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Proc Natl Acad Sci USA. A critical role for the sphingosine analog AAL-R in dampening the cytokine response during influenza virus infection.

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  • Proc Natl Acad Sci USA. A critical role for the sphingosine analog AAL-R in dampening the cytokine response during influenza virus infection.

    Proc Natl Acad Sci U S A. 2009 Jan 21. [Epub ahead of print]

    A critical role for the sphingosine analog AAL-R in dampening the cytokine response during influenza virus infection.

    Marsolais D, Hahm B, Walsh KB, Edelmann KH, McGavern D, Hatta Y, Kawaoka Y, Rosen H, Oldstone MB. - Departments of Chemical Physiology and Immunology, The Scripps Research Institute, La Jolla, CA 92037;

    Pulmonary tissue damage resulting from influenza virus infection is caused by both the cytolytic activity of the virus and the host immune response.
    Immune-mediated injury results from T cell-mediated destruction of virus-infected cells and by release of cytokines and chemokines that attract polymorphonuclear leukocytes (PML) and macrophages to the infected site.
    The cytokines/chemokines potentiate dendritic cell (DC) activation and T cell expansion, which further enhances local damage.
    Here we report that immune modulation by local administration to the respiratory tract of sphingosine analog AAL-R significantly dampens the release of cytokines and chemokines while maintaining protective neutralizing antibody and cytotoxic T cell responses.
    As a result there was a marked reduction of infiltrating PML and macrophages into the lung and resultant pulmonary tissue injury.
    DC maturation was suppressed, which limited proliferation of specific antiviral T cells in the lung and draining lymph nodes.
    Further, AAL-R was effective in controlling CD8(+) T cell accumulation in the lungs even when given 4 days after initiation of influenza virus infection.
    These data indicate that sphingosine analogs display useful potential for controlling the immunopathology caused by influenza virus.

    PMID: 19164548 [PubMed - as supplied by publisher]
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