ASSOCIATION OF IL-1B. (-511C/T) IL-IB(31T/C)GENEPOLYMORPHISM WITH ENDOPLASMIC RETICULUM STRESSMARKER LEVELS IN ACUTE DECOMPENSATED HEART FAILURE WITH LOW EJECTION FRACTION

Abstract

Inflammatory processes play an important role in the pathogenesis of heart failure. The accumulation of unfolded protiens in the endoplasmic reticulum lumen and the unfolded protien response signal path is activated. The IL-IB gene is located in the Chromsone 2.q14 region. -31 and -511 single nucleotide polymorphisms (SNPs) were detected in the IL-IB Promoter region. These two SNPs affect IL-1expression. This Study aims to investigate the presence of IL-IB (-511 C / T) and IL-IB (-31 T / C) gene polymorphisms and the relationship between ER Stress markers and the inflammatory markers. Patients who applied to the department of emergency medicine with the findings of acute decompensated heart failure. Polymorphic sites of the IL-IB gene were determined by DNA sequencing. In all study, individuals with IL-IB (-31 T / C) T allele have higher serum PERK, GRP-78, CHOP AND CRP levels median values than individuals with IL-IB (-31 T/C) C allele (p = 0.00001, p = 0.0002, p = 0.002 and p = 0.011, respectively). Serum ERK and GRP-78 Values in HF Group were higher in individuals with IL-IB (-31 T / C) T allele compared to individuals with C alle (p = 0.0001 and p = 0.0006). There was a statistically difference in serum CHOP levels in the control group with the IL-IB (-511 C / T) T allele and the individuals with the C allele in the HF group (p= 0.002). In Cnclusion we consider that the inflammatory response caused by IL-IB (-31 T / C) gene polymorphism increased and the ER stress response increased, inflammatory pathway and stress of having IL-IB (-31 T / C) T / T genotype or T allele.