Role of macrophages in the pathogenesis of endomyocardial fibrosis in murine malaria.
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.
D000818:Animals; D002448:Cell Adhesion; D002738:Chloroquine / Q000627:therapeutic use; D004699:Endocardium / Q000648:ultrastructure; D004719:Endomyocardial Fibrosis / Q000209:etiology* / Q000473:pathology; D008262:Macrophage Activation; D008264:Macrophages / Q000648:ultrastructure*; D008288:Malaria / Q000150:complications* / Q000188:drug therapy / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D008854:Microscopy, Electron
D002738:Chloroquine