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

Research output: Contribution to journalArticlepeer-review

37 Scopus citations

Abstract

We investigated the possibility that manifestations of Lyme disease in certain hosts, such as arthritis and carditis, may be autoimmunity mediated due to molecular mimicry between the bacterium Borrelia burgdorferi and self-components. We first compared amino acid sequences of Streptococcus pyogenes M protein, a known inducer of antibodies that are cross-reactive with myosin, and B. burgdorferi and found significant homologies with OspA protein. We found that S. pyogenes M5-specific antibodies and sera from B. burgdorferi-infected mice reacted with both myosin and B. burgdorferi proteins by Western blots and enzyme-linked immunosorbent assay. To investigate the relationship between self-reactivity and the response to B. burgdorferi, NZB mice, models of autoimmunity, were infected. NZB mice infected with B. burgdorferi developed higher degrees of joint swelling and higher anti-B. burgdorferi immunoglobulin M cross-reactive responses than other strains with identical major histocompatibility complex (DBA/2 and BALB/c). These studies reveal immunological cross-reactivity and suggest that B. burgdorferi may share common epitopes which mimic self-proteins. These implications could be important for certain autoimmunity-susceptible individuals or animals who become infected with B. burgdorferi.

Original languageEnglish (US)
Pages (from-to)850-856
Number of pages7
JournalJournal of clinical microbiology
Volume43
Issue number2
DOIs
StatePublished - Feb 2005

All Science Journal Classification (ASJC) codes

  • Microbiology (medical)

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