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Renal disease in chronic experimental Trypanosoma gambiense infections
Abstract:
Two recently isolated stocks of Trypanosoma brucei gambiense of human origin gave rise to a moderate to severe proliferative or membranoproliferative glomerulonephritis in 40 or 44 NMRI and C57BL/6J mice infected for 7-22 weeks. Extensive granular deposits of C3, IgG1 and IgG3 were found in the mesangium, together with smaller quantities of IgG2a, IgG2b, and IgM. No trypanosomal antigen could be detected in the deposits though specific anti-trypanosoma antibodies were found in kidney eluates. By electron microscopy, a conspicuous proliferation of mesangial and endothelial cells was observed and electron-dense deposits were seen in a mesangial and subepithelial localization. With one of these trypanosome stocks, four of seven Wistar rats infected for 9-15 weeks developed morphologically similar glomerular lesions. Four other trypanosome stocks did not evoke renal alterations in 17 other rats infected for 13-56 weeks. Experimental infection in mice or rats appears to be a suitable model for the study of renal disease in chronic African sleeping sickness.
Insights
African sleeping sickness in mice models can cause kidney disease. Researchers observed glomerulonephritis in infected mice, indicating a potential model for studying chronic kidney complications.
Area of Science:
- Immunology
- Pathology
- Infectious Diseases
Background:
- Human African trypanosomiasis, or sleeping sickness, is a parasitic disease caused by Trypanosoma brucei.
- Chronic infection can lead to severe systemic complications, including potential kidney damage.
Purpose of the Study:
- To investigate the development of glomerulonephritis in experimental animal models infected with Trypanosoma brucei gambiense.
- To establish a suitable animal model for studying the renal pathology associated with chronic African sleeping sickness.
Main Methods:
- Infection of NMRI, C57BL/6J mice, and Wistar rats with Trypanosoma brucei gambiense.
- Histopathological examination of kidney tissues.
- Immunofluorescence and electron microscopy to detect immune deposits and cellular changes.
Main Results:
- A moderate to severe proliferative or membranoproliferative glomerulonephritis developed in infected mice.
- Extensive granular deposits of complement component 3 (C3) and immunoglobulins (IgG1, IgG3) were found in the glomeruli.
- Similar glomerular lesions were observed in a subset of infected Wistar rats, but not in rats infected with other trypanosome stocks.
Conclusions:
- Experimental infection with Trypanosoma brucei gambiense can induce glomerulonephritis in mice and rats.
- The observed kidney lesions share similarities with human cases, suggesting the utility of these models.
- This research provides a valuable animal model for further investigation into the mechanisms of renal disease in chronic African sleeping sickness.