Abstract
BackgroundStudies have shown in vitro that cigarette smoke condensate stimulates monocytes to express toll-like receptor 4 (TLR4), tumor necrosis factor-α (TNF-α), and intercellular adhesion molecule 1 (ICAM-1), and enhances their adhesion to the endothelium. However, the same effects of cigarette smoking have not been explored in vivo. This study is to investigate the effect of cigarette smoking and smoking cessation on their mRNA expression in human peripheral blood mononuclear cells (PBMCs).MethodsA group of 97 smokers and 62 nonsmokers were enrolled. The RNA from PBMCs was assessed with real-time polymerase chain reaction (PCR) to determine the levels of ICAM-1, TNF-α, and TLR4. The same markers in PBMCs of 87 quitters were examined before and at one week, one month, and two months after smoking cessation.ResultsOf the 97 smokers, 85 (87.6%) were males, and 30 (48.4%) of the nonsmokers were males (p < 0.0001). The mean (SD) age of the smokers was 43.24 (10.89) years, which was younger than 43.45 (11.41) years of nonsmokers (p < 0.0001). The incidence of cardiovascular diseases was 13.4% in smokers, which was higher than 1.6% in nonsmokers (p < 0.05). Both ICAM-1 and TNF-α mRNA levels in PBMCs were higher among the smokers (p < 0.0001). In addition, TLR4 mRNA levels in PBMCs were statistically elevated in the smokers (p < 0.0001) comparing with those in the nonsmokers. The mRNA levels of TLR4 and TNF-α in PBMCs decreased in those who had quit smoking for 2 months (p < 0.0001).ConclusionsICAM-1, TNF-α, and TLR4 mRNA expression levels in PBMCs increased in smokers and decreased after being on a smoking cessation program for 2 months. This finding suggested that TLR4 expression may mediate the atherogenic inflammatory process induced by smoking.
Highlights
Cigarette smoking is a major lifestyle risk factor for atherosclerosis and cardiovascular diseases, regarded as one of the biggest threats to health worldwide
When cultured peripheral blood mononuclear cells (PBMCs) were treated with cigarette smoke extract, the expression of toll-like receptor 4 (TLR4) mRNA increased in a dose-dependent manner due to enhanced production of inflammatory cytokines such as interleukin 8 (IL-8) and tumor necrosis factor-a (TNF-a) [9]. These findings suggest that the expression of TLR4 mRNA by monocytes/macrophages may be stimulated by cigarette smoke and may be involved in the pathogenesis of atherosclerosis
The aim of our study is to investigate the effect of cigarette smoking and smoking cessation on the mRNA expression of TLR4, intercellular adhesion molecule 1 (ICAM-1), and TNF-a in PBMCs obtained from human subjects
Summary
Cigarette smoking is a major lifestyle risk factor for atherosclerosis and cardiovascular diseases, regarded as one of the biggest threats to health worldwide. The study in Japan [2] showed that smoking advanced carotid atherosclerosis as estimated on carotid intima-media thickness and increased the risk of atherothrombotic events such as acute myocardial infarction and stroke in patients with metabolic syndrome. Smoking cessation gives rise to enormous health benefits for quitters of all ages in extending lifespan and significantly reducing risks of myocardial infarction [5]. It remains unclear how smoking causes atherosclerosis, and the mechanism which improves the cardiovascular conditions after smoking cessation is poorly understood. This study is to investigate the effect of cigarette smoking and smoking cessation on their mRNA expression in human peripheral blood mononuclear cells (PBMCs)
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