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LRRK2/NF-κB信号对BCG诱导巨噬细胞RAW264.7炎症应答的调控

王启源 徐红艳 姬文兰

中国病理生理杂志2018,Vol.34Issue(3):528-532,5.
中国病理生理杂志2018,Vol.34Issue(3):528-532,5.DOI:10.3969/j.issn.1000-4718.2018.03.024

LRRK2/NF-κB信号对BCG诱导巨噬细胞RAW264.7炎症应答的调控

LRRK2/NF-κB signaling modulates inflammatory responses in BCG-in-fected RAW264.7 macrophages

王启源 1徐红艳 1姬文兰1

作者信息

  • 1. 陕西省结核病防治院内四科,陕西西安710100
  • 折叠

摘要

Abstract

AIM:To investigate the biological function and potential mechanism of leucine-rich repeat kinase 2 (LRRK2)in RAW264.7 macrophages during Mycobacterium tuberculosis infection.METHODS: The bacillus Calmette-Guerin(BCG)-infected RAW264.7 cell model was established.Colony-forming unit(CFU)analysis was used to deter-mine the mycobacterial viability.The releases of interleukin(IL)-1β,IL-6 and interferon-γ(IFN-γ)in the RAW264.7 cells were detected by ELISA.qPCR and Western blot were used to measure the mRNA and protein expression levels,re-spectively.RESULTS:LRRK2 was robustly enhanced in the RAW264.7 cells in response to BCG infection.Additional-ly,silencing of LRRK2 suppressed intracellular growth of mycobacteria during BCG challenge.Moreover, silencing of LRRK2 dramatically attenuated the accumulation of inflammatory cytokines IL-1β,IL-6 and IFN-γinduced by BCG infec-tion.More importantly,LRRK2 modulated BCG-induced inflammatory responses by positively regulating the nuclear factor-κB(NF-κB)signaling pathway.CONCLUSION: LRRK2/NF-κB signaling pathway positively modulates inflammatory responses during BCG infection,which may provide a better understanding of the pathogenesis of tuberculosis and useful in -formation for developing potential therapeutic interventions against the disease.

关键词

富亮氨酸重复序列激酶2/结核分枝杆菌/巨噬细胞/炎症应答

Key words

Leucine-rich repeat kinase 2/Mycobacterium tuberculosis/Macrophages/Inflammatory responses

分类

医药卫生

引用本文复制引用

王启源,徐红艳,姬文兰..LRRK2/NF-κB信号对BCG诱导巨噬细胞RAW264.7炎症应答的调控[J].中国病理生理杂志,2018,34(3):528-532,5.

中国病理生理杂志

OA北大核心CSCDCSTPCD

1000-4718

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