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Bacteriology

Evidence of Borrelia Autoimmunity-Induced Component of Lyme Carditis and Arthritis

Elizabeth S. Raveche, Steven E. Schutzer, Helen Fernandes, Helen Bateman, Brian A. McCarthy, Steven P. Nickell, Madeleine W. Cunningham
Elizabeth S. Raveche
1Departments of Pathology and Medicine, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, New Jersey
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Steven E. Schutzer
1Departments of Pathology and Medicine, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, New Jersey
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  • For correspondence: schutzer@umdnj.edu
Helen Fernandes
1Departments of Pathology and Medicine, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, New Jersey
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Helen Bateman
1Departments of Pathology and Medicine, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, New Jersey
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Brian A. McCarthy
1Departments of Pathology and Medicine, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, New Jersey
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Steven P. Nickell
2Department of Molecular Genetics and Microbiology, University of New Mexico, Albuquerque, New Mexico
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Madeleine W. Cunningham
3University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
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DOI: 10.1128/JCM.43.2.850-856.2005
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  • FIG. 1.
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    FIG. 1.

    Joint swelling in mice at various weeks after infection with B. burgdorferi. Mice were between 9 and 12 months of age at the time of initial infection. Data are means ± standard deviations (approximately five mice/group). Values are shown as the differences from uninfected time zero for each mouse. The NZB group was significantly different from the other groups on day 14 (P < 0.05; Student's t test).

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    FIG. 2.

    Levels of anti-B. burgdorferi antibodies in B. burgdorferi (Bb)-infected animals at various times pre- and postinfection using equivalent serum dilutions. Data in columns represent mean values for OD (O.D.) readings in an ELISA of pooled sera from each group. Sera (diluted 1:10) were obtained from animals studied at 9 to 12 months of age. Columns are IgM (left three groups) and IgG (right three groups) antibodies reactive with B. burgdorferi.

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    FIG. 3.

    Levels of IgM anti-OspA antibodies in control and B. burgdorferi-infected NZB mice infected between 5 and 6 months of age and bled on day 35 postinfection. Data in columns represent mean values for OD (O.D.) readings in an ELISA.

  • FIG. 4.
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    FIG. 4.

    The mean ELISA OD (O.D.) readings of IgM anti-myosin reactivity in pooled sera of groups of mice infected with B. burgdorferi 35 days prior to readings. The anti-S. pyogenes (Strep) M5 MAb 36.2.2 was employed for comparison.

  • FIG. 5.
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    FIG. 5.

    Levels of IgM anti-S. pyogenes M5 antibodies in B. burgdorferi-infected animals at various times pre- and postinfection. Data in columns represent mean values for OD readings in an ELISA. Pooled sera (diluted 1:10) were obtained from animals studied at 9 to 12 months of age (approximately five mice/group).

  • FIG. 6.
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    FIG. 6.

    Competition of anti-B. burgdorferi (anti-Bb) reactivity with S. pyogenes M5 protein. Sera from 9- to 12-month-old individual NZB and DBA mice obtained on day 20 postinfection with B. burgdorferi or culture supernatants from anti-S. pyogenes (Strep) MAb 36.2.2 were preincubated with 10 μg of S. pyogenes M5 protein and then tested by ELISA for reactivity with B. burgdorferi lysates. Data represent mean OD values.

  • FIG. 7.
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    FIG. 7.

    (A) Western blot immunoreactivity of serum or monoclonal antibodies to purified recombinant OspA lipoprotein. The control lane contains anti-OspA monoclonal antibody which detects the 31-kDa OspA protein. Sera were obtained from B. burgdorferi-infected NZB (lane b), DBA/2 (lane c), and BALB/c (lane d) mice 35 days following infection. Also shown are anti-S. pyogenes (Strep) M5 IgM MAbs 36.2.2 (lane e) and 54.2.8 (lane f). (Anti-OspA reactivity was detected with specific conjugated goat anti-mouse IgM in all lanes except the control lane, which was reacted with goat anti-mouse IgG.) (B) Anti-S. pyogenes monoclonal antibodies were screened for binding to ELISA plates coated with either B. burgdorferi sonicates, purified M5 protein, or control subpeptides NT3 and NT4. Data in columns represent mean values for OD readings in an ELISA.

Tables

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  • TABLE 1.

    Persistent presence of B. burgdorferi in the hearts of infected mice

    MiceTime of B. burgdorferi infection% PCR positive for OspA (no. positive/total)a
    NZBNone (control)0 (0/3)
    NZB6 weeks60 (3/5)
    NZB8 months100 (4/4)
    • ↵ a Each group was tested for the OspA gene in the heart and spleen by semiquantitative PCR.

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Evidence of Borrelia Autoimmunity-Induced Component of Lyme Carditis and Arthritis
Elizabeth S. Raveche, Steven E. Schutzer, Helen Fernandes, Helen Bateman, Brian A. McCarthy, Steven P. Nickell, Madeleine W. Cunningham
Journal of Clinical Microbiology Feb 2005, 43 (2) 850-856; DOI: 10.1128/JCM.43.2.850-856.2005

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Evidence of Borrelia Autoimmunity-Induced Component of Lyme Carditis and Arthritis
Elizabeth S. Raveche, Steven E. Schutzer, Helen Fernandes, Helen Bateman, Brian A. McCarthy, Steven P. Nickell, Madeleine W. Cunningham
Journal of Clinical Microbiology Feb 2005, 43 (2) 850-856; DOI: 10.1128/JCM.43.2.850-856.2005
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KEYWORDS

Arthritis, Infectious
Autoimmune Diseases
Borrelia burgdorferi
Lyme disease
Myocarditis

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