Abstract 10062: Immunoglobulin Treatment Suppresses Free Radical-Medicated Myocardial Injury in Experimental Autoimmune Myocarditis
Background and Purpose: Recent evidence suggests that free radicals may play a crucial role in heart failure. We tested the hypothesis that immunoglobulin ameliorated experimental autoimmune myocarditis in mice attributing to the suppression of free radicals-mediated injury.
Methods: We administered intact type of human immunoglobulin (Ig) or F(ab')2 fragments of human Ig, 1mg/kg/day, to mice with heart failure due to experimental autoimmune myocarditis produced by immunization of porcine myosin (each group; n=15∼20).
Results: Intact type of Ig, but not F(ab')2 type, markedly reduced the severity of myocarditis associated with the decrease of myocardial macrophage, CD4+ and CD8+ T cell expression by comparing the heart weight/body weight ratio, macroscopic and microscopic scores compared with untreated group. Tissue superoxide production shown by dihydroethidium staining was marked in untreated mice with myocarditis, which was suppressed by the treatment of Ig. The cytotoxic activities of lymphocytes in mice with myocarditis treated with intact Ig, but not with F (ab')2 type, were reduced compared with untreated controls.
Conclusions: Free radicals may be involved in myocarditis. Intact Ig ameliorates murine myocarditis. The cardioprotection of Ig may be due to suppression of free radicals as well as to suppressive effects for cytotoxic myocardial injury via Fc portion of immunoglobulin.
- © 2010 by American Heart Association, Inc.