title: Effects of Atorvastatin on Th polarization in patients with acute myocardial infarction.
abstract: BACKGROUND
  The development of heart failure after acute myocardial infarction (AMI) has been shown to be associated with inflammation, which is positively and negatively regulated by T helper (Th) 1 and Th2 lymphocytes, respectively. Several studies have indicated that statins can improve heart function after AMI.
  
  
  OBJECTIVE
  To study the effects of atorvastatin on Th polarization in patients with AMI.
  
  
  METHODS
  Peripheral blood mononuclear cells were collected from 20 patients with AMI treated with oral atorvastatin (10 mg/d, group AMI-A) and 18 patients with AMI (group AMI-C) who did not receive treatment with statins. Cytokine-producing Th lymphocytes were quantified by 3-color flow cytometry. After in vitro culturing in the presence or absence of atorvastatin (0, 0.3, 1 and 3 micromol/L) for 6 days, cytokine-producing Th lymphocytes were quantified again in AMI-C group.
  
  
  RESULTS
  The ratio of IFN-gamma-producing T cells was significantly higher in AMI-C group (17.8% +/- 6.4%) than in the AMI patients treated with oral atorvastatin (AMI-A, 13.1% +/- 4.6%). In vitro culturing with atorvastatin significantly reduced Th1 development in the AMI-C group. There was no significant difference on the frequencies of interleukin (IL)-4-producing T cells between each group.
  
  
  CONCLUSIONS
  Atorvastatin can reduce Th1 development but has no effect on Th2 cell-functions in AMI patients. Our findings suggest that atorvastatin can regulate the polarization of Th1/Th2, this may be one of the mechanisms through which atorvastatin improves heart function after AMI.
authors.affiliation: The Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China.
authors.forename: Xiang
authors.initials: X
authors.lastname: Cheng
authors.forename: Yu-Hua
authors.initials: YH
authors.lastname: Liao
authors.forename: Jinying
authors.initials: J
authors.lastname: Zhang
authors.forename: Bin
authors.initials: B
authors.lastname: Li
authors.forename: Hongxia
authors.initials: H
authors.lastname: Ge
authors.forename: Jing
authors.initials: J
authors.lastname: Yuan
authors.forename: Min
authors.initials: M
authors.lastname: Wang
authors.forename: Baojun
authors.initials: B
authors.lastname: Lu
authors.forename: Ying
authors.initials: Y
authors.lastname: Liu
authors.forename: Yan
authors.initials: Y
authors.lastname: Cheng
mesh_terms: D000069059:Atorvastatin; D002478:Cells, Cultured; D018450:Disease Progression; D005260:Female; D005434:Flow Cytometry; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D066298:In Vitro Techniques; D008213:Lymphocyte Activation / Q000187:drug effects*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy / Q000276:immunology / Q000473:pathology*; D011758:Pyrroles / Q000627:therapeutic use*; D016176:T-Lymphocyte Subsets; D006377:T-Lymphocytes, Helper-Inducer / Q000187:drug effects / Q000276:immunology / Q000473:pathology*
chemical_list: D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D000069059:Atorvastatin