TNF-α -238, -308, -863 polymorphisms, and brucellosis infection

• Published in: Human immunology 2016-01, Vol.77 (1), p.121-125
• Main Authors: Eskandari-Nasab, Ebrahim, Moghadampour, Mehdi, Sepanj-Nia, Adel
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; Aged; Allergy and Immunology; Brucella abortus; Brucella abortus - immunology; Brucellosis; Brucellosis - genetics; Brucellosis - immunology; Case-Control Studies; Child; Cytokine; Female; Gene Frequency; Gene polymorphism; Genetic Predisposition to Disease; Genotype; Humans; Infection; Iran; Male; Middle Aged; Polymorphism, Genetic; Promoter Regions, Genetic - genetics; Retrospective Studies; TNF-α; Tumor Necrosis Factor-alpha - genetics; Young Adult
• ISSN: 0198-8859; 1879-1166
• DOI: 10.1016/j.humimm.2015.11.010

Abstract Background Brucella abortus is an intracellular bacterium that affects humans and domestic animals. Tumor necrosis factor-alpha (TNF-α) has been shown as a key player in the induction of cell-mediated resistance against Brucella infection. We aimed to evaluate the possible influence of the TNF-α promoter polymorphisms (-308 G/A, -238 G/A, and -863 C/A) on the susceptibility of human brucellosis. Methodology A total of 153 patients with active brucellosis and 128 healthy individuals were recruited. All subjects were genotyped for the polymorphisms in the TNF-α gene by Allele-Specific polymerase chain reaction analysis. Results Our results showed that the TNF-α -308 GG genotype was significantly more frequently present in controls than in brucellosis patients (91% vs. 75%), thus was a protective factor against developing brucellosis (OR = 0.313, p = 0.001). In contrast, the -308 GA genotype (OR = 3.026, p = 0.002) and minor allele (A) (OR = 3.058, p = 0.001) as well as AAG haplotype (OR = 4.014, p = 0.001) conferred an increased risk of brucellosis. However, the -238 G/A and -863 C/A polymorphisms were not associated with the risk of brucellosis at both allelic and genotypic levels ( p > 0.05). Conclusion Our study revealed that the TNF-α -308 A allele or GA heterozygosity or AAG haplotype were associated with an increased risk of brucellosis in our population.