Effect of recombinant human macrophage colony-stimulating factor 1 on immunopathology of experimental brucellosis in mice
| Autor: | C. Barnett, Timothy L. Dunn, William J. Halliday, Anthony G. Doyle, David A. Hume |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 1992 |
| Předmět: |
Macrophage colony-stimulating factor
Cellular immunity Time Factors Immunology Hepatosplenomegaly Dose-Response Relationship Immunologic Spleen Biology Lymphocyte Activation Microbiology Brucellosis Colony-Forming Units Assay chemistry.chemical_compound Mice Macrophage Colony-Stimulating Factor 1 Immunopathology medicine Macrophage Animals Hypersensitivity Delayed RNA Messenger Lung Macrophage Colony-Stimulating Factor Macrophages Organ Size Blotting Northern Recombinant Proteins Disease Models Animal Infectious Diseases medicine.anatomical_structure chemistry Liver Antibody Formation Splenomegaly Mice Inbred CBA Parasitology Muramidase medicine.symptom Lysozyme Research Article Hepatomegaly |
| Zdroj: | Doyle, A G, Halliday, W J, Barnett, C J, Dunn, T L & Hume, D A 1992, ' Effect of recombinant human macrophage colony-stimulating factor 1 on immunopathology of experimental brucellosis in mice ', Infection and Immunity, vol. 60, no. 4, pp. 1465-72 . Scopus-Elsevier |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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