Journal
CELL HOST & MICROBE
Volume 2, Issue 1, Pages 7-18Publisher
CELL PRESS
DOI: 10.1016/j.chom.2007.06.001
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Funding
- NIAID NIH HHS [R01 AI032947, R37 AI049200, R01 AI032947-17, R01 AI041440, R37 AI049200-06] Funding Source: Medline
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The tick Ixodes scapularis is an efficient vector for microbes, including the Lyme disease agent Borrelia burgdorferi. Ticks engorging on vertebrates induce recruitment of inflammatory cells to the bite site. For efficient transmission to the vector, pathogens have to traffic through this complex feeding site while avoiding the deleterious effects of immune cells. We show that a tick protein, Salp25D, plays a critical role-in the mammalian host-for acquisition of Borrelia burgdorferi by the vector. Silencing salp25D in tick salivary glands impaired spirochete acquisition by ticks engorging on B. burgdorferi-infected mice. Immunizing mice against SaIp25D also decreased Borrelia acquisition by L scapularis. Salp25D detoxified reactive oxygen species at the vector-pathogen-host interface, thereby providing a survival advantage to B. burgdorferi at the tick feeding site in mice. These data demonstrate that pathogens can exploit arthropod molecules to defuse mammalian responses in order to successfully enter the vector.
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