Hypothetical protein Cpn0423 triggers NOD2 activation and contributes to Chlamydia pneumoniae-mediated inflammation.

Hypothetical protein Cpn0423 triggers NOD2 activation and contributes to Chlamydia pneumoniae-mediated inflammation.
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DOI:
10.1186/s12866-017-1062-y
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发表时间:
2017-07-11
期刊:
影响因子:
4.2
通讯作者:
Wu YM
Wu YM
中科院分区:
生物学3区
文献类型:
--
作者:
Chen HL;Dai GZ;Zhou AW;Li RH;Yuan HX;Xiang J;You XX;Ran O;Wu YM

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肺炎衣原体(C.pneumoniae)对人类具有致病性,可引起青少年和年轻人的肺部炎症或支气管炎。然而,将肺炎衣原体成分与炎症联系起来的分子信号仍然难以捉摸。本研究旨在探讨肺炎衣原体特异性Cpn0423对肺炎衣原体介导的炎症的影响。 Cpn0423 在肺炎衣原体包涵体之外检测到,它诱导多种细胞因子的产生,包括巨噬细胞炎症蛋白 2 (MIP-2) 和白细胞介素 (IL)。在用 NOD2-siRNA 预处理的细胞中,Cpn0423 诱导的细胞因子的产生显着减少,但用阴性对照寡核苷酸则没有。通过鼻内施用 Cpn0423 治疗的小鼠表现出肺部炎症,表现为炎症细胞浸润、肺组织学炎症评分增加、中性粒细胞募集以及 BALF 中细胞因子水平增加。 Cpn0423 可以被 NOD2 感知,NOD2 被确定为促进肺炎衣原体介导的炎症发生的途径中的重要元件。
Chlamydia pneumoniae (C. pneumoniae) is pathogenic to humans, by causing pulmonary inflammation or bronchitis in both adolescents and young adults. However, the molecular signals linking C. pneumoniae components to inflammation remain elusive. This study was to investigate the effect of Chlamydia-specific Cpn0423 of C. pneumoniae on C. pneumoniae-mediated inflammation. Cpn0423 was detected outside of C. pneumoniae inclusions, which induced production of several cytokines including macrophage inflammatory protein-2 (MIP-2) and interleukins (ILs). Production of the Cpn0423-induced cytokines was markedly reduced in cells pretreated with NOD2-siRNA, but not with negative control oligonucleotides. Mice treated with Cpn0423 through intranasal administration exhibited pulmonary inflammation as evidenced by infiltration of inflammatory cells, increased inflammatory scores in the lung histology, recruitment of neutrophils and increased cytokines levels in the BALF. Cpn0423 could be sensed by NOD2, which was identified as an essential element in a pathway contributing to the development of C. pneumoniae -mediated inflammation.
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