<abstract xmlns="http://www.w3.org/1999/xhtml"> Background: Coronary Artery Disease (CAD) is the most frequent form of heart diseases. IL-10 is an antiinflammatory cytokine and down regulates the Th1 response by suppression of pro-inflammatory cytokine. There are interindividual variations in IL-10 production, which are genetically contributed by polymorphisms within IL- 10 promoter region. Objectives: We investigated the association of IL-10 gene promoter -1082 G/A, -819 C/T, and -592 C/A polymorphism with CAD susceptibility in Pakistani individuals. Methods: Ninety-three CAD patients and ninety-nine controls were enrolled in the study. IL-10 (-1,082 G/A, -819 C/T, -592 C/A) genotyping was performed by amplification refractory mutation system-polymerase chain reaction (ARMS-PCR). Results: There is an indication that IL-10 -1082 GG (p = 0.033, OR = 0.26, 95%, CI = 0.07-0.97) has positive association while -1082 GA (p = 0.031, OR = 2.7, 95%, CI = 1.07-6.90) has negative association with CAD. IL-10 -819 TT (-592 AA) were significantly higher in control than in patients (p = 0.008, OR= 3.1, 95%, CI = 1.09-9.02). We have not found any significant association between IL-10 alleles and haplotypes and CAD. GTA/ATA was the diplotype, which showed the protective effect (p = 0.006, OR = 3.6, 95%, CI = 1.16-10.57) in CAD susceptibility. Conclusion:We found a significant distributional variation in IL-10 promoter SNPs in healthy individuals and the disease group. This difference may be manifested in IL-10 production and disturb the pro- and anti- inflammatory cytokine balance hence influencing the susceptibility of CAD.</abstract>

Background: Coronary Artery Disease (CAD) is the most frequent form of heart diseases. IL-10 is an antiinflammatory cytokine and down regulates the Th1 response by suppression of pro-inflammatory cytokine. There are interindividual variations in IL-10 production, which are genetically contributed by polymorphisms within IL- 10 promoter region. Objectives: We investigated the association of IL-10 gene promoter -1082 G/A, -819 C/T, and -592 C/A polymorphism with CAD susceptibility in Pakistani individuals. Methods: Ninety-three CAD patients and ninety-nine controls were enrolled in the study. IL-10 (-1,082 G/A, -819 C/T, -592 C/A) genotyping was performed by amplification refractory mutation system-polymerase chain reaction (ARMS-PCR). Results: There is an indication that IL-10 -1082 GG (p = 0.033, OR = 0.26, 95%, CI = 0.07-0.97) has positive association while -1082 GA (p = 0.031, OR = 2.7, 95%, CI = 1.07-6.90) has negative association with CAD. IL-10 -819 TT (-592 AA) were significantly higher in control than in patients (p = 0.008, OR= 3.1, 95%, CI = 1.09-9.02). We have not found any significant association between IL-10 alleles and haplotypes and CAD. GTA/ATA was the diplotype, which showed the protective effect (p = 0.006, OR = 3.6, 95%, CI = 1.16-10.57) in CAD susceptibility. Conclusion:We found a significant distributional variation in IL-10 promoter SNPs in healthy individuals and the disease group. This difference may be manifested in IL-10 production and disturb the pro- and anti- inflammatory cytokine balance hence influencing the susceptibility of CAD.

Influence of IL-10 polymorphism on the development of coronary artery disease in Pakistan

NUST Center of Virology and Immunology (NCVI), National University of Science and Technology, Islamabad 44000,

NUST Center of Virology and Immunology (NCVI), National University of Science and Technology (NUST), H-12, Islamabad 44000,

Asian Biomedicine

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

Background: Coronary Artery Disease (CAD) is the most frequent form of heart diseases. IL-10 is an antiinflammatory cytokine and down regulates the Th1...

Influence of IL-10 polymorphism on the development of coronary artery disease in Pakistan

Article Category: Original article

Pubblicato online: 04 feb 2017

Pagine: 159 - 165

DOI: https://doi.org/10.5372/1905-7415.0602.042

© 2017

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.