LRRK2/NF-κB signaling modulates inflammatory responses in BCG-in-fected RAW264.7 macrophages / 中国病理生理杂志
Chinese Journal of Pathophysiology
;
(12): 528-532, 2018.
Article
in Chinese
| WPRIM
| ID: wpr-701155
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Type of study:
Prognostic study
Language:
Chinese
Journal:
Chinese Journal of Pathophysiology
Year:
2018
Type:
Article
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