Expression of Borrelia burgdorferi erp genes during infection of non-human primates

Jennifer C. Miller, Kavitha Narayan, Brian Stevenson, Andrew R. Pachner

Research output: Contribution to journalArticlepeer-review

30 Scopus citations

Abstract

All examined isolates of the Lyme disease spirochete contain multiple operons encoding Erp outer membrane lipoproteins. Many Erp proteins have been demonstrated to bind the host complement regulator factor H, and may thereby help protect the bacteria from complement-mediated killing during mammalian infection. Consistent with that hypothesis, all Erp proteins are produced by Borrelia burgdorferi during transmission between tick vectors and mammalian hosts. The present study examined whether erp genes are also expressed by B. burgdorferi following establishment of mammalian infection. To that end, quantitative RT-PCR was utilized to assess erp transcription levels within different tissues of infected non-human primates, a model that closely mimics human Lyme disease. The majority of erp genes were detectably transcribed after more than 3 months of mammalian infection. Intriguingly, differences in expression levels were noted among the various erp loci. No significant differences in erp expression were apparent between examined tissues, which included central and peripheral nervous system tissue, skeletal muscle, bladder, skin and heart tissues. These data strongly suggest that Erp proteins are expressed by B. burgdorferi throughout infection of their vertebrate hosts.

Original languageEnglish
Pages (from-to)27-33
Number of pages7
JournalMicrobial Pathogenesis
Volume39
Issue number1-2
DOIs
StatePublished - Jul 2005

Bibliographical note

Funding Information:
This study was funded by US National Institutes of Health grants RO1-AI44254 to Brian Stevenson, and NO1-AI9358 to Andrew R. Pachner. Jennifer C. Miller was supported by NIH training grant T32-AI49795. We thank Robert Gilmore, Jr and Mark Wooten for assistance with LightCycler- based protocols, Kate von Lackum for helpful discussions, and Sara Bair and Natalie Mickelson for technical assistance during the course of this work.

Funding

This study was funded by US National Institutes of Health grants RO1-AI44254 to Brian Stevenson, and NO1-AI9358 to Andrew R. Pachner. Jennifer C. Miller was supported by NIH training grant T32-AI49795. We thank Robert Gilmore, Jr and Mark Wooten for assistance with LightCycler- based protocols, Kate von Lackum for helpful discussions, and Sara Bair and Natalie Mickelson for technical assistance during the course of this work.

FundersFunder number
National Institutes of Health (NIH)RO1-AI44254, NO1-AI9358
National Institute of Allergy and Infectious DiseasesT32AI049795

    Keywords

    • Borrelia burgdorferi
    • Genes
    • Lyme disease

    ASJC Scopus subject areas

    • Microbiology
    • Infectious Diseases

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