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Gern, Lise

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Gern, Lise
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https://libra.unine.ch/handle/123456789/303

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  • Publication
    Métadonnées seulement
    Quantitative analysis of Borrelia burgdorferi gene expression in naturally (tick) infected mouse strains
    (2005)
    Lederer, Sharon
    ;
    Brenner, Christiane
    ;
    Stehle, Thomas
    ;
    Gern, Lise 
    ;
    Wallich, Reinhard
    ;
    Simon, Markus M
    Adaptation of Borrelia burgdorferi in the vector and vertebrate host is mediated by mechanisms that regulate differential expression of outer surface lipoproteins (Osps). In this study, real time PCR was applied to quantify tissue-specific expression of four linear plasmid (lp54)-encoded (ospA, zs7.a36, zs7.a66 zs7.a68) and one circular plasmid (cp26)-encoded (ospC) gene from B. burgdorferi sensu stricto, in a natural setting of tick-infected immunodeficient (C.B-17 SCID) and immunocompetent (BALB/c and AKR/OlaHsd) mice for up to 120 days post-infection (p.i.). Early during infection (day 30 p.i.) high numbers of spirochetes were found in the heart and joint, but not the ear and spleen tissues of disease-susceptible SCID mice. In disease-susceptible AKR mice spirochetes colonized the ear and joint tissues, but were undetectable in tissues of disease-resistant BALB/c mice. Later in infection (day 120 p.i.), spirochetes had expanded (similar to1,000-fold) in all SCID tissues tested but were undetectable in AKR and BALB/c mice. Of the five genes analyzed, only zs7.a36 transcripts were detected in various tissues of all infected mouse strains, though at differing levels, whereas ospC transcripts were only found in tissue specimens of SCID mice. Furthermore, gene expression of ospC and zs7.a36 appears to be differentially regulated in distinct organs of individual mice. In contrast, transcripts for ospA, zs7.a66, and zs7.a68 were not detected in any of the mouse strains, independent of their immune status and/or the severity of their infection/inflammatory responses. Late during infection (day 120 p.i.), transcription of zs7.a36 and ospC was down-regulated in the tissues of SCID mice despite expansion of spirochetes. This type of quantitative analysis may be helpful to further disclose principles of pathogenesis of Lyme borreliosis and to design strategies for its therapeutic treatment.
  • Publication
    Métadonnées seulement
    T helper cell priming of mice to Borrelia burgdorferi OspA leads to induction of protective antibodies following experimental but not tick-borne infection
    (1997)
    Zhong, Weimin
    ;
    Gern, Lise 
    ;
    Kramer, Michael
    ;
    Wallich, Reinhard
    ;
    Simon, Markus M
    Antibodies to the outer surface lipoprotein A (OspA) of Borrelia burgdorferi confer protection to SCID mice against subsequent tick-borne or experimental infection. However, OspA-specific antibodies are hardly detectable in naturally infected humans, dogs, hamsters and mice. This is most probably due to limited expression of OspA on spirochetes transmitted from the vector to the host. Here we have tested whether T cell priming of mice would lead to the induction of protective OspA-specific antibodies upon infection. It is shown that AKR/N mice, previously immunized with either a single T helper cell peptide of OspA, or a mixture of 27 peptides spanning the entire molecule, develop OspA-specific IgM or IgG antibodies, including those to a prominent protective B cell epitope of OspA, LA-2, within 7 days of infection with low doses (10(3)) of culture-derived spirochetes. In marked contrast, the same groups of pre-sensitized mice failed to generate any detectable OspA-specific antibodies after tick-borne infection for more than 40 days after infection. All mice, irrespective of their state of T cell immunity to OspA or the mode of infection, produced similar levels of OspC-specific IgM and IgG antibodies as early as day 14 after infection. None of the mice previously immunized with OspA peptides were protected against experimental infection, in spite of the appearance of protective antibodies. It is clear from these data that, in contrast to culture-derived spirochetes, the naturally transmitted pathogen fails to express OspA within the mammalian host at levels sufficient for induction of B cell responses, even in the presence of pre-activated T helper cells. Together with the fact that OspA-specific antibodies are mainly operative by eliminating spirochetes from the vector during infestation, the data suggest that OspA-vaccination for T helper cell immunity alone is not sufficient to prevent Lyme disease.