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Susceptibility of selected inbred strains of mice to Encephalitozoon cuniculi
Abstract:
Selected inbred strains of mice were examined for susceptibility to peritoneal infections with Encephalitozoon cuniculi. Marked differences in susceptibility and resistance among mouse strains were not controlled by loci within the mouse major histocompatibility (H-2) complex, but resistance in BALB/c mice was influenced by a dominant gene(s) outside the H-2 complex. The lethality of peritoneal infections in hypothymic nude mice suggested that resistance to encephalitozoonosis is dependent on thymus-derived lymphocytes. Peritoneal infection with E. cuniculi was associated with slightly enhanced proliferative spleen cell responses to mitogens in BALB/c mice and significantly depressed responses in C57Bl/6 mice. Infection in BALB/c mice was accompanied by normal antibody responses to sheep erythrocyte immunogens, but C57Bl/6 mice had depressed antibody responses. The results indicate that the immune system plays a major role in determining the course of peritoneal infections with E. cuniculi and that encephalitozoonosis can modulate the host's immune system.
Insights
Mouse strain differences in Encephalitozoon cuniculi susceptibility are not linked to the H-2 complex. Resistance is influenced by genes outside H-2 and relies on thymus-derived lymphocytes, indicating the immune system
Area of Science:
- Immunology
- Genetics
- Microbiology
Background:
- Encephalitozoon cuniculi is an opportunistic pathogen causing encephalitozoonosis.
- Susceptibility to E. cuniculi varies significantly among different host species and strains.
- The genetic and immunological basis of host resistance to E. cuniculi is not fully understood.
Purpose of the Study:
- To investigate the genetic control of susceptibility to peritoneal Encephalitozoon cuniculi infection in inbred mouse strains.
- To determine the role of the major histocompatibility complex (H-2) and other genetic factors in resistance.
- To assess the contribution of thymus-derived lymphocytes and the impact of infection on host immune responses.
Main Methods:
- Infection of selected inbred mouse strains with Encephalitozoon cuniculi via peritoneal inoculation.
- Evaluation of host susceptibility and survival rates.
- Analysis of immune responses, including spleen cell proliferation to mitogens and antibody production to sheep erythrocytes.
- Assessment of infection lethality in hypothymic nude mice.
Main Results:
- Significant differences in susceptibility and resistance were observed among mouse strains, independent of the H-2 complex.
- Resistance in BALB/c mice was associated with a dominant gene(s) located outside the H-2 complex.
- Peritoneal E. cuniculi infection was lethal in hypothymic nude mice, highlighting the importance of thymus-derived lymphocytes.
- BALB/c mice showed enhanced spleen cell responses and normal antibody production, while C57Bl/6 mice exhibited depressed spleen cell responses and antibody production.
Conclusions:
- Host immune system components, particularly thymus-derived lymphocytes, play a critical role in controlling peritoneal Encephalitozoon cuniculi infections.
- Genetic factors outside the major histocompatibility complex significantly influence resistance to encephalitozoonosis.
- Encephalitozoon cuniculi infection can modulate the host's immune system, affecting both cellular and humoral responses.