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    Bacterial Lipopolysaccharide (LPS) activates Bovine Leukemia Virus (BLV) expression through Toll-like receptor 4 (2004)

    Art
    Poster
    Autoren
    Bondzio, A.
    Gabler, C.
    Beier, D.
    Risse, S.
    Einspanier, R.
    Kongress
    Herbsttagung der Gesellschaft für Biochemie und Molekularbiologie
    Münster, 19. – 22.09.2004
    Quelle
    Sprache
    Englisch
    Kontakt
    Institut für Veterinär-Biochemie

    Oertzenweg 19 b
    14163 Berlin
    Tel.+49 30 838 62225 Fax.+49 30 838-62584
    email:biochemie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    BLV is an oncogenic retrovirus and the causative agent for enzootic bovine leukosis. BLV
    infection results in a large asymptomatic period, followed by development of persistent
    lymphocytosis. Since the major target cell for this virus is the B-lymphocyte, the
    expression of BLV should respond to agents that activating these cells. LPS is one of the
    agents that can stimulate BLV expression in bovine peripheral blood mononuclear cells
    (PBMCs). However, the signalling mechanisms utilized by LPS to stimulate BLV
    expression are still incompletely understood. In this study we showed by RT-PCR that
    the initiation of PBMC response to LPS involves Toll-like receptor 4 (TLR4). Stimulation of
    PBMCs with LPS resulted in an significant increase in the expression level of TLR4 mRNA
    in PBMCs in a time-dependent manner, but the expression of TLR2 mRNA was not
    affected. In parallel, we showed that LPS activated NF-kB in bovine PBMCs and enhanced
    the secretion of IL-8 in a time- and dose-dependent manner. As demonstrated by ELISA
    the expression of viral antigens BLVp24 and gp51 in PBMCs was enhanced by LPS
    compared to the unstimulated controls. These effects were accompanied by free radical
    formation as measured with pholasin, giving further evidence for the role of reactive
    oxygen species (ROS) in activation of BLV expression, that we have previously reported
    (Bondzio et al., 2003). In summary, our results indicate that TLR4 may mediate LPSstimulated
    BLV expression via ROS.