| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 4360816 | Cell Host & Microbe | 2016 | 8 Pages |
•Ixodes ticks acquire the Lyme disease pathogen and IFNγ in blood meal from infected hosts•IFNγ in tick gut induces a tick Rho-like GTPase (IGTPase) in a STAT-dependent manner•IGTPase induces expression of the antimicrobial peptide Dae2, limiting pathogen levels
SummaryEvolution of hematophagy in blood-sucking parasites likely involves communication with their hosts. We find that Ixodes ticks are responsive to IFNγ acquired in a blood meal from mice infected with the Lyme disease-causing bacteria Borrelia burgdorferi, leading to induction of antimicrobial responses. Ixodes ticks parasitizing B. burgdorferi-infected mice upregulated an I. scapularis Rho-like GTPase (IGTPase). IGTPase knockdown enhanced B. burgdorferi levels in post-fed ticks, suggesting this protein controls spirochete survival. Notably, IGTPase was only induced during pathogen acquisition from mice and not upon transmission to naive hosts. Microinjection of ticks with IFNγ induced IGTPase, and ticks parasitizing IFNγ knockout mice, failed to upregulate IGTPase. Additionally, ticks lacking the transcription factor STAT, which signals downstream of IFNγ, did not induce IGTPase. IGTPase expression induced antimicrobial peptides, including Dae2, previously shown to inhibit B. burgdorferi. These results identify an interspecies signaling cascade allowing ticks to detect invading bacteria and mount microbicidal responses.
Graphical AbstractFigure optionsDownload full-size imageDownload high-quality image (139 K)Download as PowerPoint slide
