产后子宫细菌感染影响子宫生理和卵巢活动,造成生育问题。革兰氏阴性菌的外膜成分,脂多糖(LPS),参与局部炎症过程的启动,和其他细菌毒素,特别是脂肽,也被证明是有效的细胞因子诱导剂,通过Toll样受体2(TLR2)起作用。然而,TLR2对卵巢和黄体活动的可能不良反应尚未得到深入研究.TLR2在黄体(CL)血管中的强表达使我们假设TLR2激活可能参与黄体血管功能的破坏。因此,我们分析了Pam3CSK4(Pam3CysSerLys4)的作用,合成三酰化脂肽和TLR2/TLR1配体,关于间隙连接细胞间通信的功能,内皮细胞侵袭,在永生化的绵羊微血管内皮(OLENDO)细胞系中形成体外毛细血管样网络。Pam3CSK4处理OLENDO细胞在体外试管形成中被破坏,但对间隙连接细胞间通讯或OLENDO细胞迁移没有影响。此外,Pam3CSK4诱导NF-kB表达,OLENDO细胞中的IL6和IL8。此外,通过常规PCR确认OLENDO细胞中TLR(TLR1-10)和TLR共受体(MYD88,LY96/MD2和CD14)的基础可用性。最后,TLR2/TLR1的激活似乎改变了OLENDO细胞中毛细血管样结构的体外形成并诱导了炎症过程。
UNASSIGNED: Activation of TLR2/TLR1 alters in vitro formation of capillary-like structures and induces inflammatory processes in ovine luteal endothelial (OLENDO) cells.
UNASSIGNED: Postpartum bacterial infections of the uterus affect uterine physiology and ovarian activity, causing fertility problems. The outer membrane component of Gram-negative bacteria, lipopolysaccharide, is involved in the initiation of the local inflammatory processes, and other bacterial toxins, particularly lipopeptides, have also been shown to be potent cytokine inducers, acting via Toll-like receptor-2 (TLR2). However, the possible adverse effects of TLR2 on ovarian and luteal activities have not yet been investigated in depth. The strong expression of TLR2 in the blood vessels of the corpus luteum led us to hypothesize that TLR2 activation might participate in the disruption of luteal vascular functionality. Therefore, we analyzed the effects of Pam3CSK4 (Pam3CysSerLys4), a synthetic triacylated lipopeptide and TLR2/TLR1 ligand, on the functionality of gap junctional intercellular communication (GJIC), endothelial cell invasion, and in vitro capillary-like network formation in an immortalized ovine luteal endothelial (OLENDO) cell line. Pam3CSK4 treatment of OLENDO cells disrupted in vitro tube formation but had no effect on GJIC or migration of OLENDO cells. Furthermore, Pam3CSK4 induced the expression of NFKB, IL6, and IL8 in OLENDO cells. Additionally, the basal availability of TLRs (TLR1-10) and TLR co-receptors (MYD88, LY96/MD2, and CD14) in OLENDO cells was confirmed by conventional PCR. Finally, the activation of TLR2/TLR1 appears to alter in vitro formation of capillary-like structures and induce inflammatory processes in OLENDO cells.