Borrelia burgdorferi RevA significantly affects pathogenicity and host response in the mouse model of Lyme disease

Rebecca Byram, Robert A. Gaultney, Angela M. Floden, Christopher Hellekson, Brandee L. Stone, Amy Bowman, Brian Stevenson, Barbara J.B. Johnson, Catherine A. Brissette

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

The Lyme disease spirochete, Borrelia burgdorferi, expresses RevA and numerous outer surface lipoproteins during mammalian infection. As an adhesin that promotes bacterial interaction with fibronectin, RevA is poised to interact with the extracellular matrix of the host. To further define the role(s) of RevA during mammalian infection, we created a mutant that is unable to produce RevA. The mutant was still infectious to mice, although it was significantly less well able to infect cardiac tissues. Complementation of the mutant with a wild-type revA gene restored heart infectivity to wild-type levels. Additionally, revA mutants led to increased evidence of arthritis, with increased fibrotic collagen deposition in tibiotarsal joints. The mutants also induced increased levels of the chemokine CCL2, a monocyte chemoattractant, in serum, and this increase was abolished in the complemented strain. Therefore, while revA is not absolutely essential for infection, deletion of revA had distinct effects on dissemination, arthritis severity, and host response.

Original languageEnglish
Pages (from-to)3675-3683
Number of pages9
JournalInfection and Immunity
Volume83
Issue number9
DOIs
StatePublished - 2015

Bibliographical note

Publisher Copyright:
© 2015, American Society for Microbiology.

ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Immunology
  • Infectious Diseases

Fingerprint

Dive into the research topics of 'Borrelia burgdorferi RevA significantly affects pathogenicity and host response in the mouse model of Lyme disease'. Together they form a unique fingerprint.

Cite this