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首页> 外文期刊>Infection and immunity >Role for the Chlamydial Type III Secretion Apparatus in Host Cytokine Expression
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Role for the Chlamydial Type III Secretion Apparatus in Host Cytokine Expression

机译：衣原体III型分泌设备在宿主细胞因子表达中的作用

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In many important human pathogens, such as Shigella and Salmonella spp., the bacterial type III secretion (T3S) apparatus is required to initiate inflammation via activation of caspase-1- or NF-κB-dependent genes. Using an ex vivo infection model, the goal of the present study was to determine whether the chlamydial T3S apparatus also modulates the host inflammatory response. Infections of mouse peritoneal macrophages were performed with Chlamydia muridarum, and the expression of inflammatory cytokines was monitored by quantitative reverse transcription-PCR and enzyme-linked immunosorbent assay. Since there is no current genetic system for Chlamydia spp., blockade of T3S was accomplished pharmacologically using a T3S inhibitor called INP0007. It has been previously shown that INP0007 also blocks chlamydial growth in vitro and that the addition of exogenous iron completely reverses this deficit. The addition of iron to INP0007-treated C. muridarum-infected macrophages not only restored chlamydial growth deficit caused by INP0007 but also led to a multi-inclusion phenotype. Overall, T3S inhibition led to decreased interleukin-6 (IL-6), IL-1β, and CXCL10, whereas the tumor necrosis factor alpha levels were unchanged. Rescue of chlamydial growth by addition of iron sulfate did not restore cytokine production, implying that the decreased expression of many cytokines during infection was dependent on T3S and not solely on growth. In addition, the observation that the greatest effects of INP0007 were seen at late time points during infection suggests that a temporally regulated T3S effector protein(s) may be triggering the host cytokine response.
机译：在许多重要的人类病原体中，例如志贺氏菌和沙门氏菌 spp。，细菌III型分泌（T3S）装置需要通过激活caspase-1-或caspase-1来引发炎症。 NF-κB依赖性基因。使用离体感染模型，本研究的目的是确定衣原体T3S装置是否也调节宿主的炎症反应。用鼠膜衣原体感染小鼠腹膜巨噬细胞，并通过定量逆转录PCR和酶联免疫吸附法检测炎性细胞因子的表达。由于目前尚没有衣原体的遗传系统，因此可以通过药理学方法使用称为INP0007的T3S抑制剂来阻断T3S。以前已经证明INP0007在体外也能阻断衣原体的生长，外源铁的添加完全可以逆转这种缺陷。将铁添加到INP0007处理的 C中。感染了muridarum 的巨噬细胞不仅恢复了INP0007引起的衣原体生长缺陷，而且导致了多包涵体表型。总体而言，T3S抑制导致白介素6（IL-6），IL-1β和CXCL10降低，而肿瘤坏死因子α水平不变。通过添加硫酸铁来挽救衣原体的生长并不能恢复细胞因子的产生，这意味着感染过程中许多细胞因子表达的下降取决于T3S，而不仅取决于生长。另外，观察到INP0007的最大作用是在感染过程中的较晚时间点观察到的，这表明时间调节的T3S效应蛋白可能触发了宿主细胞因子的应答。

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