腺素 (PG) 和牛体内雌激素的产生促进胎盘功能成熟。本研究调查了发挥免疫抑制作用的外源性糖皮质激素如何影响分娩时的胎盘炎症。在自然分娩或诱导分娩后立即收集胎盘。通常使用 PGF2α 或地塞米松或使用曲安奈德和高剂量倍他米松的组合（TABET 治疗）诱导分娩。聚合酶链反应 (PCR) 阵列分析表明，9/13 C-C 基序趋化因子配体 (CCL) 在自然分娩中上调 > 两倍，CCL2 和 CCL8 高表达。CCL2、CCL8、C-C 基序趋化因子受体 1 (CCR1) 和 CCR5 在自然分娩中的表达显着高于诱导分娩。尽管地塞米松的临床剂量不影响这些 CCL 和 CCR 的表达，但 TABET 治疗增加了 CCR1 的表达。CCL8、CCR1、CCR2 和 CCR5 位于肉瘤上皮细胞中。CCR2 也位于子叶绒毛的上皮细胞中。这项研究是第一个揭示诱导分娩时牛胎盘中 CCL 和 CCR 表达中断的报告。为诱导分娩而增加糖皮质激素暴露可能会上调胎盘中 CCR1 的表达，但这种治疗并不能充分促进 CCL 的表达。此外，