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Infection and Immunity, October 2007, p. 4817-4825, Vol. 75, No. 10
0019-9567/07/$08.00+0     doi:10.1128/IAI.00532-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Human Pathogenic Borrelia spielmanii sp. nov. Resists Complement-Mediated Killing by Direct Binding of Immune Regulators Factor H and Factor H-Like Protein 1{triangledown}

Pia Herzberger,1 Corinna Siegel,1 Christine Skerka,2 Volker Fingerle,3 Ulrike Schulte-Spechtel,3 Alje van Dam,4 Bettina Wilske,3 Volker Brade,1 Peter F. Zipfel,2,5 Reinhard Wallich,6 and Peter Kraiczy1*

Institute of Medical Microbiology and Infection Control, University Hospital of Frankfurt, Paul-Ehrlich-Str. 40, D-60596 Frankfurt, Germany,1 Department of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology, Beutenbergstr. 11a, D-07745 Jena, Germany,2 Max von Pettenkofer-Institut für Medizinische Mikrobiologie und Hygiene der Ludwig-Maximilians-Universität München, D-80336 Munich, Germany,3 Department of Medical Microbiology, University Medical Center, P.O. Box 9600, 2300RC Leiden, The Netherlands,4 Friedrich Schiller University, D-07745 Jena, Germany,5 Institute of Immunology, University of Heidelberg, Im Neuenheimer Feld 305, D-69120 Heidelberg, Germany6

Received 13 April 2007/ Returned for modification 29 May 2007/ Accepted 6 July 2007

Borrelia spielmanii sp. nov. has recently been shown to be a novel human pathogenic genospecies that causes Lyme disease in Europe. In order to elucidate the immune evasion mechanisms of B. spielmanii, we compared the abilities of isolates obtained from Lyme disease patients and tick isolate PC-Eq17 to escape from complement-mediated bacteriolysis. Using a growth inhibition assay, we show that four B. spielmanii isolates, including PC-Eq17, are serum resistant, whereas a single isolate, PMew, was more sensitive to complement-mediated lysis. All isolates activated complement in vitro, as demonstrated by covalent attachment of C3 fragments; however, deposition of the later activation products C6 and C5b-9 was restricted to the moderately serum-resistant isolate PMew and the serum-sensitive B. garinii isolate G1. Furthermore, serum adsorption experiments revealed that all B. spielmanii isolates acquired the host alternative pathway regulators factor H and factor H-like protein (FHL-1) from human serum. Both complement regulators retained their factor I-mediated C3b inactivation activities when bound to spirochetes. In addition, two distinct factor H and FHL-1 binding proteins, BsCRASP-1 and BsCRASP-2, were identified, which we estimated to be approximately 23 to 25 kDa in mass. A further factor H binding protein, BsCRASP-3, was found exclusively in the tick isolate, PC-Eq17. This is the first report describing an immune evasion mechanism utilized by B. spielmanii sp. nov., and it demonstrates the capture of human immune regulators to resist complement-mediated killing.

* Corresponding author. Mailing address: Institute of Medical Microbiology and Infection Control, University Hospital of Frankfurt, Paul-Ehrlich-Str. 40, D-60596 Frankfurt, Germany. Phone: 49-69-6301-7165. Fax: 49-69-6301-5767. E-mail: Kraiczy{at}em.uni-frankfurt.de

{triangledown} Published ahead of print on 16 July 2007.

Editor: F. C. Fang

Infection and Immunity, October 2007, p. 4817-4825, Vol. 75, No. 10
0019-9567/07/$08.00+0     doi:10.1128/IAI.00532-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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