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Research Article

Effect of recombinant human macrophage colony-stimulating factor 1 on immunopathology of experimental brucellosis in mice.

A G Doyle, W J Halliday, C J Barnett, T L Dunn, D A Hume
A G Doyle
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W J Halliday
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C J Barnett
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T L Dunn
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D A Hume
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ABSTRACT

Brucella abortus injected into CBA mice replicated primarily in the spleen and liver, reaching a peak bacterial count in both organs about 7 days postinfection. The organism was eliminated from the liver but declined to a chronic phase in the spleen. The infection caused hepatosplenomegaly. An influx of macrophages into the two organs was monitored by quantitative Northern (RNA blot) analysis of the macrophage-specific marker lysozyme mRNA. Lysozyme mRNA was detectable in spleen and increased three- to fourfold during infection. In liver, lysozyme mRNA was initially undetectable, but at about the peak of infection it reached a level comparable to that in the spleen. Macrophage colony-stimulating factor 1 (CSF-1) has been reported to be elevated in the circulation of animals infected with B. abortus and is known to stimulate monocytopoiesis. To investigate the role of CSF-1 in pathogenesis, we studied the effect of further increasing the CSF-1 concentration by administration of recombinant human CSF-1. Since the infection is characterized by several distinct phases, recombinant human CSF-1 was administered at defined times relative to these phases. Pronounced effects were observed only when CSF-1 administration was begun during the developing acute phase. The consequences were decreased bacterial numbers in the spleen but an increase in the liver, reduced antibody generation, and increased hepatosplenomegaly. A feature of many chronic intracellular infections is immunosuppression. B. abortus caused a substantial diminution of responsiveness of spleen cells to T-cell mitogens, particularly concanavalin A. This action was mimicked by CSF-1 treatment of the animals prior to spleen cell isolation. The results suggest that CSF-1 plays a role in macrophage recruitment in brucellosis and that recruited macrophages contribute to the immunopathology and immunosuppression.

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Effect of recombinant human macrophage colony-stimulating factor 1 on immunopathology of experimental brucellosis in mice.
A G Doyle, W J Halliday, C J Barnett, T L Dunn, D A Hume
Infection and Immunity Apr 1992, 60 (4) 1465-1472; DOI:

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Effect of recombinant human macrophage colony-stimulating factor 1 on immunopathology of experimental brucellosis in mice.
A G Doyle, W J Halliday, C J Barnett, T L Dunn, D A Hume
Infection and Immunity Apr 1992, 60 (4) 1465-1472; DOI:
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