INTERLEUKIN-18 PROMOTER GENE POLYMORPHISMS ARE NOT ASSOCIATED WITH MYOCARDIAL INFARCTION IN TYPE 2 DIABETES IN SLOVENIA
Kariž S1*, Petrovič D2
*Corresponding Author: Stojan Kariž, Department of Internal Medicine, General Hospital Izola, Polje 35, Izola 6310, Slovenia; Tel.: +386-5-660-6480; Fax: +386-660-6305; E-mail: stojan.kariz@siol.net
page: 3

INTRODUCTION

Type 2 diabetes is a major risk factor for development of coronary artery disease (CAD) and subsequent myocardial infarction (MI). Considerable data support the hypothesis that inflammation plays a central role in pathogenesis of both atherosclerosis [1] and type 2 diabetes [2]. In particular, diabetes is associated with enhanced inflammatory responses and accelerated atherosclerosis [3]. The risk of MI is increased 2- to 4-fold in diabetic patients [4]. The genetic variability of inflammatory genes may be involved in the pathogenesis of diabetes-accelerated atherosclerosis and its complications [1-3]. Interleukin-18 (IL-18) is a pro-inflammatory cytokine with an important role in the inflammatory process that contributes to atherosclerosis [5]. High levels of IL-18 have been detected in human atherosclerotic plaques and have been related to plaque instability [6]. Animal models support the pro-atherogenic role of IL-18 [7] and the favorable effect of inhibiting IL-18 on plaque composition and progression [8]. Increased levels of circulating IL-18 have been demonstrated in patients with acute coronary syndromes [9] and in type 2 diabetic patients [10]. Diabetic patients with high IL-18 had a greater carotid intima-media thickness and a higher number of carotid plaques than those with normal IL-18 serum levels [11]. Moreover, acute hyperglycemia induces an increase in plasma IL-18 in normal subjects and in patients with impaired glucose tolerance [12]. Thus, elevated plasma IL-18 may be associated with acceleration of atherosclerosis and may play a role in acute coronary syndromes through plaque destabilization in type 2 diabetic patients.The IL-18 gene locus is located at 11q22.2-q23.3 and several polymorphisms in its promoter region have been identified [13]. Substitution of G>C at position –137 changes a histone 4 transcription factor-1 (H4TF-1) nuclear factor-binding site, while a change of C>A at position –607 disrupts a cyclic adenosine monophosphate (cAMP) responsive element proteinbinding site. These changes influence the transcriptional activity of the IL-18 gene [13]. Recently, genetic polymorphisms of the IL-18 gene have been associated with various immune and inflammatory diseases, including cardiovascular disease [14-16], type 1 diabetes mellitus [17], and Alzheimer’s disease [18]. We have investigated the association of –137 (G>C) and –607 (C>A) polymorphisms of the IL-18 gene promoter region of MI patients of Caucasian origin with type 2 diabetes in Slovenia, and also the impact of the IL-18 gene polymorphisms on serum IL-18 levels.



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