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Infection and Immunity, September 2007, p. 4227-4236, Vol. 75, No. 9
0019-9567/07/$08.00+0     doi:10.1128/IAI.00604-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Coordinated Expression of Borrelia burgdorferi Complement Regulator-Acquiring Surface Proteins during the Lyme Disease Spirochete's Mammal-Tick Infection Cycle{triangledown}

Tomasz Bykowski,1 Michael E. Woodman,1 Anne E. Cooley,1 Catherine A. Brissette,1 Volker Brade,2 Reinhard Wallich,3 Peter Kraiczy,2 and Brian Stevenson1*

Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky College of Medicine, Lexington, Kentucky,1 Institute of Medical Microbiology and Infection Control, University Hospital of Frankfurt, Frankfurt am Main, Germany,2 Department of Immunology, University of Heidelberg, Heidelberg, Germany3

Received 27 April 2007/ Returned for modification 23 May 2007/ Accepted 1 June 2007

The Lyme disease spirochete, Borrelia burgdorferi, is largely resistant to being killed by its hosts’ alternative complement activation pathway. One possible resistance mechanism of these bacteria is to coat their surfaces with host complement regulators, such as factor H. Five different B. burgdorferi outer surface proteins having affinities for factor H have been identified: complement regulator-acquiring surface protein 1 (BbCRASP-1), encoded by cspA; BbCRASP-2, encoded by cspZ; and three closely related proteins, BbCRASP-3, -4, and -5, encoded by erpP, erpC, and erpA, respectively. We now present analyses of the recently identified BbCRASP-2 and cspZ expression patterns throughout the B. burgdorferi infectious cycle, plus novel analyses of BbCRASP-1 and erp-encoded BbCRASPs. Our results, combined with data from earlier studies, indicate that BbCRASP-2 is produced primarily during established mammalian infection, while BbCRASP-1 is produced during tick-to-mammal and mammal-to-tick transmission stages but not during established mammalian infection, and Erp-BbCRASPs are produced from the time of transmission from infected ticks into mammals until they are later acquired by other feeding ticks. Transcription of cspZ and synthesis of BbCRASP-2 were severely repressed during cultivation in laboratory medium relative to mRNA levels observed during mammalian infection, and cspZ expression was influenced by culture temperature and pH, observations which will assist identification of the mechanisms employed by B. burgdorferi to control expression of this borrelial infection-associated protein.

* Corresponding author. Mailing address: Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky College of Medicine, MS 421 W.R. Willard Medical Education Building, 800 Rose Street, Lexington, KY 40536-0298. Phone: (859) 257-9358. Fax: (859) 257-8994. E-mail: brian.stevenson{at}uky.edu

{triangledown} Published ahead of print on 11 June 2007.

Editor: D. L. Burns

Infection and Immunity, September 2007, p. 4227-4236, Vol. 75, No. 9
0019-9567/07/$08.00+0     doi:10.1128/IAI.00604-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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