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Amyloidosis developing in experimental nocardia infections
British Journal of Experimental Pathology
|April 1, 1977
Abstract:
Swiss white and C57/BL/6J mice inoculated repeatedly with either Nocardia asteroides or Nocardia brasiliensis organisms developed amyloidosis over a 7-month period. Amyloidosis also developed in these mice within 6 weeks following a single large inoculum of either organism, but not in other in-bred mouse strains, suggesting a genetic influence in the pathogenesis of this form of secondary amyloidosis.
Insights
Swiss white and C57/BL/6J mice developed amyloidosis after Nocardia inoculation. Genetic factors in these mouse strains appear crucial for secondary amyloidosis development.
Area of Science:
- Microbiology
- Immunology
- Pathology
Background:
- Amyloidosis is a group of diseases characterized by the deposition of amyloid proteins.
- Secondary amyloidosis can arise from chronic inflammatory conditions.
- The role of specific bacterial infections in inducing amyloidosis requires further investigation.
Purpose of the Study:
- To investigate the potential of Nocardia asteroides and Nocardia brasiliensis to induce amyloidosis in mice.
- To explore the influence of host genetics on the development of Nocardia-induced secondary amyloidosis.
Main Methods:
- Swiss white and C57/BL/6J mice were inoculated with Nocardia asteroides or Nocardia brasiliensis.
- Inoculations were performed repeatedly over 7 months or as a single large dose.
- Control groups included other in-bred mouse strains.
Main Results:
- Both Swiss white and C57/BL/6J mice developed amyloidosis following repeated Nocardia inoculations.
- Amyloidosis was also observed in these strains after a single large Nocardia inoculum.
- Other in-bred mouse strains did not develop amyloidosis under similar conditions.
Conclusions:
- Nocardia asteroides and Nocardia brasiliensis can induce secondary amyloidosis in susceptible mouse strains.
- Genetic predisposition plays a significant role in the pathogenesis of Nocardia-induced amyloidosis.