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通过Toll样受体11激活细胞外信号调节激酶信号通路可诱导受[病原体名称未给出]刺激的腹腔巨噬细胞产生白细胞介素-12 p40。

Activation of ERK Signaling via TLR11 Induces IL-12p40 Production in Peritoneal Macrophages Challenged by .

作者信息

Jin Xiaoxia, Gong Pengtao, Zhang Xichen, Li Guojiang, Zhu Tao, Zhang Mengge, Li Jianhua

机构信息

Key Laboratory of Zoonosis, Ministry of Education - College of Veterinary Medicine, Jilin UniversityChangchun, China.

Jilin Agricultural Science and Technology UniversityJilin, China.

出版信息

Front Microbiol. 2017 Jul 26;8:1393. doi: 10.3389/fmicb.2017.01393. eCollection 2017.

DOI:10.3389/fmicb.2017.01393
PMID:28798732
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5527353/
Abstract

, an obligate intracellular protozoan parasite, can infect a large variety of vertebrate hosts including the most economically important cattle. Infection with . is a main cause of abortion in both dairy and beef cattle, which causes great economic losses worldwide. However, the mechanism of host cell infection by . has not been fully elucidated, especially in terms of inflammatory responses. In this study, the effect of TLR-ERK signaling pathway on the synthesis of pro-inflammatory interleukin-12p40 in mouse peritoneal macrophages (PMϕ) challenged by . was investigated. Our results suggested that . infection quickly activated MEK-ERK signaling via TLR11 in PMϕ. In addition, . infection also caused upregulated production of IL-12p40 by PMϕ, which was significantly reduced with the blockade of TLR11/MEK/ERK pathway, suggesting that this upregulation of IL-12 p40 was TLR11 and MEK-ERK-activation dependent.

摘要

一种专性细胞内原生动物寄生虫，可感染包括经济上最重要的牛在内的多种脊椎动物宿主。感染该寄生虫是奶牛和肉牛流产的主要原因，在全球范围内造成巨大经济损失。然而，该寄生虫感染宿主细胞的机制尚未完全阐明，尤其是在炎症反应方面。在本研究中，研究了TLR-ERK信号通路对受该寄生虫攻击的小鼠腹腔巨噬细胞（PMϕ）中促炎白细胞介素-12p40合成的影响。我们的结果表明，该寄生虫感染通过PMϕ中的TLR11迅速激活MEK-ERK信号。此外，该寄生虫感染还导致PMϕ产生的IL-12p40上调，而TLR11/MEK/ERK通路的阻断可显著降低这种上调，表明IL-12 p40的这种上调依赖于TLR11和MEK-ERK激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8d/5527353/61758aca984f/fmicb-08-01393-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8d/5527353/609fd85fb7e3/fmicb-08-01393-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8d/5527353/866e39edc3b9/fmicb-08-01393-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8d/5527353/acba3638bc3e/fmicb-08-01393-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8d/5527353/5cabbd28b753/fmicb-08-01393-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8d/5527353/61758aca984f/fmicb-08-01393-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8d/5527353/609fd85fb7e3/fmicb-08-01393-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8d/5527353/866e39edc3b9/fmicb-08-01393-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8d/5527353/acba3638bc3e/fmicb-08-01393-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8d/5527353/5cabbd28b753/fmicb-08-01393-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f8d/5527353/61758aca984f/fmicb-08-01393-g005.jpg

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