ArticleInfection and immunity1999
Expression of sialylated or paragloboside-like lipooligosaccharides are not required for pustule formation by Haemophilus ducreyi in human volunteers.
Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 33 citations in OpenAlex.
- A Class IInfection and immunity · 2019Trial
- Molecular pathogenesis ofMicrobiology and molecular biology reviews : MMBR · 2025Review
- AInfection and immunity · 2024Article
- Formate production is dispensable forInfection and immunity · 2023Article
- Interactions of the Skin PathogenFrontiers in immunology · 2020Review
- DksA and (p)ppGpp have unique and overlapping contributions to Haemophilus ducreyi pathogenesis in humans.Infection and immunity · 2015Article
- A (p)ppGpp-null mutant of Haemophilus ducreyi is partially attenuated in humans due to multiple conflicting phenotypes.Infection and immunity · 2014Article
- Carbon storage regulator A contributes to the virulence of Haemophilus ducreyi in humans by multiple mechanisms.Infection and immunity · 2013Article
- Sialylation of lipooligosaccharides is dispensable for the virulence of Haemophilus ducreyi in humans.Infection and immunity · 2012Article
- Role played by CD4+FOXP3+ regulatory T Cells in suppression of host responses to Haemophilus ducreyi during experimental infection of human volunteers.The Journal of infectious diseases · 2010Article
- Experimental infection of human volunteers with Haemophilus ducreyi: fifteen years of clinical data and experience.The Journal of infectious diseases · 2009Article
- Identification of genes involved in the expression of atypical lipooligosaccharide structures from a second class of Haemophilus ducreyi.Infection and immunity · 2007Article
- 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 requires an intact flp gene cluster for virulence in humans.Infection and immunity · 2003Article
- A humoral immune response confers protection against Haemophilus ducreyi infection.Infection and immunity · 2003Article
- Differences in host susceptibility to disease progression in the human challenge model of Haemophilus ducreyi infection.Infection and immunity · 2003Article
- The lbgAB gene cluster of Haemophilus ducreyi encodes a beta-1,4-galactosyltransferase and an alpha-1,6-DD-heptosyltransferase involved in lipooligosaccharide biosynthesis.Infection and immunity · 2002Article
- Immunopathogenesis of Haemophilus ducreyi infection (chancroid).Infection and immunity · 2002Review
- A superoxide dismutase C mutant of Haemophilus ducreyi is virulent in human volunteers.Infection and immunity · 2002Article
- Characterization of Haemophilus ducreyi-specific T-cell lines from lesions of experimentally infected human subjects.Infection and immunity · 2001Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
The lipooligosaccharide (LOS) of Haemophilus ducreyi, the etiologic agent of chancroid, chemically and immunologically resembles human glycosphingolipid antigens. To test whether LOS that contains paragloboside-like structures was required for pustule formation, an isogenic mutant (35000HP-RSM2) was constructed in losB, which encodes D-glycero-D-manno-heptosyltransferase. 35000HP-RSM2 produces a truncated LOS whose major glycoform terminates in a single glucose attached to a heptose trisaccharide core and 2-keto-3-deoxyoctulosonic acid. Five human subjects were inoculated with 35000HP and 35000HP-RSM2 in a dose-response trial. For estimated delivered doses (EDDs) of >/=25 CFU, the pustule formation rates were 80% for 35000HP and 58% for 35000HP-RSM2. Preliminary data indicated that a previously described Tn916 losB mutant made a minor glycoform that does not require DD-heptose to form the terminal N-acetyllactosamine. If 35000HP-RSM2 made this glycoform, then 35000HP-RSM2 could theoretically make a sialylated glycoform. To test whether sialylated LOS was required for pustule formation, a second trial comparing an isogenic sialyltransferase mutant (35000HP-RSM203) to 35000HP was performed in five additional subjects. For EDDs of >/=25 CFU, the pustule formation rates were 30% for both 35000HP and 35000HP-RSM203. The histopathology and recovery rates of H. ducreyi from surface cultures and biopsies obtained from mutant and parent sites in both trials were similar. These results indicate that neither the expression of a major glycoform resembling paragloboside nor sialylated LOS is required for pustule formation by H. ducreyi in humans.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.