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  • 1
    Language: English
    In: Journal of Infectious Diseases, 2016, Vol.214(3), pp.489-495
    Keywords: Haemophilus Ducreyi ; Chancroid ; Skin Ulcers ; Immunogenetics ; Humans ; Innate Immunity
    ISSN: 0022-1899
    ISSN: 1537-6613
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  • 2
    In: The Journal of Infectious Diseases, 2016, Vol. 214(3), pp.489-495
    Description: Background.  In humans inoculated with Haemophilus ducreyi , there are host effects on the possible clinical outcomes—pustule formation versus spontaneous resolution of infection. However, the immunogenetic factors that influence these outcomes are unknown. Here we examined the role of 14 single-nucleotide polymorphisms (SNPs) in 7 selected pathogen-recognition pathways and cytokine genes on the gradated outcomes of experimental infection. Methods.  DNAs from 105 volunteers infected with H. ducreyi at 3 sites were genotyped for SNPs, using real-time polymerase chain reaction. The participants were classified into 2 cohorts, by race, and into 4 groups, based on whether they formed 0, 1, 2, or 3 pustules. χ 2 tests for trend and logistic regression analyses were performed on the data. Results.  In European Americans, the most significant findings were a protective association of the TLR9 +2848 GG genotype and a risk-enhancing association of the TLR9 TA haplotype with pustule formation; logistic regression showed a trend toward protection for the TLR9 +2848 GG genotype. In African Americans, logistic regression showed a protective effect for the IL10 – 2849 AA genotype and a risk-enhancing effect for the IL10 AAC haplotype. Conclusions.  Variations in TLR9 and IL10 are associated with the outcome of H. ducreyi infection.
    Keywords: 〈Kwd〉〈Italic Toggle="Yes"〉Haemophilus Ducreyi〈/Italic〉〈/Kwd〉 ; Chancroid ; Skin Ulcers ; Immunogenetics ; Humans ; Innate Immunity
    ISSN: 0022-1899
    E-ISSN: 1537-6613
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  • 3
    Language: English
    In: The Journal of infectious diseases, 15 June 2010, Vol.201(12), pp.1839-48
    Description: Haemophilus ducreyi causes chancroid, a genital ulcer disease. Among human volunteers, the majority of experimentally infected individuals fail to clear the infection and form pustules. Here, we investigated the role played by CD4(+)FOXP3(+) regulatory T (T(reg)) cells in the formation of pustules. In pustules, there was a significant enrichment of CD4(+)FOXP3(+) T cells, compared with that in peripheral blood. The majority of lesional FOXP3(+) T cells were CD4(+), CD25(+), CD127(lo/-), and CTLA-4(+). FOXP3(+) T cells were found throughout pustules but were most abundant at their base. Significantly fewer lesional CD4(+)FOXP3(+) T cells expressed interferon gamma, compared with lesional CD4(+)FOXP3(-) effector T cells. Depletion of CD4(+)CD25(+) T cells from the peripheral blood of infected and uninfected volunteers significantly enhanced proliferation of H. ducreyi-reactive CD4(+) T cells. Our results indicate that the population of CD4(+)CD25(+)CD127(lo/-)FOXP3(+) T(reg) cells are expanded at H. ducreyi-infected sites and that these cells may play a role in suppressing the host immune response to the bacterium.
    Keywords: Immune Tolerance ; Cd4-Positive T-Lymphocytes -- Immunology ; Forkhead Transcription Factors -- Analysis ; Haemophilus Infections -- Immunology ; Haemophilus Ducreyi -- Immunology ; T-Lymphocytes, Regulatory -- Immunology
    ISSN: 00221899
    E-ISSN: 1537-6613
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  • 4
    Language: English
    In: The Journal of infectious diseases, 15 August 2009, Vol.200(4), pp.590-8
    Description: The role of natural killer (NK) cells in the host response to Haemophilus ducreyi infection is unclear. In pustules obtained from infected human volunteers, there was an enrichment of CD56bright NK cells bearing the activation markers CD69 and HLA-DR, compared with peripheral blood. To study the mechanism by which H. ducreyi activated NK cells, we used peripheral blood mononuclear cells from uninfected volunteers. H. ducreyi activated NK cells only in the presence of antigen-presenting cells. H. ducreyi-infected monocytes and monocyte-derived macrophages activated NK cells in a contact- and interleukin-18 (IL-18)-dependent manner, whereas monocyte-derived dendritic cells induced NK activation through soluble IL-12. More lesional NK cells than peripheral blood NK cells produced IFN-gamma in response to IL-12 and IL-18. We conclude that NK cells are recruited to experimental lesions and likely are activated by infected macrophages and dendritic cells. IFN-gamma produced by lesional NK cells may facilitate phagocytosis of H. ducreyi.
    Keywords: Haemophilus Ducreyi ; Chancroid -- Immunology ; Killer Cells, Natural -- Physiology ; Lymphocyte Activation -- Physiology
    ISSN: 0022-1899
    E-ISSN: 15376613
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