Chlamydia psittaci Plasmid-Encoded CPSIT_P7 Elicits Inflammatory Response in Human Monocytes via TLR4/Mal/MyD88/NF-κB Signaling Pathway.
Chlamydia psittaci Plasmid-Encoded CPSIT_P7 Elicits Inflammatory Response in Human Monocytes via TLR4/Mal/MyD88/NF-κB Signaling Pathway.
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鹦鹉热衣原体质粒编码的 CPSIT_P7 通过 TLR4/Mal/MyD88/NF-κB 信号通路在人类单核细胞中引发炎症反应。
DOI：
10.3389/fmicb.2020.578009
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发表时间：
2020
影响因子：
5.2
通讯作者：
Wu Y
中科院分区：
文献类型：
--
作者：
Chen Q;Li Y;Yan X;Sun Z;Wang C;Liu S;Xiao J;Lu C;Wu Y
衣原体质粒是一种重要的毒力因子，其编码的质粒蛋白在衣原体感染和相应的免疫反应中起重要作用。然而，鹦鹉热衣原体的毒力因素和分子机制尚不清楚。在本研究中，我们研究了鹦鹉弓形虫质粒编码蛋白CPSIT_P7在调节THP-1细胞（人单核白血病细胞系）炎症反应中的作用和机制。基于细胞因子阵列，CPSIT_P7诱导THP-1细胞中白细胞介素-6 （IL-6）、白细胞介素-8 （IL-8）和单核细胞趋化蛋白-1 （MCP-1）的表达。此外，在使用小干扰RNA沉默toll样受体4 （TLR4）基因并转染编码TLR4的显性负质粒（pZERO-hTLR4）后，CPSIT_P7刺激的IL-6、IL-8和MCP-1的表达水平下降。我们进一步证明，转染编码MyD88的显性阴性质粒（pDeNy-hMyD88）和编码Mal的显性阴性质粒（pDeNy-hMal）也可以消除相应蛋白的表达。Western blot和免疫荧光分析结果显示，CPSIT_P7可激活THP-1细胞的核因子κB （NF-κB）信号通路。总之，我们的研究结果表明，CPSIT_P7诱导TLR4/Mal/MyD88/NF-κB信号轴，因此有助于炎症细胞因子反应。
The chlamydial plasmid, an essential virulence factor, encodes plasmid proteins that play important roles in chlamydial infection and the corresponding immune response. However, the virulence factors and the molecular mechanisms of Chlamydia psittaci are not well understood. In the present study, we investigated the roles and mechanisms of the plasmid-encoded protein CPSIT_P7 of C. psittaci in regulating the inflammatory response in THP-1 cells (human monocytic leukemia cell line). Based on cytokine arrays, CPSIT_P7 induces the expression of interleukin-6 (IL-6), interleukin-8 (IL-8), and monocyte chemoattractant protein-1 (MCP-1) in THP-1 cells. Moreover, the expression levels of IL-6, IL-8, and MCP-1 stimulated by CPSIT_P7 declined after silencing of the Toll-like receptor 4 (TLR4) gene using small interfering RNA and transfection of a dominant negative plasmid encoding TLR4 (pZERO-hTLR4). We further demonstrated that transfection with the dominant negative plasmid encoding MyD88 (pDeNy-hMyD88) and the dominant negative plasmid encoding Mal (pDeNy-hMal) could also abrogate the expression of the corresponding proteins. Western blot and immunofluorescence assay results showed that CPSIT_P7 could activate nuclear factor κB (NF-κB) signaling pathways in THP-1 cells. Altogether, our results indicate that the CPSIT_P7 induces the TLR4/Mal/MyD88/NF-κB signaling axis and therefore contributes to the inflammatory cytokine response.
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影响因子：
37.8
作者：
Dechend, R;Maass, M;Gulba, DC
通讯作者：
Gulba, DC
影响因子：
3.1
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作者：
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影响因子：
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作者：
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通讯作者：
Zhong, Guangming