Bacterial lipopolysaccharide induces an endocrine switch from prostaglandin F2alpha to prostaglandin E2 in bovine endometrium.
Bacterial lipopolysaccharide induces an endocrine switch from prostaglandin F2alpha to prostaglandin E2 in bovine endometrium.
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DOI：
10.1210/en.2008-1379
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发表时间：
2009-04
期刊：
影响因子：
4.8
通讯作者：
Sheldon IM
中科院分区：
文献类型：
--
作者：
Herath S;Lilly ST;Fischer DP;Williams EJ;Dobson H;Bryant CE;Sheldon IM
子宫内膜的大肠杆菌感染会导致产后子宫疾病，并与牛卵巢周期黄体期延长有关。催产素刺激的子宫内膜上皮细胞中的前列腺素 F2α (PGF) 启动黄体期的终止。与正常动物相比，子宫内膜大肠杆菌感染的动物外周血浆中脂多糖（LPS）和前列腺素E2（PGE）浓度较高，但PGF浓度较高。子宫内膜外植体对 LPS 的反应主要在培养基中积累 PGE，并且催产素不能逆转这种效应。子宫内膜细胞表达检测 LPS 所必需的 TLR4/CD14/MD-2 受体复合物。用 LPS 处理的上皮细胞和基质细胞具有比 PGF 更高的 PGE 稳态培养基浓度。花生四烯酸通过磷脂酶 2 (PLA2) 从细胞膜中释放出来，并通过合酶转化为前列腺素。用 LPS 处理上皮细胞和基质细胞不会改变 PGE 或 PGF 合酶的水平。然而，LPS 刺激上皮细胞中 PLA2 VI 组的水平增加，但不刺激 PLA2 IV 组 C 免疫反应蛋白的水平增加。子宫内膜细胞表达对 PGE 做出反应所必需的 EP2 和 EP4 受体，PGE 可以调节炎症并具有促黄体作用。总之，子宫内膜细胞检测到的LPS刺激了PGE而不是PGF的积累，这提供了解释子宫疾病动物黄体期延长的机制，并且这种PGE对于调节子宫内膜的炎症反应也可能很重要。
Escherichia coli infection of the endometrium causes uterine disease after parturition and is associated with prolonged luteal phases of the ovarian cycle in cattle. Termination of the luteal phase is initiated by prostaglandin F2α (PGF) from oxytocin-stimulated endometrial epithelial cells. Compared with normal animals, the peripheral plasma of animals with E. coli infection of the endometrium had higher concentrations of lipopolysaccharide (LPS) and prostaglandin E2 (PGE), but not PGF. Endometrial explants accumulated predominantly PGE in the culture medium in response to LPS and this effect was not reversed by oxytocin. Endometrial cells expressed the TLR4/CD14/MD-2 receptor complex necessary to detect LPS. Epithelial and stromal cells treated with LPS had higher steady-state media concentrations of PGE rather than PGF. Arachadonic acid is liberated from cell membranes by phospholipase 2 (PLA2) enzymes and converted to prostaglandins by synthase enzymes. Treatment of epithelial and stromal cells with LPS did not change the levels of PGE or PGF synthase enzymes. However, LPS stimulated increased levels of PLA2 group VI but not PLA2 group IV C immunoreactive protein in epithelial cells. Endometrial cells expressed the EP2 and EP4 receptors necessary to respond to PGE, which regulates inflammation as well as being luteotropic. In conclusion, LPS detection by endometrial cells stimulated the accumulation of PGE rather than PGF, providing a mechanism to explain prolonged luteal phases in animals with uterine disease, and this PGE may also be important for regulating inflammatory responses in the endometrium.
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DOI：
10.1530/rep-07-0229
发表时间：
2007-11
期刊：
Reproduction (Cambridge, England)
影响因子：
--
作者：
Herath S;Williams EJ;Lilly ST;Gilbert RO;Dobson H;Bryant CE;Sheldon IM
通讯作者：
Sheldon IM
DOI：
10.1530/rep-08-0171
发表时间：
2008-09
期刊：
Reproduction (Cambridge, England)
影响因子：
--
作者：
Donofrio G;Ravanetti L;Cavirani S;Herath S;Capocefalo A;Sheldon IM
通讯作者：
Sheldon IM
影响因子：
5.8
作者：
Hirata, T;Osuga, Y;Taketani, Y
通讯作者：
Taketani, Y
影响因子：
4.8
作者：
Arosh, JA;Banu, SK;Fortier, MA
通讯作者：
Fortier, MA
DOI：
10.1016/0160-5402(89)90053-3
发表时间：
1989-05-01
期刊：
JOURNAL OF PHARMACOLOGICAL METHODS
影响因子：
--
作者：
LEWIS, EJ;BISHOP, J;CASHIN, CH
通讯作者：
CASHIN, CH