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A possible role for complement in the pathogenesis of chronic chagasic cardiomyopathy
Author(s) -
Demarchi Aiello Vera,
Martins Reis Márcia,
Alberto Benvenuti Luiz,
de Lourdes Higuchi Maria,
Antonio Franchini Ramires José,
Halperin José A.
Publication year - 2002
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1095
Subject(s) - inflammation , complement system , pathogenesis , fibrosis , cd59 , cardiomyopathy , dilated cardiomyopathy , complement membrane attack complex , immunology , myocarditis , pathology , medicine , antibody , heart failure
The membrane attack complex (MAC) of complement participates in several inflammatory and proliferative processes by releasing pro‐inflammatory cytokines and growth factors from target cells. Chronic Chagasic cardiomyopathy (CCH) is a parasitic dilated cardiopathy, characterized by severe fibrosis and inflammation, which differs from idiopathic dilated cardiomyopathy (DCM). Trypanosoma cruzi , the pathogenic organism of CCH, is a strong complement activator and can also induce alternative pathway activation by mammalian cells. This study explored whether the myocardium in CCH patients has increased MAC deposition, an expression of complement activation, compared to DCM patients. MAC was semi‐quantified in endomyocardial human samples (29 CCH subjects, 18 DCM subjects, and four controls) by immunohistochemistry. MAC was present in the sarcolemma of 38% of CCH, 5.5% of DCM ( p <0.02), and 0% of controls, and in interstitial inflammatory cells of CCH. No difference was observed in the expression of the complement regulatory protein CD59, indicating that increased MAC deposition is likely to be the result of complement activation rather than decreased protection. It is proposed that the increased MAC deposition found in CCH, but not in DCM or controls, may help to explain the diffuse myocardial fibrosis and inflammation characteristic of the disease. Copyright © 2002 John Wiley & Sons, Ltd.