Chlamydia trachomatis infection modulates trophoblast cytokine/chemokine production.

Chlamydia trachomatis infection modulates trophoblast cytokine/chemokine production.
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DOI:
10.4049/jimmunol.0800764
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发表时间:
2009-03-15
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
通讯作者:
Abrahams VM
Abrahams VM
中科院分区:
其他
文献类型:
--
作者:
de la Torre E;Mulla MJ;Yu AG;Lee SJ;Kavathas PB;Abrahams VM

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众所周知,宫内感染可能通过进入胎盘和胎儿而对妊娠构成威胁,并且临床研究表明细菌感染与早产密切相关。虽然沙眼衣原体(C. trachomatis;Ct)可以感染胎盘和蜕膜,但人们对其对滋养层细胞免疫功能的影响知之甚少。我们已经证明,Ct 感染滋养层细胞形成包涵体,并通过产生感染性基体来完成这些细胞内的生命周期。此外,Ct 感染会导致滋养层细胞产生细胞因子和趋化因子的差异调节。使用两种人类妊娠早期滋养层细胞系 Sw.71 和 H8,我们发现最显着的特征是 Ct 感染导致两种细胞系强烈诱导 IL-1β 分泌,并同时减少 MCP-1 (CCL2) 的产生。此外,我们发现滋养层的Ct感染会导致NFκB p65的裂解和降解。这些发现表明,衣原体感染对滋养层趋化因子和细胞因子分泌的影响涉及滋养层表达的先天免疫受体的激活以及细菌分泌到滋养层的毒力因子。这种改变的滋养层先天免疫反应可能对母胎界面的微环境产生深远的影响,并可能影响妊娠结局。
It is well established that intrauterine infections can pose a threat to pregnancy by gaining access to the placenta and fetus, and clinical studies have strongly linked bacterial infections with preterm labor. While Chlamydia trachomatis (C. trachomatis; Ct) can infect the placenta and decidua, little is known about its effects on trophoblast cell immune function. We have demonstrated that Ct infects trophoblast cells to form inclusions, and completes the life cycle within these cells by generating infectious elementary bodies. Moreover, infection with Ct leads to differential modulation of the trophoblast cell's production of cytokines and chemokines. Using two human first trimester trophoblast cell lines, Sw.71 and H8, the most striking feature we found was that Ct infection results in a strong induction of IL-1β secretion, and a concomitant reduction in MCP-1 (CCL2) production in both cell lines. In addition, we have found that Ct infection of the trophoblast results in the cleavage and degradation of NFκB p65. These findings suggest that the effect of a Chlamydia infection on trophoblast secretion of chemokines and cytokines involves both activation of innate immune receptors expressed by the trophoblast, and virulence factors secreted into the trophoblast by the bacteria. Such altered trophoblast innate immune responses may have a profound impact on the microenvironment of the maternal-fetal interface, and this could influence pregnancy outcome.
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