Differences in host susceptibility to disease progression in the human challenge model of Haemophilus ducreyi infection.
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Experimental infection of human volunteers with Haemophilus ducreyi: fifteen years of clinical data and experience.Haemophilus ducreyi SapA contributes to cathelicidin resistance and virulence in humansIdentification of Haemophilus ducreyi genes expressed during human infection.Host-pathogen interplay of Haemophilus ducreyi.Outer membrane protein P4 is not required for virulence in the human challenge model of Haemophilus ducreyi infectionRole played by CD4+FOXP3+ regulatory T Cells in suppression of host responses to Haemophilus ducreyi during experimental infection of human volunteersTrafficking pathways and characterization of CD4 and CD8 cells recruited to the skin of humans experimentally infected with Haemophilus ducreyi.Expression of the Flp proteins by Haemophilus ducreyi is necessary for virulence in human volunteers.A DltA mutant of Haemophilus ducreyi Is partially attenuated in its ability to cause pustules in human volunteers.Haemophilus ducreyi requires an intact flp gene cluster for virulence in humans.Haemophilus ducreyi lipooligosaccharides induce expression of the immunosuppressive enzyme indoleamine 2,3-dioxygenase via type I interferons and tumor necrosis factor alpha in human dendritic cells.Sialylation of lipooligosaccharides is dispensable for the virulence of Haemophilus ducreyi in humansThe Human Skin Microbiome Associates with the Outcome of and Is Influenced by Bacterial InfectionHaemophilus ducreyi partially activates human myeloid dendritic cellsDysregulated immune profiles for skin and dendritic cells are associated with increased host susceptibility to Haemophilus ducreyi infection in human volunteers.Expression of the LspA1 and LspA2 proteins by Haemophilus ducreyi is required for virulence in human volunteers.Permeases of the sap transporter are required for cathelicidin resistance and virulence of Haemophilus ducreyi in humansExperimental infection with Haemophilus ducreyi in persons who are infected with HIV does not cause local or augment systemic viral replication.Inactivation of the Haemophilus ducreyi luxS gene affects the virulence of this pathogen in human subjects.Mechanism of human natural killer cell activation by Haemophilus ducreyi.Human challenge studies: a review of adequacy of reporting methods and results.Host Polymorphisms in TLR9 and IL10 Are Associated With the Outcomes of Experimental Haemophilus ducreyi Infection in Human Volunteers.
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P2860
Differences in host susceptibility to disease progression in the human challenge model of Haemophilus ducreyi infection.
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name
Differences in host susceptibi ...... Haemophilus ducreyi infection.
@ast
Differences in host susceptibi ...... Haemophilus ducreyi infection.
@en
type
label
Differences in host susceptibi ...... Haemophilus ducreyi infection.
@ast
Differences in host susceptibi ...... Haemophilus ducreyi infection.
@en
prefLabel
Differences in host susceptibi ...... Haemophilus ducreyi infection.
@ast
Differences in host susceptibi ...... Haemophilus ducreyi infection.
@en
P2093
P2860
P1476
Differences in host susceptibi ...... Haemophilus ducreyi infection.
@en
P2093
Andrew L Faber
Barry P Katz
Beth E Zwickl
Carisa A Townsend
Cliffton T H Bong
Kate R Fortney
Stacy L Bennett
Stanley M Spinola
Steven D Billings
Tricia L Humphreys
P2860
P304
P356
10.1128/IAI.71.11.6658-6663.2003
P407
P577
2003-11-01T00:00:00Z