Affiliation:
1. Department of Medical Microbiology and Immunology, University of California, One Shields Avenue, Davis, California 95616
2. Texas A&M University System Health Science Center, Department of Medical Microbiology and Immunology, College Station, Texas 77843-1114
Abstract
ABSTRACT
The
Brucella abortus
type IV secretion system (T4SS), encoded by the
virB
genes, is essential for survival in mononuclear phagocytes in vitro. In the mouse model, a
B. abortus virB
mutant was initially able to colonize the spleen at the level of the wild type for approximately 3 to 5 days, which coincided with the development of adaptive immunity. To investigate the relationship between survival in macrophages cultivated in vitro and persistence in tissues in vivo, we tested the ability of mutant mice lacking components of adaptive immunity to eliminate the
virB
mutant from the spleen during a mixed infection with the
B. abortus
wild type.
Ifng
−/−
or β
2
m
−/−
mice were able to clear the
virB
mutant to the same degree as control mice. However, spleens of
Rag1
−/−
mice and
Igh6
−/−
mice were more highly colonized by the
virB
mutant than control mice after 14 to 21 days, suggesting that, in these mice, there is not an absolute requirement for the T4SS to mediate persistence of
B. abortus
in the spleen. Macrophages isolated from
Igh6
−/−
mice killed the
virB
mutant to the same extent as macrophages from control mice, showing that the reduced ability of these mice to clear the
virB
mutant from the spleen does not correlate with diminished macrophage function in vitro. These results show that in the murine model host, the T4SS is required for persistence beyond 3 to 5 days after infection and suggest that the T4SS may contribute to evasion of adaptive immune mechanisms by
B. abortus
.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
54 articles.
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