Effects of Atorvastatin on Th polarization in patients with acute myocardial infarction

被引:25
作者
Cheng, X
Liao, YH [1 ]
Zhang, JY
Lin, B
Ge, HX
Yuan, J
Wang, M
Lu, BJ
Liu, Y
Cheng, Y
机构
[1] Univ Sci & Technol, Union Hosp, Tongji Med Coll, InstCardiol,Lab Cardiovasc Immunol, Wuhan 430022, Peoples R China
[2] Univ Penn, Sch Med, Ctr Expt Therapeut, Philadelphia, PA 19104 USA
关键词
HMG-CoA reductase inhibitor; acute myocardial infarction; T lymphocyte; helper; heart failure;
D O I
10.1016/j.ejheart.2005.01.020
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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. Aims: 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 AMIA) 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 mu mol/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. V 2005 European Society of Cardiology. Published by Elsevier B.V All rights reserved.
引用
收藏
页码:1099 / 1104
页数:6
相关论文
共 27 条
[1]   Treatment of relapsing paralysis in experimental encephalomyelitis by targeting Th1 cells through atorvastatin [J].
Aktas, O ;
Waiczies, S ;
Smorodchenko, A ;
Dörr, J ;
Seeger, B ;
Prozorovski, T ;
Sallach, S ;
Endres, M ;
Brocke, S ;
Nitsch, R ;
Zipp, F .
JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 197 (06) :725-733
[2]  
Aronica MA, 1999, J IMMUNOL, V163, P5116
[3]   Peripheral blood dendritic cells in human end-stage heart failure and the early post-transplant period: evidence for systemic Th1 immune responses [J].
Athanassopoulos, P ;
Vaessen, LMB ;
Maat, APWM ;
Balk, AHMM ;
Weimar, W ;
Bogers, AJJC .
EUROPEAN JOURNAL OF CARDIO-THORACIC SURGERY, 2004, 25 (04) :619-626
[4]   Improvement of left ventricular remodeling and function by hydroxymethylglutaryl coenzyme A reductase inhibition with cerivastatin in rats with heart failure after myocardial infarction [J].
Bauersachs, J ;
Galuppo, P ;
Fraccarollo, D ;
Christ, M ;
Ertl, G .
CIRCULATION, 2001, 104 (09) :982-985
[5]   Decreased circulating Fas ligand in patients with familial combined hyperlipidemia or carotid atherosclerosis normalization by atorvastatin [J].
Blanco-Colio, LM ;
Martín-Ventura, JL ;
Sol, JM ;
Díaz, C ;
Hernández, G ;
Egido, J .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2004, 43 (07) :1188-1194
[6]  
Boyum A., 1968, SCAND J CLIN LAB INV, V21, P97
[7]  
CHENG X, 2004, EUR J HEART FAIL S1, V3, P20
[8]  
CONSTANT SL, 1997, ANNU REV IMMUNOL, V15, P279
[9]   Anti-inflammatory effect of Atorvastatin (80 mg) in unstable angina pectoris and non-Q-wave acute myocardial infarction [J].
Correia, LCL ;
Spósito, AC ;
Lima, JC ;
Magalhaes, LP ;
Passos, LCS ;
Rocha, MS ;
D'Oliveira, A ;
Esteves, JP .
AMERICAN JOURNAL OF CARDIOLOGY, 2003, 92 (03) :298-301
[10]   The inflammatory response in myocardial infarction [J].
Frangogiannis, NG ;
Smith, CW ;
Entman, ML .
CARDIOVASCULAR RESEARCH, 2002, 53 (01) :31-47