ArticleInfection and immunity2002
The Haemophilus ducreyi serum resistance antigen DsrA confers attachment to human keratinocytes.
Article in Infection and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 50 citations in OpenAlex.
- Microbial evasion of the complement system: a continuous and evolving story.Frontiers in immunology · 2023Review
- Vitronectin Binds to a Specific Stretch within the Head Region of Yersinia Adhesin A and Thereby Modulates Yersinia enterocolitica Host Interaction.Journal of innate immunity · 2017Article
- Article
- Defining Potential Vaccine Targets of Haemophilus ducreyi Trimeric Autotransporter Adhesin DsrA.Monoclonal antibodies in immunodiagnosis and immunotherapy · 2015Article
- Article
- Trimeric autotransporter DsrA is a major mediator of fibrinogen binding in Haemophilus ducreyi.Infection and immunity · 2013Article
- Article
- Host-pathogen interplay of Haemophilus ducreyi.Current opinion in infectious diseases · 2010Review
- Localization of the domains of the Haemophilus ducreyi trimeric autotransporter DsrA involved in serum resistance and binding to the extracellular matrix proteins fibronectin and vitronectin.Infection and immunity · 2009Article
- Trimeric autotransporters of Haemophilus parasuis: generation of an extensive passenger domain repertoire specific for pathogenic strains.Journal of bacteriology · 2009Article
- Outer membrane protein DsrA is the major fibronectin-binding determinant of Haemophilus ducreyi.Infection and immunity · 2008Article
- Burkholderia Hep_Hag autotransporter (BuHA) proteins elicit a strong antibody response during experimental glanders but not human melioidosis.BMC microbiology · 2007Article
- Trimeric autotransporters require trimerization of the passenger domain for stability and adhesive activity.Journal of bacteriology · 2006Article
- Expression of Haemophilus ducreyi collagen binding outer membrane protein NcaA is required for virulence in swine and human challenge models of chancroid.Infection and immunity · 2006Article
- Immunization with the Haemophilus ducreyi hemoglobin receptor HgbA protects against infection in the swine model of chancroid.Infection and immunity · 2006Article
- A DltA mutant of Haemophilus ducreyi Is partially attenuated in its ability to cause pustules in human volunteers.Infection and immunity · 2006Article
- Identification of a novel sialic acid transporter in Haemophilus ducreyi.Infection and immunity · 2005Article
- Killing of dsrA mutants of Haemophilus ducreyi by normal human serum occurs via the classical complement pathway and is initiated by immunoglobulin M binding.Infection and immunity · 2005Article
- Haemophilus ducreyi Outer membrane determinants, including DsrA, define two clonal populations.Infection and immunity · 2005Article
- Expression of the LspA1 and LspA2 proteins by Haemophilus ducreyi is required for virulence in human volunteers.Infection and immunity · 2004Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
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(v)beta(5) 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.
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