ArticleInfection and immunity2006
Expression of Haemophilus ducreyi collagen binding outer membrane protein NcaA is required for virulence in swine and human challenge models of chancroid.
Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 43 citations in OpenAlex.
- A Class IInfection and immunity · 2019Trial
- Molecular pathogenesis ofMicrobiology and molecular biology reviews : MMBR · 2025Review
- Article
- Interactions of the Skin PathogenFrontiers in immunology · 2020Review
- Type V Secretion Systems: An Overview of Passenger Domain Functions.Frontiers in microbiology · 2019Review
- Trimeric autotransporter DsrA is a major mediator of fibrinogen binding in Haemophilus ducreyi.Infection and immunity · 2013Article
- Proteinaceous determinants of surface colonization in bacteria: bacterial adhesion and biofilm formation from a protein secretion perspective.Frontiers in microbiology · 2013Review
- Sialylation of lipooligosaccharides is dispensable for the virulence of Haemophilus ducreyi in humans.Infection and immunity · 2012Article
- Expression of the Flp proteins by Haemophilus ducreyi is necessary for virulence in human volunteers.BMC microbiology · 2011Article
- Characterization of the CpxRA regulon in Haemophilus ducreyi.Infection and immunity · 2010Article
- Inactivation of the Haemophilus ducreyi luxS gene affects the virulence of this pathogen in human subjects.The Journal of infectious diseases · 2009Article
- Experimental infection of human volunteers with Haemophilus ducreyi: fifteen years of clinical data and experience.The Journal of infectious diseases · 2009Article
- A fibrinogen-binding lipoprotein contributes to the virulence of Haemophilus ducreyi in humans.The Journal of infectious diseases · 2009Article
- Haemophilus ducreyi LspA proteins are tyrosine phosphorylated by macrophage-encoded protein tyrosine kinases.Infection and immunity · 2008Article
- Outer membrane protein DsrA is the major fibronectin-binding determinant of Haemophilus ducreyi.Infection and immunity · 2008Article
- Identification of Haemophilus ducreyi genes expressed during human infection.Microbiology (Reading, England) · 2008Article
- Dysregulated immune profiles for skin and dendritic cells are associated with increased host susceptibility to Haemophilus ducreyi infection in human volunteers.Infection and immunity · 2007Article
- Experimental infection with Haemophilus ducreyi in persons who are infected with HIV does not cause local or augment systemic viral replication.The Journal of infectious diseases · 2007Article
- Complete genome sequence of Haemophilus somnus (Histophilus somni) strain 129Pt and comparison to Haemophilus ducreyi 35000HP and Haemophilus influenzae Rd.Journal of bacteriology · 2007Article
- Haemophilus ducreyi Outer membrane determinants, including DsrA, define two clonal populations.Infection and immunity · 2005Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Haemophilus ducreyi, the etiologic agent of the sexually transmitted genital ulcer disease chancroid, has been shown to associate with dermal collagen fibers within infected skin lesions. Here we describe NcaA, a previously uncharacterized outer membrane protein that is important for H. ducreyi collagen binding and host colonization. An H. ducreyi strain lacking the ncaA gene was impaired in adherence to type I collagen but not fibronectin (plasma or cellular form) or heparin. The mutation had no effect on serum resistance or binding to HaCaT keratinocytes or human foreskin fibroblasts in vitro. Escherichia coli expressing H. ducreyi NcaA bound to type I collagen, demonstrating that NcaA is sufficient to confer collagen attachment. The importance of NcaA in H. ducreyi pathogenesis was assessed using both swine and human experimental models of chancroid. In the swine model, 20% of lesions from sites inoculated with the ncaA mutant were culture positive for H. ducreyi 7 days after inoculation, compared to 73% of wild-type-inoculated sites. The average number of CFU recovered from mutant-inoculated lesions was also significantly reduced compared to that recovered from wild-type-inoculated sites at both 2 and 7 days after inoculation. In the human challenge model, 8 of 30 sites inoculated with wild-type H. ducreyi progressed to the pustular stage, compared to 0 of 30 sites inoculated with the ncaA mutant. Together these results demonstrate that the collagen binding protein NcaA is required for H. ducreyi infection.
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