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首页> 外文期刊>Microbes and infection >Microbial compounds induce the expression of pro-inflammatory cytokines, chemokines and human beta-defensin-2 in vaginal epithelial cells.
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Microbial compounds induce the expression of pro-inflammatory cytokines, chemokines and human beta-defensin-2 in vaginal epithelial cells.

机译：微生物化合物诱导阴道上皮细胞中促炎性细胞因子，趋化因子和人β-防御素2的表达。

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摘要

Vaginal epithelium has a powerful innate immune system that protects the female reproductive organs from bacterial and fungal infections. In the present study, we aimed to explore whether the Toll-like receptor (TLR) signaling pathway and the induction of pro-inflammatory cytokines and antimicrobial peptides could contribute to the protection against pathogenic microorganisms in vaginal epithelia, using an immortalized vaginal epithelial cell line PK E6/E7 as a model. We found that TLR2 and TLR4 receptors are expressed in vivo in the vaginal epithelia and in vitro in PK E6/E7 vaginal epithelial cell line. The Gram-negative cell wall compound lipopolysaccharide (LPS), the Gram-positive compound peptidoglycan (PGN), heat-killed Candida albicans and zymosan significantly (P<0.05) induced the expression of pro-inflammatory cytokines and chemokines such as TNF-alpha and IL-8/CXCL8 in vaginal epithelial cells. Furthermore, the expression and production of human beta-defensin-2 (hBD2), an antimicrobial peptide with chemotactic functions, was also up-regulated in PK E6/E7 cells after treatment with LPS, PGN or C. albicans. Treatment of vaginal epithelial cells with microbial compounds induced the activation and nuclear translocation of NF-kappaB transcription factor, a key element of innate and adaptive immune responses. In our work, we provide evidence that microbial compounds induce the production of pro-inflammatory cytokines, chemokines and antimicrobial peptides in vaginal epithelial cells. In vivo, vaginal epithelial cell-derived inflammatory mediators and antimicrobial peptides may play important roles in vaginal immune responses and in the elimination of pathogens from the female reproductive tract.
机译：阴道上皮具有强大的先天免疫系统，可保护女性生殖器官免受细菌和真菌感染。在本研究中，我们旨在探讨永生化的阴道上皮细胞系是否可以通过Toll样受体（TLR）信号通路以及促炎性细胞因子和抗菌肽的诱导来保护阴道上皮免受病原微生物的侵害。 PK E6 / E7作为模型。我们发现TLR2和TLR4受体在体内在阴道上皮中表达，在体外在PK E6 / E7阴道上皮细胞系中表达。革兰氏阴性细胞壁复合脂多糖（LPS），革兰氏阳性复合肽聚糖（PGN），热杀死的白色念珠菌和酵母聚糖显着（P <0.05）诱导促炎性细胞因子和趋化因子如TNF-α的表达阴道上皮细胞中的IL-8 / CXCL8和IL-8 / CXCL8。此外，在用LPS，PGN或白色念珠菌处理后，PK E6 / E7细胞中人β-防御素-2（hBD2）（一种具有趋化功能的抗菌肽）的表达和产生也被上调。用微生物化合物处理阴道上皮细胞可诱导NF-κB转录因子的激活和核易位，NF-κB转录因子是先天性和适应性免疫反应的关键因素。在我们的工作中，我们提供证据表明微生物化合物可诱导阴道上皮细胞中促炎性细胞因子，趋化因子和抗菌肽的产生。在体内，阴道上皮细胞来源的炎性介质和抗菌肽可能在阴道免疫反应和从女性生殖道清除病原体中发挥重要作用。

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