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Role of macrophages in the pathogenesis of endomyocardial fibrosis in murine malaria

Identifieur interne : 003559 ( Main/Exploration ); précédent : 003558; suivant : 003560

Role of macrophages in the pathogenesis of endomyocardial fibrosis in murine malaria

Auteurs : Wijnand M. C. Eling [Pays-Bas] ; Christoph R. Jerusalem [Pays-Bas] ; Ute Heinen-Borries [Pays-Bas]

Source :

RBID : ISTEX:35CC25A1F489D19B92C287D9060D540A33641E6F

English descriptors

Abstract

C57B1/Rij mice developed progressive endocardial oedema and extensive endocardial thrombosis with a predilection for the right half of the heart in the course of a lethal Plasmodium berghei infection. Chemotherapy of an ongoing infection resulted in fibrosis of affected areas. Despite a close correlation between development of lesions and parasitaemia, parasitized erythrocytes were not usually present in the affected areas. Macrophages might play, however, an important role in the pathogenesis of the lesions. Early changes included sticking of macrophages to the endocardial endothelium, migration to subendothelial areas associated with leakage, and oedema. Subsequently, subendothelial infiltrates of lymphocytes, neutrophilic granulocytes, macrophages and fibroblasts were found. Moreover, endothelial lesions, sometimes associated with cell migration, were found to be plugged by microthrombi. Mural thrombi grew out eventually until death of the host or until chemotherapy cleared the infection.

Url:
DOI: 10.1016/0035-9203(84)90169-X


Affiliations:


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<term>Eling</term>
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<term>Lamina</term>
<term>Large amounts</term>
<term>Lesion</term>
<term>Macrophage</term>
<term>Malarial pigment</term>
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<term>Murine malaria</term>
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<term>Parasite</term>
<term>Parasitized</term>
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<div type="abstract">C57B1/Rij mice developed progressive endocardial oedema and extensive endocardial thrombosis with a predilection for the right half of the heart in the course of a lethal Plasmodium berghei infection. Chemotherapy of an ongoing infection resulted in fibrosis of affected areas. Despite a close correlation between development of lesions and parasitaemia, parasitized erythrocytes were not usually present in the affected areas. Macrophages might play, however, an important role in the pathogenesis of the lesions. Early changes included sticking of macrophages to the endocardial endothelium, migration to subendothelial areas associated with leakage, and oedema. Subsequently, subendothelial infiltrates of lymphocytes, neutrophilic granulocytes, macrophages and fibroblasts were found. Moreover, endothelial lesions, sometimes associated with cell migration, were found to be plugged by microthrombi. Mural thrombi grew out eventually until death of the host or until chemotherapy cleared the infection.</div>
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