The Lyme disease agent, Borrelia burgdorferi, is maintained in a tick–mouse cycle^{1, 2}. Here we show that B. burgdorferi usurps a tick salivary protein, Salp15 (ref. 3), to facilitate the infection of mice. The level of salp15 expression was selectively enhanced by the presence of B. burgdorferi in Ixodes scapularis, first indicating that spirochaetes might use Salp15 during transmission. Salp15 was then shown to adhere to the spirochaete, both in vitro and in vivo, and specifically interacted with B. burgdorferi outer surface protein C. The binding of Salp15 protected B. burgdorferi from antibody-mediated killing in vitro and provided spirochaetes with a marked advantage when they were inoculated into naive mice or animals previously infected with B. burgdorferi. Moreover, RNA interference-mediated repression of salp15 in I. scapularis drastically reduced the capacity of tick-borne spirochaetes to infect mice. These results show the capacity of a pathogen to use a secreted arthropod protein to help it colonize the mammalian host.

1. Sections of Rheumatology and
2. Allergy and Immunology, Department of Internal Medicine, and
3. Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut 06520, USA
4. Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA
5. Department of Biology, University of North Carolina at Charlotte, Charlotte, North Carolina 28223, USA
6. Department of Entomology, Connecticut Agricultural Experiment Station, New Haven, Connecticut 06504, USA
7. L2 Diagnostics, New Haven, Connecticut 06511, USA

Correspondence to: Erol Fikrig^1,3 Correspondence and requests for materials should be addressed to E.F. (Email: erol.fikrig@yale.edu).

Received 17 March 2005; Accepted 13 May 2005

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