Nod1, but not the ASC inflammasome, contributes to induction of IL-1β secretion in human trophoblasts after sensing of Chlamydia trachomatis.

Nod1, but not the ASC inflammasome, contributes to induction of IL-1β secretion in human trophoblasts after sensing of Chlamydia trachomatis.
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DOI:
10.1038/mi.2012.63
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发表时间:
2013-03
期刊:
影响因子:
8
通讯作者:
--
中科院分区:
医学1区
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--
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沙眼衣原体(Chlamydia trachomatis,Ct)是一种专性胞内致病菌。以前,我们发现Ct感染人滋养层细胞会触发促炎细胞因子IL-1β的分泌。本研究旨在了解Ct感染后滋养细胞产生IL-1β的天然免疫途径。我们采取的方法是抑制与衣原体感染相关的关键Toll样受体(TLR)、Nod样受体(NLR)和炎性小体组分的表达或功能。在本研究中,我们报告了Ct诱导的滋养细胞IL-1β分泌与IL-1β mRNA的转录、IL-1β前体的翻译和加工以及caspase-1的激活有关。此外,我们证明了Ct诱导的滋养层IL-1β的产生和分泌不依赖于TLR 2、TLR 4、MyD 88和Nalp 3/ASC炎性体。相反,我们报告,第一次,Nod 1介导滋养层IL-1β分泌的重要性,响应Ct感染。
Chlamydia trachomatis (Ct) is an obligate intracellular bacterial pathogen. Previously, we showed that infection of human trophoblast cells by Ct triggers the secretion of the pro-inflammatory cytokine, IL-1β. The aim of this study was to understand the innate immune pathways involved in trophoblast production of IL-1β after Ct infection. The approach we took was to inhibit the expression or function of the key Toll-like receptors (TLRs), Nod-like receptors (NLRs) and inflammasome components that have been associated with chlamydia infection. In this study we report that Ct-induced trophoblast IL-1β secretion is associated with the transcription of IL-1β mRNA, the translation and processing of pro-IL-1β, and the activation of caspase-1. In addition, we demonstrate that Ct-induced IL-1β production and secretion by the trophoblast is independent of TLR2, TLR4, MyD88, and the Nalp3/ASC inflammasome. Instead we report, for the first time, the importance of Nod1 for mediating trophoblast IL-1β secretion in response to a Ct infection.
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