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首页> 外文期刊>Infection and immunity >Effects of Estradiol on Lipopolysaccharide and Pam3Cys Stimulation of CCL20/Macrophage Inflammatory Protein 3 Alpha and Tumor Necrosis Factor Alpha Production by Uterine Epithelial Cells in Culture
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Effects of Estradiol on Lipopolysaccharide and Pam3Cys Stimulation of CCL20/Macrophage Inflammatory Protein 3 Alpha and Tumor Necrosis Factor Alpha Production by Uterine Epithelial Cells in Culture

机译：雌二醇对培养的子宫上皮细胞产生脂多糖和Pam3Cys刺激CCL20 /巨噬细胞炎性蛋白3α和肿瘤坏死因子α的影响

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We have previously demonstrated that rat uterine epithelial cells (UEC) produce CCL20/macrophage inflammatory protein 3 alpha (MIP3α) and tumor necrosis factor alpha (TNF-α) in response to live and heat-killed Escherichia coli and to the pathogen-associated molecular patterns (PAMP) lipopolysaccharide (LPS) and Pam3Cys. To determine whether estradiol (E2) modulates PAMP-induced CCL20/MIP3α and TNF-α secretion, primary cultures of rat UEC were incubated with E2 for 24 h and then treated with LPS or Pam3Cys or not treated for an additional 12 h. E2 inhibited the constitutive secretion of TNF-α and CCL20/MIP3α into culture media. Interestingly, E2 pretreatment enhanced CCL20/MIP3α secretion due to LPS and Pam3Cys administration. In contrast, and at the same time, E2 lowered the TNF-α response to both PAMP. To determine whether estrogen receptors (ER) mediated the effects of E2, epithelial cells were incubated with E2 and/or ICI 182,780, a known ER antagonist. ICI 182,780 had no effect on E2 inhibition of constitutive TNF-α and CCL20/MIP3α secretion. In contrast, ICI 182,780 reversed the stimulatory effect of E2 on LPS- and/or Pam3Cys-induced CCL20/MIP3α secretion as well as partially reversed the inhibitory effect of E2 on TNF-α production by epithelial cells. Overall, these results indicate that E2 regulates the production of TNF-α and CCL20/MIP3α by UEC in the absence as well as presence of PAMP. Since CCL20/MIP3α has antimicrobial activity and is chemotactic for immune cells, these studies suggest that regulation of CCL20/MIP3α and TNF-α by E2 and PAMP may have profound effects on innate and adaptive immune responses to microbial challenge in the female reproductive tract.
机译：先前我们已经证明，大鼠子宫上皮细胞（UEC）对活的和热杀死的大肠杆菌产生CCL20 /巨噬细胞炎性蛋白3α（MIP3α）和肿瘤坏死因子α（TNF-α）。以及与病原体相关的分子模式（PAMP）脂多糖（LPS）和Pam 3 Cys。为了确定雌二醇（E 2 ）是否调节PAMP诱导的CCL20 /MIP3α和TNF-α分泌，将大鼠UEC的原代培养物与E 2 孵育24小时，然后用LPS或Pam 3 Cys处理或再不处理12小时。 E 2 抑制TNF-α和CCL20 /MIP3α向培养基的组成性分泌。有趣的是，E 2 预处理可通过LPS和Pam 3 Cys的给药增强CCL20 /MIP3α的分泌。相反，同时，E 2 降低了对两种PAMP的TNF-α反应。为了确定雌激素受体（ER）是否介导E 2 的作用，将上皮细胞与E 2 和/或ICI 182,780（一种已知的ER拮抗剂）一起孵育。 ICI 182,780对E 2 对组成型TNF-α和CCL20 /MIP3α分泌的抑制作用无效。相比之下，ICI 182,780逆转了E 2 对LPS-和/或Pam 3 Cys诱导的CCL20 /MIP3α分泌的刺激作用，以及部分逆转了E 2 E 2 对上皮细胞产生TNF-α的影响。总体而言，这些结果表明，E 2 在不存在和存在PAMP的情况下通过UEC调节TNF-α和CCL20 /MIP3α的产生。由于CCL20 /MIP3α具有抗微生物活性并且对免疫细胞具有趋化性，因此这些研究表明E 2 和PAMP对CCL20 /MIP3α和TNF-α的调节可能对自身的先天性和适应性免疫反应产生深远的影响。女性生殖道中的微生物挑战。

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