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Nature. 2005 Jul 28;436(7050):573-7.

The Lyme disease agent exploits a tick protein to infect the mammalian host.

Author information

1
Sections of Rheumatology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.

Abstract

The Lyme disease agent, Borrelia burgdorferi, is maintained in a tick-mouse cycle. 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.

PMID:
16049492
PMCID:
PMC4306560
DOI:
10.1038/nature03812
[Indexed for MEDLINE]
Free PMC Article

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