Open AccessAn Ixodes scapularis Protein Disulfide Isomerase Contributes to Borrelia burgdorferi Colonization of the Vector
Author(s) -
Yongguo Cao,
Connor Rosen,
Gunjan Arora,
Akash Gupta,
Carmen J. Booth,
Kristen E. Murfin,
Jiří Černý,
Alejandro Marín López,
Yu-Min Chuang,
XiaoTian Tang,
Utpal Pal,
Aaron M. Ring,
Sukanya Narasimhan,
Erol Fikrig
Publication year - 2020
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.00426-20
Subject(s) - ixodes scapularis , borrelia burgdorferi , biology , tick , lyme disease , microbiology and biotechnology , ixodes , vector (molecular biology) , borrelia , virology , colonization , spirochaetaceae , ixodidae , antibody , immunology , recombinant dna , biochemistry , gene
Borrelia burgdorferi causes Lyme disease, the most common tick-transmitted illness in North America. When Ixodes scapularis feed on an infected vertebrate host, spirochetes enter the tick gut along with the bloodmeal and colonize the vector. Here, we show that a secreted tick protein, I . s capularis p rotein d isulfide i somerase A3 (IsPDIA3), enhances B. burgdorferi colonization of the tick gut. I. scapularis ticks in which ispdiA3 has been knocked down using RNA interference have decreased spirochete colonization of the tick gut after engorging on B. burgdorferi -infected mice. Moreover, administration of IsPDIA3 antiserum to B. burgdorferi -infected mice reduced the ability of spirochetes to colonize the tick when feeding on these animals. We show that IsPDIA3 modulates inflammatory responses at the tick bite site, potentially facilitating spirochete survival at the vector-host interface as it exits the vertebrate host to enter the tick gut. These data provide functional insights into the complex interactions between B. burgdorferi and its arthropod vector and suggest additional targets to interfere with the spirochete life cycle.