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Infection and Immunity, December 2002, p. 6811-6816, Vol. 70, No. 12
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.12.6811-6816.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Immunization with the N-Terminal Portion of Treponema pallidum Repeat Protein K Attenuates Syphilitic Lesion Development in the Rabbit Model

Cecilia A. Morgan,1 Sheila A. Lukehart,1,2 and Wesley C. Van Voorhis1,2*

Departments of Pathobiology,1 Medicine, University of Washington, Seattle, Washington 981952

Received 14 June 2002/ Returned for modification 13 August 2002/ Accepted 29 August 2002

When used as an immunogen, Treponema pallidum repeat protein K (TprK) has been shown to attenuate syphilitic lesions upon homologous intradermal challenge in the rabbit model. To further explore this protein as a potential vaccine component, we sought to identify the immunogenic regions of TprK. The abilities of three recombinant peptides encompassing TprK to elicit T- and B-cell responses and to protect against challenge were examined. All three fragments elicited proliferative responses from splenocytes taken from infected rabbits. However, enzyme-linked immunosorbent assays indicated that only fragments 1 and 3 were consistently recognized by antisera from infected rabbits. Each fragment was also used to immunize rabbits that were subsequently challenged intradermally with infectious T. pallidum. All lesions on unimmunized control rabbits ulcerated and contained treponemes, while the lesions on rabbits immunized with fragment 1 were the least likely to have detectable treponemes (25%) and the least likely to ulcerate (37.5%). The lesions on rabbits immunized with fragment 3 showed intermediate results, and rabbits immunized with fragment 2 were the most likely of all those on immunized rabbits to have detectable treponemes (91.7%) and to ulcerate (66.7%). These results demonstrate that epitopes in fragment 1 are recognized by T cells and antibodies during infection and that immunization with this portion of TprK most effectively attenuates syphilitic lesion development.

* Corresponding author. Mailing address: University of Washington, Box 357185, Seattle, WA 98195. Phone: (206) 543-0821. Fax: (206) 685-8681. E-mail: wesley{at}u.washington.edu.

Editor: D. L. Burns

Infection and Immunity, December 2002, p. 6811-6816, Vol. 70, No. 12
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.12.6811-6816.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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