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首页> 外文期刊>Endocrinology >Epithelial and stromal cells of bovine endometrium have roles in innate immunity and initiate inflammatory responses to bacterial lipopeptides in vitro via Toll-like receptors TLR2, TLR1, and TLR6
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Epithelial and stromal cells of bovine endometrium have roles in innate immunity and initiate inflammatory responses to bacterial lipopeptides in vitro via Toll-like receptors TLR2, TLR1, and TLR6

机译：牛子宫内膜的上皮和基质细胞在先天免疫中发挥作用，并通过Toll样受体TLR2，TLR1和TLR6在体外对细菌脂肽发起炎症反应

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Bacteria often infect the endometrium of cattle to cause endometritis, uterine disease, and infertility. Lipopeptides are commonly foundamongbacteria and are detected by the Toll-like receptor (TLR) cell surface receptor TLR2 on immune cells. Heterodimers of TLR2 with TLR1 or TLR6 activate MAPK and nuclear factor-κB intracellular signaling pathways to stimulate inflammatory responses. In the endometrium, epithelial and stromal cells are the first to encounter invading bacteria, so the present study explored whether endometrial cells can also mount inflammatory responses to bacterial lipopeptides via TLRs. The supernatants of pure populations of primary bovine endometrial epithelial and stromal cells accumulated the cytokine IL-6 and the chemokine IL-8 in response to triacylated or diacylated bacterial lipopeptides. The accumulation of IL-6 and IL-8 in response to triacylated lipopeptides was reduced by small interfering RNA targeting TLR2 or TLR1 but not TLR6, whereas cellular responses to diacylated lipopeptide were reduced by small interfering RNA targeting TLR2, TLR1, or TLR6. Both lipopeptides induced rapid phosphorylation of ERK1/2, p38, and nuclear factor-κB in endometrial cells, and inhibitorsofERK1/ 2orp38limitedtheaccumulationofIL-6.Theovariansteroidsestradiolandprogesterone had little impact on inflammatory responses to lipopeptides. The endometrial epithelial and stromal cell responses to lipopeptides via TLR2, TLR1, and TLR6 provide a mechanism linking a wide range of bacterial infections to inflammation of the endometrium.
机译：细菌经常感染牛的子宫内膜，引起子宫内膜炎，子宫疾病和不育。脂肽通常在细菌中发现，并由免疫细胞上的Toll样受体（TLR）细胞表面受体TLR2检测。 TLR2与TLR1或TLR6的异二聚体可激活MAPK和核因子-κB细胞内信号通路，从而刺激炎症反应。在子宫内膜中，上皮细胞和基质细胞是最先遇到细菌侵袭的，因此本研究探讨了子宫内膜细胞是否还可以通过TLRs对细菌脂肽产生炎症反应。纯牛原代子宫内膜上皮细胞和基质细胞的上清液会响应三酰化或二酰化细菌脂肽积聚细胞因子IL-6和趋化因子IL-8。通过靶向TLR2或TLR1的小分子干扰RNA减少了对三酰脂肽反应的IL-6和IL-8的积累，但是通过针对TLR2，TLR1或TLR6的小分子干扰RNA减少了对二酰化脂肽的细胞反应。两种脂肽均能诱导子宫内膜细胞中ERK1 / 2，p38和核因子-κB的快速磷酸化，ERK1 / 2orp38的抑制剂限制了IL-6的积累。卵巢甾体类雌激素孕酮对脂肽的炎症反应影响很小。经由TLR2，TLR1和TLR6对脂肽的子宫内膜上皮和基质细胞应答提供了一种机制，可将多种细菌感染与子宫内膜炎症联系起来。

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