Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 214, Issue 3, Pages 489-495Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiw164
Keywords
Haemophilus ducreyi; chancroid; skin ulcers; immunogenetics; humans; innate immunity
Categories
Funding
- National Institutes of Health [U19 AI31494, AI27863S1, AI059384]
- Indiana Clinical and Translational Sciences Institute
- Indiana Clinical Research Center [UL RR052761]
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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. chi(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.
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