**4. Discussion**

The results of the current study indicated that rs2569190A>G in *CD14* was associated with increased levels of Tchol and LDL-C and decreased levels of HDL-C. This might point to a possible role for *CD14* in the pathophysiology of hypercholesterolemia.

Human *CD14* is located on the long arm of chromosome 5 (q23-31), which encodes the membrane (m)*CD14*, binds to lipopolysaccharides, and activates various TLRs and downstream proinflammatory pathways [14]. Additionally, *CD14* exists in a soluble form (s)*CD14* [15]. In response to interleukin-6, its expression is increased; therefore, it is regarded as an acute phase protein [16]. Of interest, Reiner et al. reported that (s)*CD14* was positively correlated with LDL-C and HTN and negatively correlated with HDL-C [7]. When combined with our results, the above suggests that the *CD14* gene and protein might be implicated in CVDs.

Increasing experimental evidence is suggesting that rs2569190A>G in the *CD14* promoter could contribute to the genetic etiology of human atherosclerosis [17,18]. This SNP was shown to be functional and increase the transcriptional activity of *CD14* [10], which leads to higher (m)*CD14* protein levels and an increased risk of myocardial infarction [17,18].

The current study is not the first to find a link between elements of the innate immune system (*CD14*) and CVD risk factors, since activated innate immune system elements and dysfunction in metabolic pathways could lead to the chronic inflammation and pathologic conditions associated with CVDs [19]. Benachour et al. reported that the expression of the antimicrobial peptide *LL-37* (a component of the immune system) was positively correlated with CVD risk factors such as systolic BP and triglyceride levels, and negatively with plasma levels of HDL-C, in a sample of 90 apparently healthy men [20]. Another component of the innate immune system that has a noteworthy association with CVD risk factors is the human formyl peptide receptor 1 (*FPR1*) [21]. We have previously identified that, in 1012 French middle-aged adults equally divided between healthy and hypertensive individuals, *FPR1* C32T (rs5030878) is associated with increased BP levels [21].

It is noteworthy to mention that a Hardy–Weinberg equilibrium for rs2569190 was found despite the participants belonging to the Middle Eastern population, where consanguinity rates are higher than in European populations. This might be explained by the fact that the majority of the studied individuals came from a northern large city (not villages), making mating less consanguineous and more random.
