Interaction of primary human endometrial cells with Neisseria gonorrhoeae expressing green fluorescent protein
Interaction of primary human endometrial cells with Neisseria gonorrhoeae expressing green fluorescent protein
复制标题
DOI：
10.1046/j.1365-2958.2000.01694.x
复制
发表时间：
2000-01-01
影响因子：
3.6
通讯作者：
Heckels, JE
中科院分区：
文献类型：
--
作者：
Christodoulides, M;Everson, JS;Heckels, JE
淋病奈瑟菌感染子宫内膜是女性盆腔炎发展的关键阶段。体外培养的原代人子宫内膜细胞模型的开发，以研究淋球菌宿主细胞的相互作用。为了促进这些研究，淋球菌用含有来自维多利亚水母的gfp基因（编码绿色荧光蛋白（GFP））的杂合穿梭载体转化，以产生固有荧光细菌。该模型证明pill和Opa蛋白对于介导淋球菌与子宫内膜细胞的相互作用和诱导促炎细胞因子和趋化因子的分泌都是重要的。Pil（+）淋球菌表现出高水平的粘附和侵袭，与Opa表达无关，这与IL-8趋化因子分泌增加和IL-6细胞因子分泌减少有关。淋球菌攻击也引起TNF-α细胞因子分泌增加，但这与皮利或Opa表达无关，表明非粘附细菌组分的释放可能参与TNF-α诱导。因此，使用培养的原代子宫内膜细胞，连同淋球菌表达绿色荧光蛋白，有可能大大扩展我们的知识，在分子水平上，这种重要的人类病原体在盆腔炎性疾病的免疫生物学的作用。
Infection of the endometrium by Neisseria gonorrhoeae is a pivotal stage in the development of pelvic inflammatory disease in women. An ex vivo model of cultures of primary human endometrial cells was developed to study gonococcal-host cell interactions. To facilitate these studies, gonococci were transformed with a hybrid shuttle vector containing the gfp gene from Aequoria victoria, encoding the green fluorescent protein (GFP), to produce intrinsically fluorescent bacteria, The model demonstrated that both pill and Opa proteins were important for both mediating gonococcal interactions with endometrial cells and inducing the secretion of pro-inflammatory cytokines and chemokines. Pil(+) gonococci showed high levels of adherence and invasion, regardless of Opa expression, which was associated with increased secretion of IL-8 chemokine and reduced secretion of IL-6 cytokine, Gonococcal challenge also caused increased secretion of TNF-alpha cytokine, but this did not correlate with expression of pili or Opa, suggesting that release of components from non-adherent bacteria may be involved in TNF-alpha induction. Thus, the use of cultured primary endometrial cells, together with gonococci expressing green fluorescent protein, has the potential to extend significantly our knowledge, at the molecular level, of the role of this important human pathogen in the immunobiology of pelvic inflammatory disease.