Chronic murine Chagas' disease:: the impact of host and parasite genotypes

被引:25
作者
Andersson, J [1 ]
Örn, A [1 ]
Sunnemark, D [1 ]
机构
[1] Karolinska Inst, Ctr Microbiol & Tumor Biol, S-17177 Stockholm, Sweden
关键词
pathogenesis; immunohistochemistry; Trypanosoma cruzi;
D O I
10.1016/S0165-2478(03)00019-1
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Chagas' disease is a protozoan infection caused by the flagellate Trypanosoma cruzi. Herein we utilise experimental infections of different mouse and parasite strains to investigate the relative importance of the host and parasite genotype, respectively, in causing Chagas' disease in mice. CBA/J and BALB/c mice infected with the Tulahuen strain of T. cruzi develop a severe acute disease characterised by transient parasitaemia and a high rate of mortality. While the acute phases in these mice are indistinguishable, they display differential outcomes of the infection since CBA/J mice eventually develop polymyositis and mild myocarditis whereas BALB/c mice are resistant to chronic disease. In contrast, BALB/c mice infected with the CA-1 clone of T. cruzi exhibit a mild acute phase, develop no polymyositis but do develop severe myocarditis. Thus both the parasite and host genotype, but not the severity of the acute phase, are important in determining the eventual outcome of T. cruzi infection. We also present a murine model suitable for investigating which host factors may be necessary to induce a chronic inflammatory disease after T cruzi infection. (C) 2003 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:207 / 212
页数:6
相关论文
共 24 条
[1]   MONOCLONAL-ANTIBODY ANALYSIS OF MONONUCLEAR-CELLS IN MYOPATHIES .1. QUANTITATION OF SUBSETS ACCORDING TO DIAGNOSIS AND SITES OF ACCUMULATION AND DEMONSTRATION AND COUNTS OF MUSCLE-FIBERS INVADED BY T-CELLS [J].
ARAHATA, K ;
ENGEL, AG .
ANNALS OF NEUROLOGY, 1984, 16 (02) :193-208
[2]   IFN-γ in human Chagas' disease:: Protection or pathology? [J].
Bahia-Oliveira, LMG ;
Gomes, JAS ;
Rocha, MOC ;
Moreira, MCV ;
Lemos, EM ;
Luz, ZMP ;
Pereira, MES ;
Coffman, RL ;
Dias, JCP ;
Cancado, JR ;
Gazzinelli, G ;
Correa-Oliveira, R .
BRAZILIAN JOURNAL OF MEDICAL AND BIOLOGICAL RESEARCH, 1998, 31 (01) :127-131
[3]   DETECTION OF PARASITE DNA IN CHAGAS HEART-DISEASE [J].
BRANDARIZ, S ;
SCHIJMAN, A ;
VIGLIANO, C ;
ARTEMAN, P ;
VIOTTI, R ;
BELDJORD, C ;
LEVIN, MJ .
LANCET, 1995, 346 (8986) :1370-1371
[4]   Activation of toll-like receptor-2 by glycosylphosphatidylinositol anchors from a protozoan parasite [J].
Campos, MA ;
Almeida, IC ;
Takeuchi, O ;
Akira, S ;
Valente, EP ;
Procópio, DO ;
Travassos, LR ;
Smith, JA ;
Golenbock, DT ;
Gazzinelli, RT .
JOURNAL OF IMMUNOLOGY, 2001, 167 (01) :416-423
[5]   CARDIAC PARASYMPATHETIC ABNORMALITIES - CAUSE OR CONSEQUENCE OF CHAGAS HEART-DISEASE [J].
DAVILA, DF ;
ROSSELL, RO ;
DONIS, JH .
PARASITOLOGY TODAY, 1989, 5 (10) :327-329
[6]   Cysteine protease inhibitors cure an experimental Trypanosoma cruzi infection [J].
Engel, JC ;
Doyle, PS ;
Hsieh, I ;
McKerrow, JH .
JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 188 (04) :725-734
[7]   HLA and β-myosin heavy chain do not influence susceptibility to Chagas' disease cardiomyopathy [J].
Faé, KC ;
Drigo, SA ;
Cunha-Neto, E ;
Ianni, B ;
Mady, C ;
Kalil, J ;
Goldberg, AC .
MICROBES AND INFECTION, 2000, 2 (07) :745-751
[8]   Cell-specific activation of nuclear factor-κB by the parasite Trypanosoma cruzi promotes resistance to intracellular infection [J].
Hall, BS ;
Tam, W ;
Sen, R ;
Pereira, MEA .
MOLECULAR BIOLOGY OF THE CELL, 2000, 11 (01) :153-160
[9]   Chagas' disease and the autoimmunity hypothesis [J].
Kierszenbaum, F .
CLINICAL MICROBIOLOGY REVIEWS, 1999, 12 (02) :210-+
[10]   HLA-C*03 is a risk factor for cardiomyopathy in Chagas disease [J].
Layrisse, Z ;
Fernandez, MT ;
Montagnani, S ;
Matos, M ;
Balbas, O ;
Herrera, F ;
Colorado, IA ;
Catalioti, F ;
Acquatella, H .
HUMAN IMMUNOLOGY, 2000, 61 (09) :925-929