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Cardiovascular Research 2004 64(3):412-420; doi:10.1016/j.cardiores.2004.09.014
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

HMG-CoA reductase inhibitor attenuates experimental autoimmune myocarditis through inhibition of T cell activation

Ryoko Wakizono Azuma, Jun-ichi Suzuki, Masahito Ogawa, Hideki Futamatsu, Noritaka Koga, Yasuyuki Onai, Hisanori Kosuge and Mitsuaki Isobe*

Department of Cardiovascular Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan

* Corresponding author. Tel.: +81 3 5803 5951; fax: +81 3 5803 0238. Email address: isobemi.cvm{at}tmd.ac.jp

Objective: This study tested the hypothesis that 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitor affects T cell-mediated autoimmunity through inhibition of nuclear factor-{kappa}B (NF{kappa}B) and reduces the severity of experimental autoimmune myocarditis (EAM).

Methods: EAM was induced in Lewis rats by immunization with myosin. High-dose or low-dose fluvastatin or vehicle was administered orally for 3 weeks to rats with EAM.

Results: Fluvastatin reduced the pathophysiological severity of myocarditis. Fluvastatin inhibited expression of NF{kappa}B in the nuclei of myocardium in EAM. Fluvastatin reduced production of Th1-type cytokines, including interferon (IFN)-{gamma} and interleukin (IL)-2, and inhibited expression of inflammatory cytokine mRNAs in the myocardium. Infiltration of CD4-positive T cells into the myocardium and T cell proliferative responses were suppressed by fluvastatin. Plasma lipid levels did not differ between the groups.

Conclusions: Fluvastatin ameliorates EAM by inhibiting T cell responses and suppressing Th1-type and inflammatory cytokines via inactivation of nuclear factor-{kappa}B, and this activity is independent of cholesterol reduction.

KEYWORDS HMG-CoA reductase inhibitor; Myocarditis; Nuclear factor-{kappa}B; Cytokine; T cell response; Inflammation; Immunology

Time for primary review 17 days


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