Program Schedule

1348
­­­Immune response to endothelial cell growth factor is elevated during acute Lyme borreliosis but not in post-Lyme disease syndrome

Session: Poster Abstract Session: Biomarkers of Immune Responses
Saturday, October 11, 2014
Room: The Pennsylvania Convention Center: IDExpo Hall BC
Posters
  • IDWeek 2014 Poster KT Rev3.pdf (487.3 kB)
  • Background: Lyme disease is caused by spirochetes of the Borrelia burgdorferi species complex.  Some of the symptoms of Lyme disease are thought to result from the body’s immune response during infection. Recently, immune reactivity to endothelial cell growth factor (ECGF), a self-antigen, has been reported to be elevated in patients with Lyme disease. As such, the ECGF protein has been proposed as an autoantibody target in manifestations that are thought to involve infection-induced immune-mediated mechanisms, including refractory Lyme arthritis and post-Lyme disease syndrome (PLDS).

    Methods: We aimed to evaluate this hypothesis through analysis of antibody response to recombinant human ECGF in serum from 90 individuals with a range of early to late manifestations of Lyme disease, including single EM, multiple EM, early neurologic, late neurologic, arthritis, and refractory arthritis, as well as 93 PLDS patients, 25 post-Lyme healthy individuals, and 30 healthy individuals without a history of Lyme disease.  In addition, ECGF’s potential as a target of B. burgdorferi cross-reactive antibodies in Lyme disease was examined through competition experiments. 

    Results: In comparison to non-Lyme healthy individuals, Lyme disease patients with multiple EM (p<0.001), early neurologic (p<0.001), late neurologic (p<0.001), arthritis (p<0.001), and refractory arthritis (p<0.05) manifestations displayed significantly increased antibody reactivity to ECGF.  There was not a significant difference in anti-ECGF antibody reactivity between PLDS patients and post-Lyme healthy individuals.  Antibodies from rabbits immunized with B. burgdorferi whole protein extract did not cross-react with ECGF.  Patient serum antibody reactivity to ECGF could not be inhibited by competition with B. burgdorferi proteins. 

    Conclusion: Our data indicate that antibody reactivity to ECGF is elevated throughout the course of acute Lyme disease, with the highest levels occurring after the dissemination of infection.  However, immune response to ECGF is not specifically associated with refractory Lyme arthritis or with post-Lyme disease syndrome.  In addition, the anti-ECGF antibody response in Lyme disease does not appear to be a result of cross-reactivity.

    Kevin Tang, PhD1, Mary Ajamian1, Brian Fallon1, Gary P. Wormser, MD2, Adriana Marques, MD3 and Armin Alaedini1, (1)Columbia University, New York, NY, (2)New York Medical College, Valhalla, NY, (3)NIH, Bethesda, MD

    Disclosures:

    K. Tang, None

    M. Ajamian, None

    B. Fallon, None

    G. P. Wormser, None

    A. Marques, None

    A. Alaedini, None

    Findings in the abstracts are embargoed until 12:01 a.m. EDT, Oct. 8th with the exception of research findings presented at the IDWeek press conferences.

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