Diverse Lyme disease spirochetes bind integrin α(IIb)β3 on human platelets

J. Coburn, Stephen W Barthold, J. M. Leong

Research output: Contribution to journalArticle

59 Scopus citations

Abstract

Lyme disease is a chronic, multisystemic infection caused by Borrelia burgdorferi sensu lato. An infectious strain of B. burgdorferi was previously shown to bind to human platelets via the integrin α(IIb)β3. In this study, a diverse group of Lyme disease spirochetes was tested for platelet- and α(IIb)β3-binding activity. This collection included representatives of each of the three species that cause Lyme disease, B. burgdorferi (sensu stricto). B. garinii, and B. afzelii. Strains were characterized for infectivity in mouse models or were low-passage isolates from human patients. Each of the 11 infectious strains bound to platelets immobilized in microtiter wells and in suspension. Binding to platelets in suspension was specifically inhibited by a blocking anti-α(IIb)β3 antibody, and representatives of each species bound to purified α(IIb)β3. The strains that did not bind α(IIb)β3 or platelets were all noninfectious. No obvious relationship was observed between binding to platelets and expression of the bacterial outer surface protein OspA, OspB, or OspC, as assessed by immunoblotting. These results demonstrate that integrin α(IIb)β3-binding activity is widespread among the Borrelia species that cause Lyme disease and are consistent with a role for α(IIb)β3 binding in the transmission and/or pathogenesis of Lyme disease.

Original languageEnglish (US)
Pages (from-to)5559-5567
Number of pages9
JournalInfection and Immunity
Volume62
Issue number12
StatePublished - 1994
Externally publishedYes

ASJC Scopus subject areas

  • Immunology

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