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首页> 外文期刊>Prostaglandins, Leukotrienes, and Essential Fatty Acids >PGE(2) downregulates LPS-induced inflammatory responses via the TLR4-NF-kappa B signaling pathway in bovine endometrial epithelial cells
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PGE(2) downregulates LPS-induced inflammatory responses via the TLR4-NF-kappa B signaling pathway in bovine endometrial epithelial cells

机译：PGE（2）通过牛子宫内膜上皮细胞中的TLR4-NF-Kappa B信号通路下调LPS诱导的炎症反应

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摘要

Postpartum bacterial infections of the uterus cause endometritis in dairy cows. Inflammatory responses to bacterial infections in the bovine uterus were generated through pattern recognition receptors (PRRs) that bind to pathogen-associated molecules such as lipopolysaccharide (LPS) from Escherichia coli. Among these PRRs, Toll-like receptor 4 (TLR4) is primarily responsible for LPS recognition, which triggers inflammatory responses via mitogen-activated protein kinases (MAPKs) and NF-kappa B signaling activation, resulting in the expression of inflammatory mediators in mammals such as IL-8 and IL-6. Previous studies indicate that PGE(2) plays an important role in bacterial endometritis, although details on the mechanism underlying how it regulates LPS-induced inflammatory responses in bovine endometrial epithelial cells (bEECs) remain elusive. In the present study, bEECs were pre-treated with exogenous PGE(2) and/or PGF(2 alpha) prior to LPS stimulation. With PGE(2) pretreatment, we observed an augmentation in LPS-stimulated PKA, ERK, and I kappa B alpha phosphorylation and cyclooxygenase-2 (COX-2) and anti-inflammatory cytokine IL-6 expression and downregulation of prostaglandin E-2 receptor 4 (EP4) and TLR4 in bEECs. These results indicate that LPS-induced inflammatory responses through TLR4 signaling in bEECs could be downregulated by exogenous PGE(2) pre-treatment, but not PGF(2 alpha).
机译：子宫的产后细菌感染导致奶牛的子宫内膜炎。通过与来自大肠杆菌的病原体相关分子（PRRS）结合的图案识别受体（PRR）产生对牛子宫的细菌感染的炎症反应。在这些PRR中，Toll样受体4（TLR4）主要负责LPS识别，其通过丝裂原激活的蛋白激酶（MAPK）和NF-κB信号传导激活触发炎性反应，导致哺乳动物中的炎症介质表达作为IL-8和IL-6。以前的研究表明，PGE（2）在细菌子宫内膜炎中起重要作用，尽管关于它如何调节牛子宫内膜上皮细胞（BEECs）的LPS诱导的LPS诱导的炎症反应的机制的细节仍然难以捉摸。在本研究中，在LPS刺激之前用外源PGE（2）和/或PGF（2α）预处理BEEC。通过PGE（2）预处理，我们观察到LPS刺激的PKA，ERK和I KappaBα磷酸化和环氧氧酶-2（COX-2）和抗炎细胞因子IL-6表达和前列腺素E-2中的增强受体4（EP4）和TLR4在Beecs中。这些结果表明，通过在BEECs中通过TLR4信号传导的LPS诱导的炎症反应可以通过外源PGE（2）预处理来下调，但不是PGF（2α）。

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    Shen Yuan; Liu Bo; Mao Wei; Gao Ruifeng; Feng Shuang; Qian Yinghong; We Jindi; Zhang Shuangyi; Gao Long; Fu Changqi; Li Qianru; Deng Yang; Cao Jinshan;

  • 作者单位

    Inner Mongolia Agr Univ Coll Vet Med Lab Vet Pharmacol 306 Zhaowuda Rd Hohhot 010018 Peoples R;

    Inner Mongolia Agr Univ Coll Vet Med Lab Vet Pharmacol 306 Zhaowuda Rd Hohhot 010018 Peoples R;

    Inner Mongolia Agr Univ Coll Vet Med Lab Vet Pharmacol 306 Zhaowuda Rd Hohhot 010018 Peoples R;

    Inner Mongolia Agr Univ Coll Vet Med Lab Vet Pharmacol 306 Zhaowuda Rd Hohhot 010018 Peoples R;

    Inner Mongolia Agr Univ Minist Agr Key Lab Clin Diag &

    Treatment Tech Anim Dis 306 Zhaowuda Rd;

    Inner Mongolia Agr &

    Anim Husb Sci 22 Zhaojun Rd Hohhot 010031 Peoples R China;

    Inner Mongolia Agr Univ Coll Vet Med Lab Vet Pharmacol 306 Zhaowuda Rd Hohhot 010018 Peoples R;

    Inner Mongolia Agr Univ Coll Vet Med Lab Vet Pharmacol 306 Zhaowuda Rd Hohhot 010018 Peoples R;

    Inner Mongolia Agr Univ Coll Vet Med Lab Vet Pharmacol 306 Zhaowuda Rd Hohhot 010018 Peoples R;

    Inner Mongolia Agr Univ Coll Vet Med Lab Vet Pharmacol 306 Zhaowuda Rd Hohhot 010018 Peoples R;

    Inner Mongolia Agr Univ Coll Vet Med Lab Vet Pharmacol 306 Zhaowuda Rd Hohhot 010018 Peoples R;

    Inner Mongolia Agr Univ Coll Vet Med Lab Vet Pharmacol 306 Zhaowuda Rd Hohhot 010018 Peoples R;

    Inner Mongolia Agr Univ Coll Vet Med Lab Vet Pharmacol 306 Zhaowuda Rd Hohhot 010018 Peoples R;

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  • 正文语种 eng
  • 中图分类 生物化学;
  • 关键词

    PGE(2); Bovine endometrial epithelial cells; TLR4; Inflammatory response;

    机译：PGE（2）;牛子宫内膜上皮细胞;TLR4;炎症反应;

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