Association of tumor necrosis factor–α-308 (G→A) polymorphism and susceptibility to brucellosis
Jafari-Shakib Reza, Rafiei Alireza, Ansari Mostafa, Khalilian Alireza, Hajilooi Mehrdad
Department of Immunology and Microbiology, Rasht Medical School, Guilan University of Medical Sciences, Rasht; Cellular and Molecular Biology Research Center, Sari Medical School, Mazandaran University of Medical Sciences, Sari; Department of Internal Medicine, Ekbatan Hospital, Medical School, University of Medical Sciences; and Department of Immunology, Molecular Medicine Research Center, Hamadan University of Medical Sciences, Hamadan, Iran
Received: May 16, 2007
Revised: January 12, 2008
Accepted: June 6, 2008
Corresponding author:
Dr. Hajilooi Mehrdad, Department of Immunology, Molecular Medicine Research Center, Hamadan University of Medical Sciences, Hamadan, Iran. E-mail: Hajilooi Mehrdad
Background and purpose:
A critical response against intracellular organisms such as Brucella spp. is production of tumor necrosis factor–α (TNF-α), which enhances the initial response of infected macrophages. Polymorphism in the TNF-α gene promoter has an effect on the level of TNF-α production. Therefore, this study investigated the possible association of G-308A polymorphism of the TNF-α gene and susceptibility to brucellosis.
Methods:
Genotyping was performed on DNA extracted from the peripheral leukocytes of 260 patients with brucellosis and 217 healthy control participants using the sequence-specific primer polymerase chain reaction method.
Results:
The TNF-α-308(A/A) homozygote was significantly higher in patients than in controls (14.2% vs 5.5%; p = 0.001). Logistic regression analysis showed a significant association between the TNF-α-308 (A/A) genotype and brucellosis (odds ratio, 2.4; 95% confidence interval, 1.2-4.8; p = 0.01).
Conclusion:
The results of this study suggest that TNF-α (G-308A) polymorphism might be involved in susceptibility to brucellosis.
Key words:
Brucellosis; Polymorphism, genetic; Tumor necrosis factor-alpha
J Microbiol Immunol Infect. 2009;42:22-26.
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