Experimental infection in rabbits with a human isolate of Trypanosoma rhodesiense led to the formation of circulating immune complexes and glomerulonephritis. Granular deposits of C3 and lesser amounts of IgM and IgG were seen deposited in the glomeruli in a primarily mesangial pattern. The glomeruli became hypercellular beginning on day 7. This was associated with diffuse swelling and vacuolation of endothelial cells with focal loss of fenestrae, as well as vacuolation of mesangial cells processes protruding into the capillary lumina. The hypercellularity became maximal on day 21 and was accompanied by proteinuria and increased tubular hyaline droplets. The hypercellularity was in large part due to the accumulation of monocytes as demonstrated by nonspecific cytoplasmic esterase stains. Counts of the number of monocytic cellular profiles per glomerulus showed that maximal numbers were reached on the 21st day of the infection. Ultrastructural examination confirmed the presence of monocytes within capillary lumina and macrophages within mesangial regions. Electron-dense deposits were rarely seen by transmission electron microscopy, and the heavy granular deposits of IgM and C3 observed by immunofluorescence were attributed to ingested proteins within macrophages. This study implies an active role for monocytes and macrophages in immune complex-mediated glomerulonephritis.
|Original language||English (US)|
|Number of pages||12|
|State||Published - 1982|
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Molecular Biology
- Cell Biology