Evidence ofBorreliaAutoimmunity-Induced Component of Lyme Carditis and Arthritis

Publisher Website
Google Scholar
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 bacteriumBorrelia burgdorferiand self-components. We first compared amino acid sequences ofStreptococcus pyogenesM protein, a known inducer of antibodies that are cross-reactive with myosin, andB. burgdorferiand found significant homologies with OspA protein. We found thatS. pyogenesM5-specific antibodies and sera fromB. burgdorferi-infected mice reacted with both myosin andB. burgdorferiproteins by Western blots and enzyme-linked immunosorbent assay. To investigate the relationship between self-reactivity and the response toB. burgdorferi, NZB mice, models of autoimmunity, were infected. NZB mice infected withB. burgdorferideveloped higher degrees of joint swelling and higher anti-B. burgdorferiimmunoglobulin 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 thatB. burgdorferimay share common epitopes which mimic self-proteins. These implications could be important for certain autoimmunity-susceptible individuals or animals who become infected withB. burgdorferi.