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Genetic control of Propionibacterium acnes-induced protection of mice against Babesia microti
Abstract:
Using various strains of inbred mice, we found that Propionibacterium acnes-induced protection against the hemoprotozoan parasite Babesia microti was controlled by a dominant gene(s) not linked to the major histocompatibility gene (H2) complex of mice. P. acnes-induced resistance to infection was not merely an amplification of the normal immune response to B. microti, since innate resistance to infection was controlled by different genes. Expression of the nonspecific protection induced by P. acnes was found to be transferable with cells of bone marrow origin, and it did not necessarily accompany the induction of hepatosplenomegaly. The implication of these results for the understanding of the mechanism of P. acnes-induced protection is discussed.
Insights
Propionibacterium acnes confers resistance to Babesia microti infection in mice, controlled by a dominant gene. This protection, transferable via bone marrow cells, is distinct from the innate immune response.
Area of Science:
- Immunology
- Parasitology
- Genetics
Background:
- Babesia microti is a hemoprotozoan parasite causing significant morbidity.
- Propionibacterium acnes can modulate host immune responses.
- Understanding genetic control of parasite resistance is crucial for developing interventions.
Purpose of the Study:
- To investigate the genetic basis of Propionibacterium acnes-induced protection against Babesia microti infection.
- To determine if this protection is linked to the major histocompatibility complex.
- To elucidate the cellular mechanisms underlying P. acnes-mediated resistance.
Main Methods:
- Utilized various strains of inbred mice for infection studies.
- Administered Propionibacterium acnes to induce protection.
- Assessed resistance to Babesia microti infection.
- Investigated gene linkage and cell transfer experiments.
Main Results:
- Protection against Babesia microti by P. acnes was controlled by dominant gene(s).
- The resistance genes were not linked to the H2 complex.
- P. acnes-induced resistance was distinct from innate resistance mechanisms.
- Protection was transferable with bone marrow-derived cells and not always associated with hepatosplenomegaly.
Conclusions:
- A dominant genetic factor, independent of the H2 complex, controls P. acnes-induced resistance to B. microti.
- The protective mechanism involves bone marrow-derived cells and represents a specific, non-innate immune response.
- These findings offer insights into the complex interplay between microbial colonization and host defense against parasitic infections.