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Infection and Immunity, July 2000, p. 4169-4173, Vol. 68, No. 7
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Lyme Arthritis Resolution with Antiserum to a 37-Kilodalton Borrelia burgdorferi Protein

Sunlian Feng, Emir Hodzic, and Stephen W. Barthold*

Center for Comparative Medicine, Schools of Medicine and Veterinary Medicine, University of California, Davis, California 95616

Received 28 January 2000/Returned for modification 6 March 2000/Accepted 12 April 2000

A 37-kDa protein from Borrelia burgdorferi (the agent of Lyme disease) was identified as a target for immune-mediated resolution of Lyme arthritis. Studies in a mouse model have shown that arthritis resolution can be mediated by antibodies (against unknown target antigens) within immune sera from actively infected mice. Immune sera from infected mice were therefore used to screen a B. burgdorferi genomic expression library. A gene was identified whose native product is a putative lipoprotein of approximately 37 kDa, referred to here as arthritis-related protein (Arp). Active and passive immunization of mice with recombinant Arp or Arp antiserum, respectively, did not protect mice from challenge inoculation. However, when Arp antiserum was administered to severe combined immunodeficient (SCID) mice with established infections and with ongoing arthritis and carditis, treatment selectively induced arthritis resolution without affecting the status of carditis or influencing the status of infection, including spirochetemia. The selective arthritis-resolving effect of Arp antiserum mimics the activity of immune serum from immunocompetent mice when such serum is transferred into SCID mice with established infections. The arp gene could not be amplified from unrelated B. burgdorferi isolates but hybridized with those isolates only under very-low-stringency conditions. Arp antiserum reacted against proteins of similar size in a wide range of B. burgdorferi isolates.


* Corresponding author. Mailing address: University of California, Center for Comparative Medicine, One Shields Ave., Davis, CA 95616. Phone: (530) 752-1245. Fax: (530) 752-7914. E-mail: swbarthold{at}ucdavis.edu.


Infection and Immunity, July 2000, p. 4169-4173, Vol. 68, No. 7
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.



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