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  • Induction of Multiple Chemokine and Colony-Stimulating Factor Genes in Experimental Burkholderia pseudomallei Infection

    Author(s)
    Barnes, JL
    Ulett, GC
    Ketheesan, N
    Clair, T
    Summers, PM
    Hirst, RG
    Griffith University Author(s)
    Ulett, Glen C.
    Year published
    2001
    Metadata
    Show full item record
    Abstract
    Melioidosis is a disease of the tropics caused by the facultative intracellular bacterium Burkholderia pseudomallei. In human infection, increased levels of IFN-g in addition to the chemokines interferon-g-inducible protein 10 (IP-10) and monocyte interferon-g-inducible protein (Mig) have been demonstrated. However, the role of these and other chemokines in the pathogenesis of melioidosis remains unknown. Using BALB/c and C57BL/6 mice as models of the acute and chronic forms of human melioidosis, the induction of mRNA was assessed for various chemokines and CSF (G-CSF, M-CSF, GM-CSF, IP-10, Mig, RANTES, MCP-1, KC and MIP-2) ...
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    Melioidosis is a disease of the tropics caused by the facultative intracellular bacterium Burkholderia pseudomallei. In human infection, increased levels of IFN-g in addition to the chemokines interferon-g-inducible protein 10 (IP-10) and monocyte interferon-g-inducible protein (Mig) have been demonstrated. However, the role of these and other chemokines in the pathogenesis of melioidosis remains unknown. Using BALB/c and C57BL/6 mice as models of the acute and chronic forms of human melioidosis, the induction of mRNA was assessed for various chemokines and CSF (G-CSF, M-CSF, GM-CSF, IP-10, Mig, RANTES, MCP-1, KC and MIP-2) in spleen and liver following B. pseudomallei infection. Patterns of chemokine and CSF induction were similar in liver and spleen; however, responses were typically greater in spleen, which reflected higher tissue bacterial loads. In BALB/c mice, high-level expression of mRNA for all chemokines and CSF investigated was demonstrated at day 3 postinfection, correlating with peak bacterial load and extensive infiltration of leucocytes. In contrast, increased mRNA expression and bacterial numbers in C57BL/6 mice were greatest between 4 and 14 days following infection. This paralleled increases in the size and number of abscesses in liver and spleen of C57BL/6 mice at days 3 and 14 postinfection. Earlier induction of cytokine-induced neutrophil chemoattractant (KC), macrophage inflammatory protein-2 (MIP-2), monocyte chemoattractant protein-1 (MCP-1), granulocyte-macrophage CSF (GM-CSF) and macrophage CSF (M-CSF) mRNA was demonstrated in spleen, while MIP-2, MCP-1, IP-10 and Mig were demonstrated in liver of BALB/c mice when compared to spleen and liver of C57BL/6. The magnitude of cellular responses observed in the tissue correlated with increased levels of the chemokines and CSF investigated, as well as bacterial load. Compared with C57BL/6 mice, greater infiltration of neutrophils was observed in liver and spleen of BALB/c mice at day 3. In contrast, early lesions in C57BL/6 mice predominantly comprised macrophages. These results suggest that the inability of BALB/c mice to contain the infection at sites of inflammation may underlie the susceptible phenotype of this mouse strain towards B. pseudomallei infection.
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    Journal Title
    Immunology and Cell Biology
    Volume
    79
    Issue
    5
    Publisher URI
    https://onlinelibrary.wiley.com/doi/10.1046/j.1440-1711.2001.01038.x
    DOI
    https://doi.org/10.1046/j.1440-1711.2001.01038.x
    Copyright Statement
    © 2001 Nature Publishing Group. Please refer to the journal's website for access to the definitive, published version.This is the author-manuscript version of this paper. Reproduced in accordance with the copyright policy of the publisher.
    Subject
    Biochemistry and cell biology
    Immunology
    Medical bacteriology
    Publication URI
    http://hdl.handle.net/10072/25833
    Collection
    • Journal articles

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