alexa Association of TNF-α and IL-10 polymorphisms with tuberculosis in Tunisian populations.
Immunology

Immunology

Journal of Clinical & Cellular Immunology

Author(s): BenSelma W, Harizi H, Boukadida J

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Abstract Cytokine Th1/Th2 balance is known to play a key role in controlling Mycobacterium tuberculosis infection. Based upon the functional role of the TNF-α [-308 G(low) → A(high) (rs1800629)] and IL-10 [-1082 A(low) → G(high) (rs1800870), -819 T(low) → C(high) (rs1800871) and -592 A(low) → C(high) (rs1800872)] single nucleotide polymorphisms (SNPs) on production levels, we genotyped 76 patients with pulmonary tuberculosis (TB) (pTB), 55 patients with extrapulmonary TB (epTB) and 95 healthy blood donors by polymerase chain reaction fragment length polymorphism (PCR-RFLP). We observed that -308 A allele was associated with increased risk susceptibility to epTB (OR = 1.96; 95\% CI, 1.04-3.71; P = 0.024). The -1082 AG genotype was significantly associated with increased risk development of epTB (odds ratio [OR] = 3.69; 95\% confidence intervals [CI], 1.73-7.92; P corrected for the number of genotypes [Pc] = 0.0003). By contrast, -1082 AA genotype appeared to be associated with resistance to pTB (OR = 0.38; 95\% CI, 0.19-0.74; Pc = 0.006) and epTB (OR = 0.22; 95\% CI, 0.1-0.48; Pc = 0.00006). High-producer IL-10 GCC haplotype seemed to be associated with 2.11-fold (95\% CI, 1.28-3.46; Pc = 0.003) and 2.57-fold (95\% CI, 1.5-4.4; Pc = 0.0006) increased susceptibility to pTB and epTB, respectively. Combination of TNF-α/IL-10 high producer genotypes was associated with increased 3.13-fold (95\% CI, 1.23-8.05; Pc = 0.028) susceptibility to epTB. However, combined TNF-α/IL-10 low producer genotypes appeared to have protect effect to pTB (OR = 0.44, 95\% CI, 0.21-0.89; Pc = 0.04) and epTB (OR = 0.26, 95\% CI, 0.1-0.62; Pc = 0.0028). Collectively, our results showed that analysed SNPs in the TNF-α and IL-10 gene polymorphisms play key role in susceptibility to or protection against TB development in Tunisian populations. Copyright © 2011 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved. This article was published in Microbes Infect and referenced in Journal of Clinical & Cellular Immunology

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