Differences in resistance to Trypanosoma musculi infection among strains of inbred mice
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Abstract:
Inbred strains of mice were inoculated with Trypanosoma musculi, and the course of the ensuing parasitemia was followed. The mouse strains fell into three groups: those displaying high and moderate (fivefold less) parasitemia and C57BL/6 (B/6) mice which had exceptionally low infections. To gain insight concerning the mechanisms responsible for interstrain variations in infections, several types of experiments were performed. Comparison of the ability of spleen cells from the various strains to provide the growth-promoting substances required by T. musculi for growth in culture revealed that B/6 cells were deficient; this suggested one mechanism for regulating parasite infections. Exposure of C3H (high parasitemia) and B/6 mice to graded levels of ionizing radiation revealed that B/6 mice have much greater innate resistance to infection than do C3H mice. The effects of treating mice with silica dust or mercaptoethanol indicated that relative resistance to infection is not primarily associated with macrophage activity or limited growth-promoting substances. We conclude that variations in immune responsiveness to parasite antigens (probably not associated with the H-2 complex), possibly in concert with variations in a non-immunological mechanism, account for interstrain variation in resistance to T. musculi infections.
Insights
Mouse strains show varying resistance to Trypanosoma musculi infections. C57BL/6 mice exhibit exceptional resistance, linked to immune response and non-immunological factors, unlike high-parasitemia strains.
Area of Science:
- Immunology
- Parasitology
- Infectious Disease Research
Background:
- Trypanosoma musculi infections in mice exhibit significant interstrain variations in parasitemia.
- Understanding these variations is crucial for elucidating host-parasite interactions and immune mechanisms.
Purpose of the Study:
- To investigate the mechanisms underlying interstrain differences in resistance to Trypanosoma musculi infections in mice.
- To identify factors contributing to the exceptionally low parasitemia observed in C57BL/6 mice.
Main Methods:
- Inoculation of inbred mouse strains with Trypanosoma musculi to monitor parasitemia.
- In vitro culture of T. musculi with spleen cells from different mouse strains to assess growth-promoting substances.
- Exposure of mice to ionizing radiation, silica dust, or mercaptoethanol to evaluate innate resistance and cellular contributions.
Main Results:
- Mouse strains were categorized into high, moderate, and low parasitemia groups, with C57BL/6 mice showing exceptionally low infections.
- C57BL/6 spleen cells were deficient in providing growth-promoting substances for T. musculi in vitro.
- C57BL/6 mice demonstrated significantly greater innate resistance to infection compared to high-parasitemia strains like C3H, even after radiation exposure.
Conclusions:
- Interstrain variations in resistance to Trypanosoma musculi are attributed to differences in immune responsiveness to parasite antigens, potentially independent of the H-2 complex.
- Non-immunological mechanisms likely contribute in concert with immune variations to host resistance.
- Spleen cell-derived growth factors play a role in regulating parasite infections, with B/6 cells showing a deficiency.
