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
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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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