Monocyte chemoattractant protein-1 (MCP1)-2581 A/G and interferon gamma (IFNγ) +874 T/A polymorphisms in Iranian population with pulmonary tuberculosis

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Jamalli Ailar; Zare Ebrahimabad Mojtaba; Zhand Sareh; Khosravi Ayyoob

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Journal Paper

Paper Information

Journal: JORJANI BIOMEDICINE JOURNAL Year:621 | Volume: | Issue: Page(s): 24-27

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Title

Monocyte chemoattractant protein-1 (MCP1)-2581 A/G and interferon gamma (IFNγ) +874 T/A polymorphisms in Iranian population with pulmonary tuberculosis

Author(s)

Jamalli Ailar | Zare Ebrahimabad Mojtaba | Zhand Sareh | Khosravi Ayyoob | Issue Writer Certificate

Keywords

Monocyte chemoattractant protein-1Q4

Interferon-gammaQ4

Genetic PolymorphismQ4

Pulmonary tuberculosisQ4

Abstract

Background: Genetic Polymorphisms are predictors of the immune response and susceptibility to certain infectious diseases, including Pulmonary tuberculosis (TB). We evaluated the association of Monocyte chemoattractant protein-1 (MCP1) (-2581 A/G) and Interferon-gamma (IFNγ) (+874 T/A) polymorphisms with susceptibility to pulmonary TB in an Iranian population. Methods: A total of 124 patients with Pulmonary tuberculosis and 244 healthy subjects (121 related normal controls and 123 unrelated subjects) were included. The MCP1 polymorphic region (-2518 A/G) was genotyped by PCR-RFLP, while ARMS-PCR was used to amplify and detect IFNγ (+874 T/A). SNPStats and SPSS v. 20 were used for the statistical analysis of the data. Results: The comparison of MCP1 (-2518 A/G) alleles and genotypes in TB patients and healthy subjects showed no significant association in all the constructed heredity models. No association was observed between TB patients and normal subjects in all the constructed inheritance models for IFNγ (+874 T/A) alleles and genotypes. Conclusion: Due to the lack of association between MCP1 (-2518 A/G) and IFNγ (874 T/A) polymorphisms and susceptibility to PT in our study and the conflicting results of some previous studies, further clinical and molecular research is needed to clarify the role of the studied polymorphisms in the pathogenesis of tuberculosis.

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