Prostaglandin E2 promotes Pam3CSK4-induced inflammation in endometrial epithelial cells of cattle
Prostaglandin E2 promotes Pam3CSK4-induced inflammation in endometrial epithelial cells of cattle
复制标题
前列腺素 E2 促进 Pam3CSK4 诱导的牛子宫内膜上皮细胞炎症。
DOI：
10.1016/j.anireprosci.2018.11.010
复制
发表时间：
2019-01-01
影响因子：
2.2
通讯作者：
Cao, Jinshan
中科院分区：
文献类型：
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作者：
Shen, Yuan;Feng, Shuang;Cao, Jinshan
细菌污染经常损害牛的子宫功能，导致子宫疾病，如子宫内膜炎。牛子宫对细菌感染的炎症反应是通过模式识别受体产生的，包括负责识别Pam3CSK4的Toll样受体2(TLR2)。这种细胞反应通过刺激丝裂原活化蛋白激酶(MAPKs)和核因子(NF)-kappaB信号激活来诱导炎症反应，刺激炎症介质的表达。前列腺素(PG)E-2在细菌性子宫内膜炎中具有重要作用，尽管这些机制调控Pam3CSK4诱导的牛子宫内膜上皮细胞(BEECs)炎症反应的细节尚不清楚。在本研究中，观察了外源性PGE(2)在Pam3CSK4诱导的炎症反应中的作用。在Pam3CSK4作用前，外源性PGE(2)可增强Pam3CSK4刺激的蛋白激酶A(PICA)、细胞外信号调节激酶(ERK)和I-kappa B-α的磷酸化，刺激TLR2、环氧合酶-2和白介素6的功能，抑制PGE(2)受体4的激活。因此，外源性PGE(2)可增强Pam3CSK4通过TLR2信号在bEECs中诱导的炎症反应。
Bacterial contamination often impairs uterine function in cattle leading to uterine diseases such as endometritis. Inflammatory responses to bacterial infections in the uterus of cattle are generated through pattern recognition receptors, including Toll-like receptor 2 (TLR2), which is responsible for Pam3CSK4 recognition. This cellular response induces inflammatory responses through stimulation of mitogen-activated protein kinases (MAPKs) and nuclear factor (NF)-kappa B signaling activation, stimulating the expression of inflammatory mediators. Prostaglandin (PG) E-2 has important actions in bacterial endometritis, although details through which these mechanisms regulate Pam3CSK4-induced inflammatory responses in cattle endometrial epithelial cells (bEECs) remain unclear. In the present study there was examination of the actions of exogenous PGE(2) in Pam3CSK4-induced inflammatory responses. The bEECs pre-treated with exogenous PGE(2) prior to Pam3CSK4 treatment had an augmented Pam3CSK4-stimulated phosphorylation of protein kinase A (PICA), extracellular signal-regulated kinase (ERK), and I kappa B-alpha; stimulation of TLR2, cyclooxygenase-2, and interleukin-6 functions; and suppression of the activation of PGE(2) receptor 4. Thus, Pam3CSK4-induced inflammatory responses through TLR2 signaling in bEECs were enhanced by exogenous PGE(2) pre-treatment.