Abstract:
:The Lyme disease agent Borrelia burgdorferi is primarily transmitted to vertebrates by Ixodes ticks. The classical and alternative complement pathways are important in Borrelia eradication by the vertebrate host. We recently identified a tick salivary protein, designated P8, which reduced complement-mediated killing of Borrelia. We now discover that P8 interferes with the human lectin complement cascade, resulting in impaired neutrophil phagocytosis and chemotaxis and diminished Borrelia lysis. Therefore, P8 was renamed the tick salivary lectin pathway inhibitor (TSLPI). TSLPI-silenced ticks, or ticks exposed to TSLPI-immune mice, were hampered in Borrelia transmission. Moreover, Borrelia acquisition and persistence in tick midguts was impaired in ticks feeding on TSLPI-immunized, B. burgdorferi-infected mice. Together, our findings suggest an essential role for the lectin complement cascade in Borrelia eradication and demonstrate how a vector-borne pathogen co-opts a vector protein to facilitate early mammalian infection and vector colonization.
journal_name
Cell Host Microbejournal_title
Cell host & microbeauthors
Schuijt TJ,Coumou J,Narasimhan S,Dai J,Deponte K,Wouters D,Brouwer M,Oei A,Roelofs JJ,van Dam AP,van der Poll T,Van't Veer C,Hovius JW,Fikrig Edoi
10.1016/j.chom.2011.06.010subject
Has Abstractpub_date
2011-08-18 00:00:00pages
136-46issue
2eissn
1931-3128issn
1934-6069pii
S1931-3128(11)00219-8journal_volume
10pub_type
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