Abstract:
:The Lyme disease agent, Borrelia burgdorferi, colonizes the gut of the tick Ixodes scapularis, which transmits the pathogen to vertebrate hosts including humans. Here we show that B. burgdorferi colonization increases the expression of several tick gut genes including pixr, encoding a secreted gut protein with a Reeler domain. RNA interference-mediated silencing of pixr, or immunity against PIXR in mice, impairs the ability of B. burgdorferi to colonize the tick gut. PIXR inhibits bacterial biofilm formation in vitro and in vivo. Abrogation of PIXR function in vivo results in alterations in the gut microbiome, metabolome and immune responses. These alterations influence the spirochete entering the tick gut in multiple ways. PIXR abrogation also impairs larval molting, indicative of its role in tick biology. This study highlights the role of the tick gut in actively managing its microbiome, and how this impacts B. burgdorferi colonization of its arthropod vector. Borrelia burgdorferi, the causative agent of Lyme disease, is transmitted by the tick Ixodes scapularis. Here, the authors show that a tick secreted protein (PIXR) modulates the tick gut microbiota and facilitates B. burgdorferi colonization.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Narasimhan S,Schuijt TJ,Abraham NM,Rajeevan N,Coumou J,Graham M,Robson A,Wu MJ,Daffre S,Hovius JW,Fikrig Edoi
10.1038/s41467-017-00208-0subject
Has Abstractpub_date
2017-08-04 00:00:00pages
184issue
1issn
2041-1723pii
10.1038/s41467-017-00208-0journal_volume
8pub_type
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