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    Online-Ressource
    Online-Ressource
    The American Association of Immunologists ; 2010
    In:  The Journal of Immunology Vol. 184, No. 1_Supplement ( 2010-04-01), p. 37.6-37.6
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 184, No. 1_Supplement ( 2010-04-01), p. 37.6-37.6
    Kurzfassung: C3H/HeN (C3H) mice develop severe arthritis whereas; C57BL/6J (C57) mice develop mild arthritis after experimental infection with the Lyme disease spirochete Borrelia burgdorferi. We hypothesize that these host responses may depend on differences in the expression and regulation of inflammatory mediators induced by spirochetes during the early stage of Lyme disease. In the present study, bone marrow-derived macrophages from C3H and C57 mice were stimulated with live B. burgdorferi or with its lipoprotein outer surface protein A; supernatants were collected and subjected to proteome analysis using multiplex ELISA. Both stimulants induced significantly higher levels of IL-6, TNF-α, IFN-γ, KC, IL-9, MCP1/CCL2, IL-5, GM-CSF, and IL-12p70 in cells of C3H than in those of C57 mice. In contrast, MIP1α/CCL3, MIP1β/CCL4, RANTES/CCL5, IP-10/CXCL10, MIP2/CXCL2, IL-17, IL-1α, IL-1β, LIX/CXCL5, G-CSF, CXCL9/MIG and IL-10 levels were significantly greater in C57 than in C3H mice. Exogenous IL-10 abrogated the expression levels of inflammatory mediators. Neutralization of endogenous IL-10 resulted in enhanced production of mediators; the effect was more evident in C57 mice. Our data show differential expression and regulation of inflammatory mediators in B. burgdorferi-stimulated macrophages of C57 and C3H mice. The potent action of endogenous IL-10, especially in C57, suggests a key role played by IL-10 to abrogate inflammation during the early stage of Lyme disease in this mouse strain.
    Materialart: Online-Ressource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: The American Association of Immunologists
    Publikationsdatum: 2010
    ZDB Id: 1475085-5
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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