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Borrelia burgdorferi and other related spirochetes bind to galactocerebroside

Department of Pathology (Drs. Garcia Monco, Fernandez Villar, Szczepanski, Wheeler, and Benach, and R.C. Rogers) and State of New York Department of Health (Dr. Benach), Health Sciences Center, State University of New York at Stony Brook, Stony Brook, NY. The present address of Dr. Juan Carlos Garcia Monco is Department of Neurology, Hospital de Galdacano, Galdacano, Vizcaya 48960, Spain.

Spirochetes are agents of neurologic disease that may utilize specific neural cell surface molecules for adhesion. Borrelia burgdorferi, the etiologic agent of Lyme disease, bound to galactocerebroside (GalCer) in numbers that were two- to threefold greater than to ceramide and glucocerebroside, and four- to fivefold greater than to sphingosine, psychosine, sulfatide, cholesterol, and three membrane phospholipids. The adherence was greater to GalCer and ceramide with a higher content of a-hydroxyl fatty acids. Treponema phagedenis Reiter and Borrelia hermsii also bound to GalCer. The binding of B burgdorferi to GalCer was inhibited in a concentration-dependent manner by rabbit polyclonal and murine monoclonal antibodies to this glycosphingolipid component of myelin. The monoclonal antibody to GalCer also inhibited adhesion of the organisms to Schwann cells. Neither free D or L monosaccharides nor the lectin peanut agglutinin inhibited binding. Since B burgdorferi and other spirochetes cause neurologic disease, these results suggest a role for GalCer as a binding site in both the central and peripheral nervous systems.

Address correspondence and reprint requests to Dr. J.L. Benach, Department of Pathology, State University of New York at Stony Brook, Stony Brook, NY 11794.

Supported by grant NIH A1 27044 and by a grant from the G.H. and L.Y. Mathers Charitable Foundation, both to Dr. Benach.

Received October 7, 1991. Accepted for publication in final form December 12, 1991.

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