Role of triggering receptor expressed on myeloid cells-1 on coxcackievirus B3-induced inflammation and cardiomyocyte injury
10.3760/cma.j.issn.0253-3758.2012.05.012
- VernacularTitle:髓系触发受体-1在柯萨奇病毒B3导致的炎症反应及心肌细胞损伤中作用的实验研究
- Author:
Xian ZHANG
1
;
Xing-Gang WANG
;
Yu-Quan XIE
;
Ye-Qing XIE
;
Xu-Jie LIU
;
Ming-Hui LI
;
Yong YU
;
Qi GUO
;
Rui-Zhen CHEN
Author Information
1. 复旦大学附属中山医院
- Keywords:
Myocarditis;
Enterovirus B,human;
Macrophages;
Triggering receptor expressed on myeloid cells-1
- From:
Chinese Journal of Cardiology
2012;40(5):411-415
- CountryChina
- Language:Chinese
-
Abstract:
Objective To determine the expression of TREM-1 (triggering receptor expressed on myeloid cells-1 ) in macrophages after coxsackievirus B3 ( CVB3 ) infection and the cardiomyocytes viability after culturing with supernatant of macrophages in the absence and presence of TREM-1 inhibitor LP-17 to explore if TREM-1 is involved in the pathogenesis of CVB3 infection induced inflammation and cardiomyocytes injury.Methods TREM-1 mRNA and TREM-1 and DAP-12 protein expression in macrophages were detected by Real-time PCR at 0,1,4,8 and 12 h and by Western blot at 0,16,24 and 48 h post CVB3 infection. TNF-α secretion of macrophages was measure by ELISA,vitality and the apoptosis degree of cardiomyocytes was assessed by CCK8 and Annexin V-FITC after the cardiomyocytes were cultured with the supernatant of macrophages in normal control group,CVB3 infection group and LP-17 pretreated CVB3 infection group.Results TREM-1 mRNA expression was significantly upregalated at 4,8,and 12 h (peaked at 8 h) and TREM-1 protein expression was significantly upregulated at 16 and 24 h and returned to baseline level at 48 h after CVB3 infection.The protein expression of DAP-12,a direct downstream signaling molecule of TREM-1,also significantly increased at 24 and 48 h post CVB3 infection ( P ＜ 0.01 ).Level of macrophages secreted TNF-α post CVB3 infection was significantly reduced in LP-17 pretreated cells ( P ＜ 0.01 ),LP-17 pretreatment also significantly improved viability and significantly reduced apoptosis of cardiomyocytes cultured with supernatant of CVB3 infected macrophages (P ＜ 0.01 ).Conclusion TREM-1 might be an important mediator post CVB3 infection and a major player on inducing excess macrophages-related inflammation and resulting in an indirect injury to cardiomyocytes.
