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Rasouli M.,Prof Alborzi Clinical Microbiology Research Center | Asaei S.,Prof Alborzi Clinical Microbiology Research Center | Kalani M.,Prof Alborzi Clinical Microbiology Research Center | Kalani M.,Shiraz University of Medical Sciences | And 2 more authors.
Cytokine | Year: 2013

On the subject of brucellosis, it seems that Th1/Th2 cytokines balance may be involved in the resistance or susceptibility to Brucella infection. In this respect, Th1 cytokines confer resistance, while Th2 cytokines predispose brucellosis. It is also clarified that IL-17 is required for the induction of IFN-γ and IL-12 in macrophages and dendritic cells. Then, it seems that IL-17 can affect the induction of Th1 immunity which is necessary for controlling Brucella. In the present study, we tried to investigate probable relationship between IL-17A genetic variants and susceptibility to the human brucellosis. One hundred and seventy six patients with brucellosis and 84 healthy animal husbandmen, who consumed contaminated raw milk and dairy products from animals with brucellosis, were included in this study. All individuals were genotyped for 9 single nucleotide polymorphisms (SNPs) (rs4711998AG, rs8193036CT, rs3819024AG, rs2275913AG, rs3819025AG, rs8193038AG, rs3804513AT, rs1974226AG and rs3748067AG) being selected by using NCBI SNP database and literature using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The distribution of IL-17 rs4711998, rs8193038, rs3748067 AA genotypes and AAGAA haplotype were significantly more frequent in the patients than in the controls (P= 0.008, 0.0019, 0.003 and 0.002, respectively) while IL-17 genotypes rs3819024GG and rs3819025AA were more frequent in the controls than the patients (P= 0.001 and 0.0035, respectively). Based on the results, IL-17 rs4711998, rs8193038, rs3748067 AA genotypes and AAGAA haplotype could be considered as susceptibility factors for brucellosis while the inheritance of IL-17 rs3819024GG and rs3819025AA genotypes might be resistance factors against the disease. © 2012 Elsevier Ltd. Source

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