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Smoking and Endothelial Dysfunction
Abstract and Figures
Cigarette smoking is one the most important health concerns worldwide. Even though the rate of smoking is declining in developed countries, it is still experiencing growth in developing regions. Many studies have examined the relationship between smoking, as an established risk factor, and cardiovascular diseases. We provide an updated review of the underlying mechanisms of smoking-induced cardiovascular diseases, with a focus on the relationship between smoking and oxidative stress, particularly from the perspective of endothelial cell dysfunction. We review smoking-induced oxidative stress as a trigger for a generalized vascular inflammation associated with cytokine release, adhesion of inflammatory cells and, ultimately, disruption of endothelial integrity as a protective barrier layer. We also briefly discuss the harms related to the vaping of electronic cigarettes, which many erroneously consider as a safe alternative for smoking. We conclude that even though e-cigarette could be a helpful device during the transition period of cigarette quitting, it is by no means a safe substitute.
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... Özellikle akciğer kanseri, kronik obstrüktif akciğer hastalığı (KOAH), kalp hastalığı, diyabet, inme ve nörodejeneratif hastalıkların patogenezinde ROT'ların rolü büyük olup, klinik sonuçlarda belirgin değişikliklere neden olabilir. [9][10][11][12][13][14][15][16][17][18][19][20][21] AnTiOKSidAn TEdAvilER vE pOTAnSiYEl ETKilERi ...
Smoking is a major health problem worldwide, and reactive oxygen species (ROS) and free radicals in cigarette smoke are harmful to health. This article addresses the health effects of ROS and free radical load in smokers.. Smoking creates oxidative stress by increasing lipid peroxidation and protein oxidation in cells. These molecular effects can cause damage to different molecular components of the cell, including lipids, proteins, genomic structures and DNA, causing cellular damage through different pathogenetic pathways. ROS and free radicals can suppress the immune system, leading to immune system weakening and increased inflammation. Smoking may contribute to the development of a number of diseases in which ROS play a role. The ROS and free radical load in smokers increases the risks of cancer, heart attack, and other serious health problems. Quitting smoking is the most effective way to prevent these negative effects. Therefore, it is important to promote smoking cessation programs and support anti-smoking policies in society.
... Smoking induces significant vascular inflammation, characterized by a surge in cytokines and inflammatory cells, compromising endothelial integrity and exacerbating oxidative stress. Intriguingly, even newer devices like electronic cigarettes may pose risks to the endothelium and should be avoided [65]. ...
Atrial fibrillation, a prevalent type of arrhythmia, is increasingly contributing to the economic burden on healthcare systems. The development of innovative treatments, notably catheter ablation, has demonstrated both impressive and promising outcomes. However, these treatments have not yet fully replaced pharmaceutical approaches, primarily due to the relatively high incidence of atrial fibrillation recurrence post-procedure. Recent insights into endothelial dysfunction have shed light on its role in both the onset and progression of atrial fibrillation. This emerging understanding suggests that endothelial function might significantly influence the effectiveness of catheter ablation. Consequently, a deeper exploration into endothelial dynamics could potentially elevate the status of catheter ablation, positioning it as a primary treatment option for atrial fibrillation.
... Smoking is closely related to the development of CVD. Tobacco ingredients, including carbon monoxide and oxidants, may increase oxidative stress and reduce the level of nitric oxide that causes endothelial damage, inflammation, and insulin resistance to affect atherosclerosis (63)(64)(65). Smoking can also induce cancer through ROS and oxidative damage (66). ...
It has been shown that patients with cancer have a longer expected life duration, benefiting from advanced medical therapy. Meanwhile, the risk of suffering from cardiovascular disease (CVD) has been increasing with ageing. A growing number of studies have elucidated the association between cancer and CVD. Cancer, atrial fibrillation (AF) and coronary artery disease share some common factors and interact with each other, such as obesity, aging, diabetes, and inflammation, but the potential specific mechanism is still unclear. In addition, cancer-specific and therapy-related factors may increase the risk of embolism and bleeding in patients with cancer than in general population. However, current available embolic and bleeding risk scores applied in patients with CVD may not be applicable for risk assessment in cancer patients, which would be difficult for clinicians to select an appropriate antithrombotic regimen and ensure the balance between bleeding and embolism. Moreover, different types of cancer have distinct risks, which may increase the complexity of antithrombotic therapy. In this review, we review the literature related to cancer, AF, and acute coronary syndrome, focusing on the epidemiological status, physiological mechanism, embolism and bleeding risks, and strategies of antithrombotic therapy.
... The underlying mechanisms of vaping on the vascular endothelium are not completely understood. E-cigarette aerosol and flavorings may cause oxidative stress and generalized inflammation which is detrimental for the endothelium [81]. El-Mahdy et al. have shown, that vaping induced the expression of NOX and inhibited the endothelial NO synthase (eNOS), resulting in the production of reactive oxygen species, thus reducing the beneficial vasodilatory effect of NO [82]. ...
... A prolonged time of return to daily and sport activities and worst functional scores were found among smokers [9]. Blood supply during meniscal healing is compromised in smokers [5,20,59]. The present systematic review has several limitations. ...
Purpose:
Meniscal injuries are common. Outside-in meniscal repair is one of the techniques advocated for the management of traumatic meniscal tears. This systematic review investigated the outcomes of the outside-in repair technique for the management of traumatic tears of the menisci. The outcomes of interest were to investigate whether PROMs improved and to evaluate the rate of complications.
Methods:
Following the 2020 PRISMA statement, in May 2023, PubMed, Web of Science, Google Scholar, and Embase were accessed with no time constraints. All the clinical investigations which reported data on meniscal repair using the outside-in technique were considered for inclusion. Only studies which reported data on acute traumatic meniscal tears in adults were considered. Only studies which reported a minimum of 24 months of follow-up were eligible.
Results:
Data from 458 patients were extracted. 34% (155 of 458) were women. 65% (297 of 458) of tears involved the medial meniscus. The mean operative time was 52.9 ± 13.6 min. Patients returned to their normal activities at 4.8 ± 0.8 months. At a mean of 67-month follow-up, all PROMs of interest improved: Tegner scale (P = 0.003), Lysholm score (P < 0.0001), International Knee Documentation Committee (P < 0.0001). 5.9% (27 of 458) of repairs were considered failures. Four of 186 (2.2%) patients experienced a re-injury, and 5 of 458 (1.1%) patients required re-operation.
Conclusion:
Meniscal repair using the outside-in technique can be effectively performed to improve the quality of life and the activity level of patients with acute meniscal tears.
Level of evidence:
Level IV.
... Therefore, elderly EH patients with a long course of disease need more active evaluation of CAD, early diagnosis, and early treatment. Studies have confirmed that smoking is one of the traditional risk factors of CAD [5,13,14], and its mechanism may be related to oxidative stress and inflammation [32]. This study found that smokers with EH were 1.47 times more likely to develop CAD than non-smokers, suggesting that quitting smoking is of great significance for the prevention and treatment of CAD. ...
Background
There is currently a lack of a precise, concise, and practical clinical prediction model for predicting coronary artery disease (CAD) in patients with essential hypertension (EH). This study aimed to construct a nomogram to predict CAD in patients with EH based on flow-mediated dilation (FMD) of brachial artery and traditional risk factors.
Methods
Clinical data of 1752 patients with EH were retrospectively collected. High-resolution vascular ultrasound was used to detect FMD in all patients at the Fujian Hypertension Research Institute, China. Patients were divided into two groups, i.e. training group (n = 1204, from August 2000 to December 2013) and validation group (n = 548, from January 2014 to May 2016) according to the time of enrollment. Independent predictors of CAD were analyzed by multivariable logistic regression in the training group, and a nomogram was constructed accordingly. Finally, we evaluated the discrimination, calibration, and clinical applicability of the model using the area under curve (AUC) of receiver operating characteristic analysis, calibration curve combined with Hosmer-Lemeshow test, and decision curve, respectively.
Results
There were 263 (21.8%) cases of EH combined with CAD in the training group. Multivariate logistic regression showed that FMD, age, duration of EH, waist circumference, and diabetes mellitus were independent influencing factors for CAD in EH patients. Smoking which was close to statistical significance (P = 0.062) was also included in the regression model to increase the accuracy. Ultimately, the nomogram for predicting CAD in EH patients was constructed according to above predictors after proper transformation. The AUC values of the training group and the validation group were 0.799 (95%CI 0.770–0.829) and 0.836 (95%CI 0.787–0.886), respectively. Calibration curve and Hosmer-Lemeshow test showed that the model had good calibration (training group: χ² = 0.55, P = 0.759; validation group: χ² = 1.62, P = 0.446). The decision curve also verified the clinical applicability of the nomogram.
Conclusion
The nomogram based on FMD and traditional risk factors (age, duration of EH disease, smoking, waist circumference and diabetes mellitus) can predict CAD high-risk group among patients with EH.
Cardiovascular diseases (CVDs) remain the leading cause of mortality and morbidity globally. Studies have shown that infections especially bacteraemia and sepsis are associated with increased risks for endothelial dysfunction and related CVDs including atherosclerosis. Extracellular vesicles (EVs) are small, sealed membrane‐derived structures that are released into body fluids and blood from cells and/or microbes and are critically involved in a variety of important cell functions and disease development, including intercellular communications, immune responses and inflammation. It is known that EVs‐mediated mechanism(s) is important in the development of endothelial dysfunction in infections with a diverse spectrum of microorganisms including Escherichia coli , Candida albicans , SARS‐CoV‐2 (the virus for COVID‐19) and Helicobacter pylori . H. pylori infection is one of the most common infections globally. During H. pylori infection, EVs can carry H. pylori components, such as lipopolysaccharide, cytotoxin‐associated gene A, or vacuolating cytotoxin A, and transfer these substances into endothelial cells, triggering inflammatory responses and endothelial dysfunction. This review is to illustrate the important role of EVs in the pathogenesis of infectious diseases, and the development of endothelial dysfunction in infectious diseases especially H. pylori infection, and to discuss the potential mechanisms and clinical implications.
Chronic smoking causes dysfunction of vascular endothelial cells, evident as a reduction of flow-mediated dilation in smokers, but the role of nicotine is still controversial. Given the increasing use of e-cigarettes and other nicotine products, it appears essential to clarify this issue. We studied extracts from cigarette smoke (CSE) and vapor from e-cigarettes (EVE) and heated tobacco (HTE) for their effects on vascular relaxation, endothelial nitric oxide signaling, and the activity of soluble guanylyl cyclase. The average nicotine concentrations of CSE, EVE, and HTE were 164, 800, and 85 µM, respectively. At a dilution of 1:3, CSE almost entirely inhibited the relaxation of rat aortas and porcine coronary arteries to acetylcholine and bradykinin, respectively, while undiluted EVE, with a 15-fold higher nicotine concentration, had no significant effect. With about 50% inhibition at 1:2 dilution, the effect of HTE was between CSE and EVE. Neither extract affected endothelium-independent relaxation to an NO donor. At the dilutions tested, CSE was not toxic to cultured endothelial cells but, in contrast to EVE, impaired NO signaling and inhibited NO stimulation of soluble guanylyl cyclase. Our results demonstrate that nicotine does not mediate the impaired endothelium-dependent vascular relaxation caused by smoking.
Ethnopharmacological relevance:
Smilax china L., an extensively used traditional Chinese medicine, is known as Baqia in China. It has been used to treat various inflammatory disorders, particularly pelvic inflammation.
Aim of the review:
The present paper aims to provide an up-to-date review at the advancements of the investigations on the ethnopharmacology, phytochemistry, pharmacological effect and actual and potential applications of S. china. Besides, the possible tendency and perspective for future research of this plant are discussed, as well.
Materials and methods:
This article uses "Smilax china L." "S. china" as the keyword and collects relevant information on Smilax china L. plants through electronic searches (Elsevier, PubMed, ACS, CNKI, Google Scholar, Baidu Scholar, Web of Science), relevant books, and classic literature about Chinese herb.
Results:
134 chemical constituents, among which steroid saponins and flavonoids are the predominant groups, have been isolated and identified from S. china. S. china with its active compounds is possessed of wide-reaching biological activities, including anti-inflammatory, anti-cancer, anti-oxidant, detoxify nicotine, anti-diabetes, anti-obesity, anti-hyperuricaemia, anti-hypertension, promoting skin wound and barrier repair and anti-bacterial activity. Besides, S. china is also applied to other fields, such as food industry and detection technology.
Conclusions:
Based on the review of the existing phytochemical studies on Smilax china L., the structural characterization of Smilax china L. extract can continue to be the focus of future research. Pharmacological studies in vitro and in vivo have demonstrated some of the traditional uses of Smilax china L. extract, while other traditional uses still need to be confirmed by research.
Electronic cigarettes (e-cigs) are customizable tobacco products that allow users to select e-liquid composition, flavors, and (in some devices) adjust wattage or heat used to generate e-cig aerosol. This study compared vascular outcomes in a conducting vessel (thoracic aorta) and a resistance artery (middle cerebral artery, MCA) in C57Bl/6 mice exposed to e-cig aerosol generated from either pure vegetable glycerin (VG) or pure propylene glycol (PG) over 60-min (Study 1), and separately the effect of using 5- vs. 30-watt settings with an exposure of 100-min (Study 2). In Study 1, aortic endothelial-dependent-dilation (EDD) was only impaired with PG- exposure (p < 0.05) compared with air. In the MCA, EDD response was impaired by ~50% in both VG and PG groups compared with air (p < 0.05). In Study 2, the aortic EDD responses were not different for either 5- or 30-watt exposed groups compared with air controls; however, in the MCA, both 5- and 30-watt groups were impaired by 32% and 55%, respectively, compared with air controls (p < 0.05). These pre-clinical data provide evidence that chronic exposure to aerosol produced by either VG or PG, and regardless of the wattage used, leads to vascular dysfunction at multiple levels within the arterial system. For all exposures, we observed greater impairment of arterial reactivity in a resistance artery (i.e. MCA) compared with the aorta. These data could suggest the smaller arteries may be more sensitive or first to be affected, or that different mechanism(s) for impairment may be involved depending on arterial hierarchy.
Background: Reports from previous studies on the effects of adenosine and caffeine on blood glucose are controversial and inconclusive. The present study sought to investigate the effect of acute adenosine infusion and caffeine injection on blood glucose level in rats. Materials and Methods: Thirty-four male albino rats (300-400 g) were randomly divided in a blinded-fashion into six groups, namely, Group I (n = 6) received normal saline (0.1-0.2 ml), Group II (n = 6) received adenosine (347.8 µg/kg/min), Group III (n = 5) received caffeine (6 mg/kg), followed by adenosine (347.8 µg/kg/min), Group IV (n = 5) were diabetic rats that received adenosine (347.8 µg/kg/min), Group V (n = 6) received caffeine (6 mg/kg), and Group VI (n = 6) received nifedipine (300µg/kg), followed by caffeine (6 mg/kg). Administrations were done through the femoral vein, while blood samples were taken from the carotid artery for glucose measurement. Results: Adenosine caused a reduction in blood glucose level in normal and diabetic rats, though the reduction was more noticeable in diabetic rats. Pretreatment of rats with caffeine completely abolished the adenosine-induced reduction in blood glucose and produced an exaggerated increase in blood glucose comparable to the level seen in rats that received caffeine alone. Pretreatment of rats with nifedipine reduced the caffeine-induced hyperglycemia by two-third. Conclusion: This study suggests that adenosine receptors could be of therapeutic target in the treatment of Type 1 diabetes due to its blood glucose-lowering potential in both diabetic and normal rats. It also suggests that intracellular calcium mobilization is more implicated in caffeine-induced hyperglycemia than adenosine receptor antagonism, even though other unidentified mechanism(s) remain to be explored.
Objective
Vaping may increase the cytotoxic effects of e-cigarette liquid (ECL). We compared the effect of unvaped ECL to e-cigarette vapour condensate (ECVC) on alveolar macrophage (AM) function.
Methods
AMs were treated with ECVC and nicotine-free ECVC (nfECVC). AM viability, apoptosis, necrosis, cytokine, chemokine and protease release, reactive oxygen species (ROS) release and bacterial phagocytosis were assessed.
Results
Macrophage culture with ECL or ECVC resulted in a dose-dependent reduction in cell viability. ECVC was cytotoxic at lower concentrations than ECL and resulted in increased apoptosis and necrosis. nfECVC resulted in less cytotoxicity and apoptosis. Exposure of AMs to a sub-lethal 0.5% ECVC/nfECVC increased ROS production approximately 50-fold and significantly inhibited phagocytosis. Pan and class one isoform phosphoinositide 3 kinase inhibitors partially inhibited the effects of ECVC/nfECVC on macrophage viability and apoptosis. Secretion of interleukin 6, tumour necrosis factor α, CXCL-8, monocyte chemoattractant protein 1 and matrix metalloproteinase 9 was significantly increased following ECVC challenge. Treatment with the anti-oxidant N-acetyl-cysteine (NAC) ameliorated the cytotoxic effects of ECVC/nfECVC to levels not significantly different from baseline and restored phagocytic function.
Conclusions
ECVC is significantly more toxic to AMs than non-vaped ECL. Excessive production of ROS, inflammatory cytokines and chemokines induced by e-cigarette vapour may induce an inflammatory state in AMs within the lung that is partly dependent on nicotine. Inhibition of phagocytosis also suggests users may suffer from impaired bacterial clearance. While further research is needed to fully understand the effects of e-cigarette exposure in humans in vivo, we caution against the widely held opinion that e-cigarettes are safe.
Smoking increases the risk of atherosclerosis-related events, such as myocardial infarction and ischemic stroke. Recent studies have examined the expression levels of altered microRNAs (miRNAs) in various diseases. The profiles of tissue miRNAs can be potentially used in diagnosis or prognosis. However, there are limited studies on miRNAs following exposure to cigarette smoke (CS). The present study was designed to dissect the effects and cellular/molecular mechanisms of CS-induced atherosclerogenesis. Apolipoprotein E knockout (ApoE KO) mice were exposed to CS for five days a week for two months at low (two puffs/min for 40 min/day) or high dose (two puffs/min for 120 min/day). We measured the area of atherosclerotic plaques in the aorta, representing the expression of miRNAs after the exposure period. Two-month exposure to the high dose of CS significantly increased the plaque area in aortic arch, and significantly upregulated the expression of atherosclerotic markers (VCAM-1, ICAM-1, MCP1, p22phox, and gp91phox). Exposure to the high dose of CS also significantly upregulated the miRNA-155 level in the aortic tissues of ApoE KO mice. Moreover, the expression level of miR-126 tended to be downregulated and that of miR-21 tended to be upregulated in ApoE KO mice exposed to the high dose of CS, albeit statistically insignificant. The results suggest that CS induces atherosclerosis through increased vascular inflammation and NADPH oxidase expression and also emphasize the importance of miRNAs in the pathogenesis of CS-induced atherosclerosis. Our findings provide evidence for miRNAs as potential mediators of inflammation and atherosclerosis induced by CS.
Background:
The course of multiple sclerosis (MS) shows substantial inter-individual variability. The underlying determinants of disease severity likely involve genetic and environmental factors.
Objective:
The aim of this study was to assess the impact of APOE and HLA polymorphisms as well as smoking and body mass index (BMI) in the very early MS course.
Methods:
Untreated patients ( n = 263) with a recent diagnosis of relapsing-remitting (RR) MS or clinically isolated syndrome underwent standardized magnetic resonance imaging (MRI). Genotyping was performed for single-nucleotide polymorphisms (SNPs) rs3135388 tagging the HLA-DRB1*15:01 haplotype and rs7412 (Ɛ2) and rs429358 (Ɛ4) in APOE. Linear regression analyses were applied based on the three SNPs, smoking and BMI as exposures and MRI surrogate markers for disease severity as outcomes.
Results:
Current smoking was associated with reduced gray matter fraction, lower brain parenchymal fraction and increased cerebrospinal fluid fraction in comparison to non-smoking, whereas no effect was observed on white matter fraction. BMI and the SNPs in HLA and APOE were not associated with structural MRI parameters.
Conclusions:
Smoking may have an unfavorable effect on the gray matter fraction as a potential measure of MS severity already in early MS. These findings may impact patients' counseling upon initial diagnosis of MS.
Objective
To use the relation between cigarette consumption and cardiovascular disease to quantify the risk of coronary heart disease and stroke for light smoking (one to five cigarettes/day).
Design
Systematic review and meta-analysis.
Data sources
Medline 1946 to May 2015, with manual searches of references.
Eligibility criteria for selecting studies
Prospective cohort studies with at least 50 events, reporting hazard ratios or relative risks (both hereafter referred to as relative risk) compared with never smokers or age specific incidence in relation to risk of coronary heart disease or stroke.
Data extraction/synthesis
MOOSE guidelines were followed. For each study, the relative risk was estimated for smoking one, five, or 20 cigarettes per day by using regression modelling between risk and cigarette consumption. Relative risks were adjusted for at least age and often additional confounders. The main measure was the excess relative risk for smoking one cigarette per day (RR1_per_day−1) expressed as a proportion of that for smoking 20 cigarettes per day (RR20_per_day−1), expected to be about 5% assuming a linear relation between risk and consumption (as seen with lung cancer). The relative risks for one, five, and 20 cigarettes per day were also pooled across all studies in a random effects meta-analysis. Separate analyses were done for each combination of sex and disorder.
Results
The meta-analysis included 55 publications containing 141 cohort studies. Among men, the pooled relative risk for coronary heart disease was 1.48 for smoking one cigarette per day and 2.04 for 20 cigarettes per day, using all studies, but 1.74 and 2.27 among studies in which the relative risk had been adjusted for multiple confounders. Among women, the pooled relative risks were 1.57 and 2.84 for one and 20 cigarettes per day (or 2.19 and 3.95 using relative risks adjusted for multiple factors). Men who smoked one cigarette per day had 46% of the excess relative risk for smoking 20 cigarettes per day (53% using relative risks adjusted for multiple factors), and women had 31% of the excess risk (38% using relative risks adjusted for multiple factors). For stroke, the pooled relative risks for men were 1.25 and 1.64 for smoking one or 20 cigarettes per day (1.30 and 1.56 using relative risks adjusted for multiple factors). In women, the pooled relative risks were 1.31 and 2.16 for smoking one or 20 cigarettes per day (1.46 and 2.42 using relative risks adjusted for multiple factors). The excess risk for stroke associated with one cigarette per day (in relation to 20 cigarettes per day) was 41% for men and 34% for women (or 64% and 36% using relative risks adjusted for multiple factors). Relative risks were generally higher among women than men.
Conclusions
Smoking only about one cigarette per day carries a risk of developing coronary heart disease and stroke much greater than expected: around half that for people who smoke 20 per day. No safe level of smoking exists for cardiovascular disease. Smokers should aim to quit instead of cutting down to significantly reduce their risk of these two common major disorders.
Smoking is an established risk factor for atherosclerosis through several underlying pathways. Moreover, in the development of atherosclerotic plaque formation, obesity, defined as excess fat mass accumulation, also plays a vital role in dyslipidemia and insulin resistance. Substantial evidence shows that cigarette smoking induces multiple pathological effects in adipose tissue, such as differentiation of adipocytes, lipolysis, and secretion properties in adipose tissue. Therefore, there is an emerging speculation in which adipose tissue abnormality induced by smoking or nicotine is likely to accelerate the progression of atherosclerosis. Herein, this review aims to investigate the possible interplay between smoking and adipose tissue dysfunction in the development of atherosclerosis.
Cardiovascular disease (CVD) is a major comorbidity in chronic obstructive pulmonary disease (COPD). Although the mechanism of its development remains largely unknown, it appears to be associated with cigarette consumption and reduced lung function. Therefore, the aim of this study was to investigate the potential link between water-soluble cigarette smoke extract (CSE)-induced endothelial dysfunction and the function of CXCL16/CXCR6 axis on the initial attachment of leukocytes, in addition to its possible impact on COPD-associated systemic inflammation. To do this, we employed several experimental approaches, including RNA silencing and flow cytometry analysis, the dynamic flow chamber technique, and intravital microscopy in the cremasteric arterioles of animals exposed to cigarette smoke (CS). CSE-induced arterial CXCL16 expression, leading to increased platelet–leukocyte and mononuclear cell adhesiveness. CSE-induced CXCL16 expression was dependent on Nox5 expression and subsequent RhoA/p38 MAPK/NF-κB activation. Flow cytometry analysis revealed that COPD patients (n = 35) presented greater numbers of activated circulating platelets (PAC-1⁺ and P-selectin⁺) expressing CXCL16 and CXCR6 as compared with age-matched controls (n = 17), with a higher number of CXCR6⁺-platelets in the smoking COPD group than in ex-smokers. This correlated with enhanced circulating CXCR6⁺-platelet–leukocyte aggregates in COPD patients. The increase in circulating numbers of CXCR6-expressing platelets and mononuclear cells resulted in enhanced platelet–leukocyte and leukocyte adhesiveness to CSE-stimulated arterial endothelium, which was greater than that found in age-matched controls and was partly dependent on endothelial CXCL16 upregulation. Furthermore, CS exposure provoked CXCL16-dependent leukocyte–arteriolar adhesion in cremasteric arterioles, which was significantly reduced in animals with a nonfunctional CXCR6 receptor. In conclusion, we provide the first evidence that increased numbers of CXCR6-expressing circulating platelets and mononuclear leukocytes from patients with COPD might be a marker of systemic inflammation with potential consequences in CVD development. Accordingly, CXCL16/CXCR6 axis blockade might constitute a new therapeutic approach for decreasing the risk of CVD in COPD patients.
http://www.bmj.com/content/360/bmj.j5855/rr-1