title: Preexposure to PM2.5 exacerbates acute viral myocarditis associated with Th17 cell.
abstract: BACKGROUND
  It is increasingly recognized that exposure to ambient fine particles (PM(2.5)) is a risk factor for the development of cardiovascular events. This study was to explore the link between PM(2.5) exposure and viral myocarditis in the functional mechanism of Th17 cells.
  
  
  METHODS
  Male BALB/c mice were administered an intratracheal (i.t.) instillation of 10 mg/kg b.w. PM(2.5) particles. Twenty-four hours later, the mice were injected intraperitoneally (i.p.) with 100 μl of coxsackievirus B3 (CVB3) diluted in Eagle's minimal essential medium (EMEM). Seven days after the treatment, pulmonary and cardiac tissues were examined.
  
  
  RESULTS
  The results showed that preexposure to PM(2.5) increased the cardiac and pulmonary injuries and viral replication in the heart of CVB3-infected mice along with an increase in CD4(+) IL-17(+) cells in the spleen and heart. The mRNA expressions of interleukin-17A (IL-17A), perforin, transforming growth factor-β (TGF-β) and RORγt were up-regulated in PM(2.5)-pretreated mice than that in the virus-treated mice. Additionally, compared to virus-treated mice, the cardiac protein expressions of IL-17A and matrix metalloproteinases-2 (MMP-2) were increased, but interferon-γ (IFN-γ) and metalloproteinases-1 (TIMP-1) were decreased in PM(2.5)-pretreated mice. Interestingly, PM(2.5) caused IFN-γ decreased, whereas CVB3 caused a dramatic increase in IFN-γ. Subsequently, preexposure to PM(2.5) induced a slight increase of IFN-γ in the sera of CVB3-infected mice.
  
  
  CONCLUSIONS
  These results demonstrated that PM(2.5) exposure exacerbated virus-induced myocarditis possibly through the increase in Th17-mediated viral replication, perforin response and imbalance of MMP-2/TIMP-1. These findings provided supportive evidence for the epidemiological research that ambient particles could increase the occurrence and development of cardiovascular diseases.
authors.affiliation: Department of Cardiology, Xinhua Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, 200092 China.
authors.forename: Yuquan
authors.initials: Y
authors.lastname: Xie
authors.forename: Xian
authors.initials: X
authors.lastname: Zhang
authors.forename: Zhenyong
authors.initials: Z
authors.lastname: Tian
authors.forename: Rongfang
authors.initials: R
authors.lastname: Jiang
authors.forename: Ruizhen
authors.initials: R
authors.lastname: Chen
authors.forename: Weimin
authors.initials: W
authors.lastname: Song
authors.forename: Jinzhuo
authors.initials: J
authors.lastname: Zhao
mesh_terms: D000208:Acute Disease; D000818:Animals; D003384:Coxsackievirus Infections / Q000139:chemically induced* / Q000378:metabolism; D029822:Enterovirus B, Human; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009205:Myocarditis / Q000139:chemically induced / Q000378:metabolism / Q000821:virology*; D052638:Particulate Matter / Q000633:toxicity*; D058504:Th17 Cells / Q000378:metabolism / Q000821:virology*
chemical_list: D052638:Particulate Matter
keywords: Immune system; Myocarditis; PM(2.5); Th17