Interleukin 10 gene promoter polymorphisms in women with early-onset pre-eclampsia

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Abstract

Summary: Pre-eclampsia is one of the most serious disorders of human pregnancy and T helper type 1 (Th1)/Th2 imbalance plays a major role in its aetiology. The Th2 cytokine, interleukin (IL)-10, plays a significant role in the maintenance of pregnancy. The present study is aimed at understanding the role of IL-10 promoter polymorphisms (-1082 G/A; -592 A/C and -819 C/T) and their haplotypes in early-onset pre-eclampsia. A total of 120 patients and an equal number of women with normal pregnancy, from Government Maternity Hospital, Petlaburz, Hyderabad, India, were considered for the present study. A standard amplification refractory mutation system-polymerase chain reaction (ARMS-PCR) was carried out for genotyping followed by agarose gel electrophoresis. Appropriate statistical methods were applied to test for the significance of the results. It was found that the IL-10 -819 C allele (P=0·003) and -592 A (P=0·005) allele frequencies increased significantly in patients compared to controls. No significant difference was found with regard to -1082 promoter polymorphism. Haplotype analysis of the IL-10 single nucleotide polymorphisms (SNPs) revealed a significant association with ACC haplotype with a twofold increased risk in patients compared to controls. The frequencies of two common IL-10 haplotypes (GCC and ATA) did not show any significant difference. Further, the diplotype analysis revealed five genotypes: -1082A with -819C (P=0·0016); -1082G with -819C (P=0·0018); -819C with -592C (P=0·001); -1082A with -592C (P=0·032); and -1082G with -592C (P=0·005) associated with the disease. These findings support the concept of contribution of IL-10 gene polymorphisms in the pathogenesis of early-onset pre-eclampsia.

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Sowmya, S., Sri Manjari, K., Ramaiah, A., Sunitha, T., Nallari, P., Jyothy, A., & Venkateshwari, A. (2014). Interleukin 10 gene promoter polymorphisms in women with early-onset pre-eclampsia. Clinical and Experimental Immunology, 178(2), 334–341. https://doi.org/10.1111/cei.12402

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