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Infection and Immunity, November 2002, p. 6158-6165, Vol. 70, No. 11
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.11.6158-6165.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

The Haemophilus ducreyi Serum Resistance Antigen DsrA Confers Attachment to Human Keratinocytes

Leah E. Cole,1 Thomas H. Kawula,1* Kristen L. Toffer,1,{dagger} and Christopher Elkins2

Department of Microbiology & Immunology,1 Department of Medicine, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 275992

Received 7 May 2002/ Returned for modification 20 June 2002/ Accepted 10 July 2002

Haemophilus ducreyi is the etiologic agent of the sexually transmitted genital ulcer disease chancroid. H. ducreyi serum resistance protein A (DsrA) is a member of a family of multifunctional outer membrane proteins that are involved in resistance to killing by human serum complement. The members of this family include YadA of Yersinia species, the UspA proteins of Moraxella catarrhalis, and the Eib proteins of Escherichia coli. The role of YadA, UspA1, and UspA2H as eukaryotic cell adhesins and the function of UspA2 as a vitronectin binder led to our investigation of the cell adhesion and vitronectin binding properties of DsrA. We found that DsrA was a keratinocyte-specific adhesin as it was necessary and sufficient for attachment to HaCaT cells, a keratinocyte cell line, but was not required for attachment to HS27 cells, a fibroblast cell line. We also found that DsrA was specifically responsible for the ability of H. ducreyi to bind vitronectin. We then theorized that DsrA might use vitronectin as a bridge to bind to human cells, but this hypothesis proved to be untrue as eliminating HaCaT cell binding of vitronectin with a monoclonal antibody specific to integrin {alpha}vß5 did not affect the attachment of H. ducreyi to HaCaT cells. Finally, we wanted to examine the importance of keratinocyte adhesion in chancroid pathogenesis so we tested the wild-type and dsrA mutant strains of H. ducreyi in our swine models of chancroid pathogenesis. The dsrA mutant was less virulent than the wild type in both the normal and immune cell-depleted swine models of chancroid infection.

* Corresponding author. Mailing address: Department of Microbiology & Immunology, Campus Box 7290, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599. Phone (919) 966-9699. Fax: (919) 962-8103. E-mail: kawula{at}med.unc.edu.

Editor: D. L. Burns

{dagger} Present address: Groton Laboratories, Pfizer Inc., Groton, Conn.

Infection and Immunity, November 2002, p. 6158-6165, Vol. 70, No. 11
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.11.6158-6165.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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