Plasmodium berghei infection in mice. An ultrastructural study of immune complex nephritis.
Renal glomeruli of Plasmodium berghei infected mice were studied electron microscopically. The endothelial cell proliferation and endothelial cytoplasmic changes were greatly stimulated on day 7, at the time when there were collections of dense granular aggregates in the glomerular capillary lumens and electron-dense deposits in the mesangial areas. The basement membrane lesion developed with the infiltration of polymorphonuclear leucocytes on day 14 with more electron-dense deposits in the mesangial areas and in the basement membrane. On the basis of these ultrastructural alterations and on previous findings of immune complex (P berghei antigen, mouse globulin and mouse beta1C globulin) deposits by immunofluorescent study, we concluded that glomerular lesions in P berghei infected mice are induced by immune mechanism.
D000818:Animals; D000936:Antigen-Antibody Complex; D005260:Female; D005455:Fluorescent Antibody Technique; D007105:Immune Complex Diseases / Q000473:pathology; D007154:Immune System Diseases / Q000473:pathology*; D007668:Kidney / Q000473:pathology; D007678:Kidney Glomerulus / Q000473:pathology; D008288:Malaria / Q000276:immunology*; D008297:Male; D051379:Mice; D008854:Microscopy, Electron; D009393:Nephritis / Q000276:immunology* / Q000473:pathology; D010962:Plasmodium berghei
D000936:Antigen-Antibody Complex