Binding of human complement regulators FHL-1 and factor H to CRASP-1 orthologs of Borrelia burgdorferi

The complement regulator-acquiring surface protein (CRASP)-1 is a member of the paralogous gene family gbb54 and the dominant FHL-1 and factor H binding protein of Borrelia burgdorferi sensu stricto (s.s.). It was shown recently that expression of BbCRASP-1 directly correlates with serum resistance...

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Main Authors: Kraiczy, Peter (Author) , Rossmann, Evelyn (Author) , Brade, Volker (Author) , Simon, Markus M. (Author) , Skerka, Christine (Author) , Zipfel, Peter F. (Author) , Wallich, Reinhard (Author)
Format: Article (Journal)
Language:English
Published: November 2006
In: Wiener klinische Wochenschrift
Year: 2006, Volume: 118, Issue: 21/22, Pages: 669-676
ISSN:1613-7671
DOI:10.1007/s00508-006-0691-1
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1007/s00508-006-0691-1
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Author Notes:Peter Kraiczy, Evelyn Rossmann, Volker Brade, Markus M. Simon, Christine Skerka, Peter F. Zipfel & Reinhard Wallich

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520 |a The complement regulator-acquiring surface protein (CRASP)-1 is a member of the paralogous gene family gbb54 and the dominant FHL-1 and factor H binding protein of Borrelia burgdorferi sensu stricto (s.s.). It was shown recently that expression of BbCRASP-1 directly correlates with serum resistance of B. burgdorferi s.s. isolates. In the present study we have elucidated the putative potential of other members of the gbb54 paralogous family, including orthologs ZSA66, ZSA69, ZSA70, ZSA71, ZSA72 and ZSA73 of the European B. burgdorferi s.s. strain ZS7, to bind human FHL-1 and factor H. In spite of their overall similarity in protein sequence, between 47% and 67%, and the fact that the C-terminal region of ZSA69 shows 70% similarity with BbCRASP-1, none of the orthologous proteins was able to bind human FHL-1 and/or factor H. BbCRASP-1 is the only member of the paralogous gene family gbb54 that binds to human complement regulators, supporting the notion that BbCRASP-1 plays a critical role in evasion of complement by B. burgdorferi s.s. and thus may be helpful in the development of novel therapeutic strategies against Lyme borreliosis. 
650 4 |a Bacterial Proteins 
650 4 |a Base Sequence 
650 4 |a Blood Donors 
650 4 |a Borrelia burgdorferi 
650 4 |a Complement Activation 
650 4 |a Complement C3b Inactivator Proteins 
650 4 |a Complement Factor H 
650 4 |a DNA, Bacterial 
650 4 |a Humans 
650 4 |a Immunity, Innate 
650 4 |a Lyme Disease 
650 4 |a Membrane Proteins 
650 4 |a Reverse Transcriptase Polymerase Chain Reaction 
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