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Original Research ARTICLE

Front. Microbiol., 01 July 2011 | http://dx.doi.org/10.3389/fmicb.2011.00141

Analysis of Borrelia burgdorferi surface proteins as determinants in establishing host cell interactions

  • Bacterial Diseases Branch, Division of Vector Borne Diseases, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, Fort Collins, CO, USA

Borrelia burgdorferi infection causes Lyme borreliosis in humans, a condition which can involve a systemic spread of the organism to colonize various tissues and organs. If the infection is left untreated by antimicrobials, it can lead to manifestations including, arthritis, carditis, and/or neurological problems. Identification and characterization of B. burgdorferi outer membrane proteins that facilitate cellular attachment and invasion to establish infection continue to be investigated. In this study, we sought to further define putative cell binding properties of surface-exposed B. burgdorferi proteins by observing whether cellular adherence could be blocked by antibodies. B. burgdorferi mixed separately with monoclonal antibodies (mAbs) against outer surface protein (Osp) A, OspC, decorin-binding protein (Dbp) A, BBA64, and RevA antigens were incubated with human umbilical vein endothelial cells (HUVEC) and human neuroglial cells (H4). B. burgdorferi treated with anti-OspA, -DbpA, and -BBA64 mAbs showed a significant decrease in cellular association compared to controls, whereas B. burgdorferi treated with anti-OspC and anti-RevA showed no reduction in cellular attachment. Additionally, temporal transcriptional analyses revealed upregulated expression of bba64, ospA, and dbpA during coincubation with cells. Together, the data provide evidence that OspA, DbpA, and BBA64 function in host cell adherence and infection mechanisms.

Keywords: Borrelia burgdorferi, cell attachment, gene expression

Citation: Schmit VL, Patton TG and Gilmore RD Jr. (2011) Analysis of Borrelia burgdorferi surface proteins as determinants in establishing host cell interactions. Front. Microbio. 2:141. doi: 10.3389/fmicb.2011.00141

Received: 19 May 2011; Accepted: 14 June 2011;
Published online: 01 July 2011.

Edited by:

Robert Heinzen, NIH/NIAID-RML, USA

Reviewed by:

Michael F. Minnick, The University of Montana, USA
Edward Shaw, Oklahoma State University, USA

Copyright: © 2011 Schmit, Patton and Gilmore. This is an open-access article subject to a non-exclusive license between the authors and Frontiers Media SA, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and other Frontiers conditions are complied with.

*Correspondence: Robert D. Gilmore Jr., Division of Vector Borne Diseases, Centers for Disease Control and Prevention, 3150 Rampart Rd., Fort Collins, CO 80521, USA. e-mail: rbg9@cdc.gov