title: [Role of triggering receptor expressed on myeloid cells-1 on coxsackievirus B3-induced inflammation and cardiomyocyte injury].
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 upregulated 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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Shanghai Institute of Cardiovascular Diseases, Shanghai, China.
authors.forename: Xian
authors.initials: X
authors.lastname: Zhang
authors.forename: Xing-gang
authors.initials: XG
authors.lastname: Wang
authors.forename: Yu-quan
authors.initials: YQ
authors.lastname: Xie
authors.forename: Ye-qing
authors.initials: YQ
authors.lastname: Xie
authors.forename: Xu-Jie
authors.initials: XJ
authors.lastname: Liu
authors.forename: Ming-hui
authors.initials: MH
authors.lastname: Li
authors.forename: Yong
authors.initials: Y
authors.lastname: Yu
authors.forename: Qi
authors.initials: Q
authors.lastname: Guo
authors.forename: Rui-zhen
authors.initials: RZ
authors.lastname: Chen
mesh_terms: D000818:Animals; D003384:Coxsackievirus Infections / Q000378:metabolism*; D017077:Culture Media, Conditioned; D008264:Macrophages / Q000378:metabolism*; D008297:Male; D009205:Myocarditis / Q000378:metabolism* / Q000821:virology; D032383:Myocytes, Cardiac / Q000166:cytology / Q000821:virology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011971:Receptors, Immunologic / Q000378:metabolism*
chemical_list: D017077:Culture Media, Conditioned; D011971:Receptors, Immunologic; C473366:TREML1 protein, human