Jafari-Shakib Reza¹, Rafiei Alireza², Ansari Mostafa³, Khalilian Alireza³, Hajilooi Mehrdad^4
1Department of Immunology and Microbiology, Rasht Medical School, Guilan University of Medical Sciences, Rasht; ²Cellular and Molecular Biology Research Center, Sari Medical School, Mazandaran University of Medical Sciences, Sari; ³Department of Internal Medicine, Ekbatan Hospital, Medical School, University of Medical Sciences; and ⁴Department of Immunology, Molecular Medicine Research Center, Hamadan University of Medical Sciences, Hamadan, Iran

Received: June 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: This e-mail address is being protected from spam bots, you need JavaScript enabled to view it

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.