http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0015830
Outer Surface Protein C Is a Dissemination-Facilitating Factor of Borrelia
burgdorferi during Mammalian Infection
Abstract
Background
The Lyme disease spirochete Borrelia burgdorferi dramatically upregulates
outer surface protein C (OspC) in response to fresh bloodmeal during
transmission from the tick vector to a mammal, and abundantly produces the
antigen during early infection. As OspC is an effective immune target, to
evade the immune system B. burgdorferi downregulates the antigen once the
anti-OspC humoral response has developed, suggesting an important role for
OspC during early infection.
Methodology/Principal Findings
In this study, a borrelial mutant producing an OspC antigen with a
5-amino-acid deletion was generated. The deletion didn't significantly
increase the 50% infectious dose or reduce the tissue bacterial burden
during infection of the murine host, indicating that the truncated OspC can
effectively protect B. burgdorferi against innate elimination.
However, the deletion greatly impaired the ability of B. burgdorferi to
disseminate to remote tissues after inoculation into mice.
Conclusions/Significance
The study indicates that OspC plays an important role in dissemination of
B.
burgdorferi during mammalian infection.
Citation: Seemanapalli SV, Xu Q, McShan K, Liang FT (2010) Outer Surface
Protein C Is a Dissemination-Facilitating Factor of Borrelia burgdorferi
during Mammalian Infection. PLoS ONE 5(12): e15830.
doi:10.1371/journal.pone.0015830
Editor: Laurent Rénia, Singapore Immunology Network-A*STAR, Singapore
Received: October 1, 2010; Accepted: November 27, 2010; Published:
December 31, 2010
Copyright: © 2010 Seemanapalli et al. This is an open-access article
distributed under the terms of the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any
medium, provided the original author and source are credited.
Funding: This work was supported in part by AI077733, AR053338, and
RR020159 from the National Institutes of Health. The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
Competing interests: The authors have declared that no competing interests
exist.
* E-mail: fliang@vetmed.lsu.edu
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