17 research outputs found

    <i>B</i>. <i>burgdorferi</i> culture results of Experiment II at 6, 9 and 15 weeks of infection.

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    <p><i>B</i>. <i>burgdorferi</i> culture results of Experiment II at 6, 9 and 15 weeks of infection.</p

    IgG antibody levels in mouse serum samples.

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    <p>Antibody levels were measured using enzyme immunoassays with whole <i>B</i>. <i>burgdorferi</i> lysate as antigen. In panel A, the results are from Experiment II, in panel B from Experiment IV, and in panels C and D combined from Experiments II and III. The results in each panel are obtained from an individual analysis. Each symbol represents the result of one animal. Results are expressed as OD492 values and all samples were analysed in duplicate. The line indicates the mean of each group. Groups with the same letter do not differ at 5% level of probability (Tukey’s HSD test, panels A and B). * P ≤ 0.05, *** P ≤ 0.001.</p

    <i>B</i>. <i>burgdorferi</i> PCR results of Experiment II at 15 weeks of infection.

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    <p>a One sample not available for <i>flaB</i> PCR</p><p><i>B</i>. <i>burgdorferi</i> PCR results of Experiment II at 15 weeks of infection.</p

    Joint swelling and histology.

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    <p>In experiment I (A), II (B) and IV (C), the development of joint swelling was monitored by measuring the medio-lateral diameter of the hind tibiotarsal joints once a week. Each curve represents the mean of the study group. Asterisks denote significant difference from uninfected mice (P ≤ 0.05). Paraffin-embedded tissue sections were prepared from Δ<i>dbpAB</i>/<i>dbpAB</i> (D; group 7) and Δ<i>dbpAB</i> (E; group 8) infected and uninfected control (F; group 6) mice at 15 weeks of infection and stained for HE. Arrowheads indicate the synovial membrane, and asterisks indicate articular cartilage surface in panels D and E. The original magnification in panels D and E is ×400 and in panel <i>F</i> ×20. Panel F indicates the anatomical structure shown in panels D and E. “Cef” Ceftriaxone treatment, “aTα” anti-TNF-alpha treatment.</p

    Design of the mouse experiments.

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    <p>In Experiment I, four Δ<i>dbpAB</i>/<i>dbpAB</i> (group 2), eight Δ<i>dbpAB</i>/<i>dbpA</i> (group 3), eight Δ<i>dbpAB</i>/<i>dbpB</i> (group 4), two Δ<i>dbpAB</i> (group 5) infected animals and two uninfected control animals (group 1) were killed at seven weeks of infection. In Experiment II, 16 infected animals (groups 4 and 5) were treated with ceftriaxone and 16 (groups 6 and 7) with ceftriaxone and anti-TNF-alpha. The ceftriaxone treatment was started at two weeks (25 mg/kg twice a day for 5 days) and the anti-TNF-alpha treatment at seven weeks of infection (10 mg/kg once a week for 4 weeks). Ear biopsy samples were collected at 6 and 9 weeks of infection to monitor the dissemination of the infection. In Experiment III, mice were killed at two weeks to study infection kinetics and bacterial load in joints. In Experiment IV, eight infected animals were treated with ceftriaxone at six weeks of infection (groups 14 and 15).</p

    <i>B</i>. <i>burgdorferi</i> culture and PCR results of Experiment III at two weeks of infection.

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    <p><i>B</i>. <i>burgdorferi</i> culture and PCR results of Experiment III at two weeks of infection.</p

    <i>B</i>. <i>burgdorferi</i> culture and PCR results of Experiment IV at 15 weeks of infection.

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    <p>ND Not determined</p><p><i>B</i>. <i>burgdorferi</i> culture and PCR results of Experiment IV at 15 weeks of infection.</p

    <i>B</i>. <i>burgdorferi</i> culture results of Experiment I at seven weeks of infection.

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    <p>a One sample not available for culture</p><p><i>B</i>. <i>burgdorferi</i> culture results of Experiment I at seven weeks of infection.</p

    Decorin Binding Proteins of <i>Borrelia burgdorferi</i> Promote Arthritis Development and Joint Specific Post-Treatment DNA Persistence in Mice

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    <div><p>Decorin binding proteins A and B (DbpA and B) of <i>Borrelia burgdorferi</i> are of critical importance for the virulence of the spirochete. The objective of the present study was to further clarify the contribution of DbpA and B to development of arthritis and persistence of <i>B</i>. <i>burgdorferi</i> after antibiotic treatment in a murine model of Lyme borreliosis. With that goal, mice were infected with <i>B</i>. <i>burgdorferi</i> strains expressing either DbpA or DbpB, or both DbpA and B, or with a strain lacking the adhesins. Arthritis development was monitored up to 15 weeks after infection, and bacterial persistence was studied after ceftriaxone and immunosuppressive treatments. Mice infected with the <i>B</i>. <i>burgdorferi</i> strain expressing both DbpA and B developed an early and prominent joint swelling. In contrast, while strains that expressed DbpA or B alone, or the strain that was DbpA and B deficient, were able to colonize mouse joints, they caused only negligible joint manifestations. Ceftriaxone treatment at two or six weeks of infection totally abolished joint swelling, and all ceftriaxone treated mice were <i>B</i>. <i>burgdorferi</i> culture negative. Antibiotic treated mice, which were immunosuppressed by anti-TNF-alpha, remained culture negative. Importantly, among ceftriaxone treated mice, <i>B</i>. <i>burgdorferi</i> DNA was detected by PCR uniformly in joint samples of mice infected with DbpA and B expressing bacteria, while this was not observed in mice infected with the DbpA and B deficient strain. In conclusion, these results show that both DbpA and B adhesins are crucial for early and prominent arthritis development in mice. Also, post-treatment borrelial DNA persistence appears to be dependent on the expression of DbpA and B on <i>B</i>. <i>burgdorferi</i> surface. Results of the immunosuppression studies suggest that the persisting material in the joints of antibiotic treated mice is DNA or DNA containing remnants rather than live bacteria.</p></div

    LrpCBA pilus-mediated effects on cellular biofilm formation.

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    <p>Normalized cultures of <i>L</i>. <i>ruminis</i> cells and the recombinant GRS1224 (WT) and GRS1225 (LrpC-deleted) lactococci were assessed for static biofilm formation using a crystal violet staining assay. Various cellular controls were used and treated in the same manner. These included the pilus-less GRS71 and GRS1052 lactococci, the recombinant WT and SpaC-deleted SpaCBA-piliated (GRS1185 and GRS1211, respectively) and WT and SpaF-deleted SpaFED-piliated (GRS1189 and GRS1226, respectively) lactococcal clones, and the SpaCBA-piliated <i>L</i>. <i>rhamnosus</i> GG strain. Multiple measurements were taken and an average value calculated (<i>n</i> = 7). Limit bars show the SEM. Statistical differences for individual pairwise comparisons against the GRS71 control are indicated as *** = <i>P</i> ≤ 0.001 (highly significant) or <i>ns</i> = <i>P</i> > 0.05 (not significant).</p
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