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The data are presented as means ± SD. Profile of plasma levels of tumor necrosis factor-α (TNF-α), interleukin- (IL-) 6, and IL-10 (a) and of monocyte chemoattractant protein-1 (MCP-1) (b) in the coronary artery disease (CAD), unstable angina pectoris (UAP), and acute myocardial infarction (AMI) groups. P∗<0.05; P∗∗<0.01.
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Objective. We evaluated inflammatory cytokines and chemokine in peripheral blood mononuclear cells (PBMCs) in patients with either acute coronary syndrome (ACS) or stable coronary artery disease (CAD). Methods. We enrolled 20 ACS patients and 50 stable CAD patients without previous history of ACS who underwent cardiac catheterization. Patients with...
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family cytokine, exerts a critical role in immune regulation in the context of infection and autoimmunity. IL-33,
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Citations
... Our results further suggest an association between the TCF21 CC homozygote genotype in both the occurrence of stable angina and STEMI in a Han Taiwanese cohort. The precise role of TCF21 polymorphisms in stable angina and STEMI has yet to be confirmed, although chronic inflammatory cytokines have been implicated [38][39][40]. Previous studies have shown that chemokines, including macrophage inflammatory protein-alpha, IFN-γ-inducible protein, monocyte chemoattractant protein-1, and eotaxin, play key roles in the pathogenesis of CAD via chronic inflammation [41]. ...
Background: Transcription factor 21 (TCF21, epicardin, capsuling, pod-1) is expressed in the epicardium and is involved in the regulation of cell fate and differentiation via epithelial-mesenchymal transformation during development of the heart. In addition, TCF21 can suppress the differentiation of epicardial cells into vascular smooth muscle cells and promote cardiac fibroblast development. This study aimed to explore whether TCF21 gene (12190287G/C) variants affect coronary artery disease risk.
Methods: We enrolled 381 patients who had stable angina, 138 with ST elevation myocardial infarction (STEMI), and 276 healthy subjects. Genotyping of rs12190287 of the TCF21 gene was performed.
Results: Higher frequencies of the CC genotype were found in the patients with stable angina/STEMI than in the healthy controls. After adjusting for diabetes mellitus, hypertension, age, sex, smoking, body mass index and hyperlipidemia, the patients with the CC genotype of the TCF21 gene were associated with 2.49- and 9.19-fold increased risks of stable angina and STEMI, respectively, compared to the patients with the GG genotype. Furthermore, TCF21 CC genotypes showed positive correlations with both stable angina and STEMI, whereas TCF21 GG genotypes exhibited a negative correlation with STEMI. Moreover, the stable angina and STEMI patients with the CC genotype had significantly elevated high-sensitivity C-reactive protein levels than those with the GG genotype. In addition, significant associations were found between type 2 diabetes mellitus, hypertension, and hyperlipidemia with TCF21 gene polymorphisms (p for trend < 0.05).
Conclusion: TCF21 gene polymorphisms may increase susceptibility to stable angina and STEMI.
... Therefore, further research is required to validate the actual results. In ACS patients, low expression levels of IL-10 in serum samples have been associated with an increased risk of cardiovascular events and high IL-10 expression levels have been associated with a decreased risk [18,19]. In present study, the level of IL-10 is lower in ACS patients as compared to controls but the difference is not statistically significant. ...
Objectives: Inflammatory pathways play a significant role in atherosclerosis that leads to acute coronary syndrome (ACS). The initial stages of atherosclerosis are often asymptomatic; when atherosclerotic plaques become unstable it leads to ACS. Therefore, early detection, diagnosis, and treatment of atherosclerosis must be sought. These circumstances underpin the need for diagnostic values of inflammatory markers, warranting their routine clinical application to develop anti-atherosclerotic therapeutic approaches. The aim of this case-control observational study was to evaluate the plasma levels of interleukin (IL)-6, IL-18, IL-1β, and IL-10. Methods: The research was conducted at Hasan Sadikin Hospital from September to December 2021. Patients were recruited based on the typical clinical history of ACS (non-ST-elevation myocardial infarction, ST-elevation myocardial infarction, and unstable angina) and electrocardiographic and cardiac enzyme data. Healthy subjects having no more than one cardiovascular disease risk factor at admission were included. A total of 43 subjects were included in the study, of which 23 subjects were patients diagnosed with ACS and 20 were healthy controls. Results: The results showed that the mean plasma levels of IL-6 (298.6±432.9 pg/mL) in ACS patients were significantly higher than the mean concentration of IL-6 (33.7±96.6 pg/mL) in the control group (p < 0.05). Similarly, the mean plasma level of IL-18 (181.4±81.4 pg/mL) in ACS patients was significantly higher compared to the mean concentration (125.0±29.8 pg/mL) in the control group (p < 0.05), suggesting that both IL-6 and IL-18 were associated with ACS. However, there is no statistically significant difference between IL-1β and IL-10 levels. A Pearson’s correlation analysis showed that a positive correlation exists between IL-6 and IL-18. Conclusions: Both IL-6 and IL-18 are associated with ACS.
... IL-33 was also found in abundance in the presence of vulnerable atherosclerotic plaques, and correlated with the degree of inflammatory cell infiltration [74]. However, conflicting results have also been reported, indicating IL-33 s ambiguous role in atherosclerosis [75]. A subsequent study stressed the prognostic significance of IL-33 in patients after revascularized acute coronary syndrome, with higher levels indicating a higher disease complexity and poorer 1-year prognosis [76]. ...
Coronary atherosclerosis is a chronic pathological process that involves inflammation together with endothelial dysfunction and lipoprotein dysregulation. Experimental studies during the past decades have established the role of inflammatory cytokines in coronary artery disease, namely interleukins (ILs), tumor necrosis factor (TNF)-α, interferon-γ, and chemokines. Moreover, their value as biomarkers in disease development and progression further enhance the validity of this interaction. Recently, cytokine-targeted treatment approaches have emerged as potential tools in the management of atherosclerotic disease. IL-1β, based on the results of the CANTOS trial, remains the most validated option in reducing the residual cardiovascular risk. Along the same line, colchicine was also proven efficacious in preventing major adverse cardiovascular events in large clinical trials of patients with acute and chronic coronary syndrome. Other commercially available agents targeting IL-6 (tocilizumab), TNF-α (etanercept, adalimumab, infliximab), or IL-1 receptor antagonist (anakinra) have mostly been assessed in the setting of other inflammatory diseases and further testing in atherosclerosis is required. In the future, potential targeting of the NLRP3 inflammasome, anti-inflammatory IL-10, or atherogenic chemokines could represent appealing options, provided that patient safety is proven to be of no concern.
... According to these data obtained, TOS caused by cellular stress during the inflammation of the coronary arteries directly triggered OSI, and the level of IL 33 may have increased in order to prevent damage to the cells due to TOS and OSI. In a study conducted in patients with CAD, it was reported that IL 33 expression was high, circulating IL 33 levels were associated with the pathogenesis of atherosclerosis in patients with acute coronary syndrome and could be used as diagnostic indicators in terms of a new index value in these diseases [18]. ...
Investigation of oxidative stress and Interleukin 33 in pericardial fluid Investigation of oxidative stress and Interleukin 33 (IL33) level in pericardial fluid of patients with coronary artery bypass surgery Abstract Aim: Pericardial fluid composition changes in coronary artery disease. This study aims to investigate interleukin 33 (IL 33), total antioxidant status (TAS), total oxidative stress (TOS), and oxidative stress index (OSI) levels in the pericardial fluid and blood plasma of patients who have undergone coronary artery bypass surgery and contribute to the understanding of the pathophysiology of the disease. Material and Methods: In the study, IL 33, TAS, TOS, and OSI levels were determined in the pericardial fluid and blood plasma of 40 patients who had undergone coronary artery bypass surgery, and the relationship between these parameters was investigated. Results: IL 33 level in pericardial fluid (51.44 pq/mL) was found to be higher than Plasma IL 33 level (32.31 pq/mL). A significant positive correlation was found between OSI and TOS in pericardial fluid and plasma (p<0.01). A significant negative correlation was found between OSI and TAS in pericardial fluid (p<0.01). Discussion: IL 33 level was found to be low in patients with coronary artery disease. A higher IL 33 level in pericardial fluid indicates that IL 33 is specific to the heart tissue and passes from the heart tissue to the pericardial space. TOS caused by cellular stress during the inflammation of the coronary arteries directly triggered OSI. IL 33 level may be increased to prevent damage to cells due to TOS and OSI. This study shows us that pericardial fluid can reflect physiological and biochemical changes in the heart, and therefore pericardial fluid can be used for diagnostic and therapeutic purposes.
... Pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) have a significant role in endothelial dysfunction and atherosclerosis development [4]. TNF-α level was elevated in the plasma of patients with acute coronary syndrome [5], while deletion of TNF-α gene reduced the formation of atherosclerosis in mice [6]. TNF-α promotes Life 2022, 12, 1462 2 of 11 atherogenesis by activating a transcription factor, nuclear factor kappaB (NF-κB). ...
Persicaria minor (Huds.) Opiz is an herb with anti-inflammatory, antioxidant, and anti-atherosclerosis effects. Nevertheless, the mechanism underlying its anti-atherosclerosis effect is poorly comprehended. This in vitro study assessed the protective effects of standardized aqueous extract of P. minor leaves (PM) on tumor necrosis factor-α (TNF-α)-induced monocyte adhesion to human umbilical vein endothelial cells (HUVEC), which is one of the pivotal early steps in atherogenesis. The results showed that PM decreased the mRNA and protein expression of cellular adhesion molecules, vascular adhesion molecule-1 and intercellular adhesion molecule-1, resulting in reduced adhesion of monocytes to HUVEC. Additionally, PM inhibited nuclear factor kappaB (NF-κB) activation as indicated by reduced NF-κB p65 levels in TNF-α-induced HUVEC. Overall, PM could prevent in vitro atherogenesis by inhibiting NF-κB activation and adhesion of monocytes to HUVEC. The effects of PM are probably mediated by its bioactive compound, quercetin-3-O-glucuronide. The findings may provide a rationale for the in vivo anti-atherosclerosis effect of PM, and support its potential use in atherosclerosis.
... Vitamin D is also thought to play a role in bile acid synthesis in the liver and may have a direct impact on lipid metabolism. Al Shahi et al., (16) and Camaré et al., (17) reported that vitamin D deficiency in diabetic coronary patients may be one of the factors contributing to instability of atherosclerotic plaques and as a result, the development of a local blood clot and eventual myocardial infarction. A cornerstone of CAD prevention is identifying and managing the risk of dyslipidaemia in T2DM. ...
Background/aim:
Vitamin D deficiency accelerates the onset of type 2 diabetes mellitus (T2DM). Polymorphisms in the vitamin D receptor (VDR) have been linked to coronary artery disease (CAD). This study aimed to evaluate the association of vitamin D deficiency and VDR polymorphism with CAD in T2DM.
Patients and methods:
A total of 150 adult male and female subjects, aged from 40 to 60 years, were divided into three groups, each with 50 subjects; control group, T2DM, and T2DM with CAD. Fasting blood glucose (FBG), total cholesterol (TC), triglycerides (TG), HDL-C, LDL-C, glycosylated hemoglobin (HbA1c), and 25-hydroxyvitamin D (25-OH D) were assessed. VDR genotypes (BsmI, Taq1 and FOK1) were investigated by polymerase chain reaction fragment length polymorphism.
Results:
There was a significant negative correlation between serum 25-OH D and FBG, TC, TG, and LDL-C levels, and a positive correlation with HDL-C levels in all diabetic patient groups. The risk of CAD was markedly higher in the group of T2DM with CAD in comparison to the control (p<0.0001) and the T2DM group. Regarding Taq1, there was also a significantly higher risk of CAD in Tt+tt genotypes and t allele in the T2DM with CAD group compared to control (p<0.001, 0.031 respectively). In addition, 25-OH D concentrations and the prevalence of VDR polymorphisms (BsmI, Taq1) were correlated with the risk of CAD.
Conclusion:
Deficiency of vitamin D and the prevalence of VDR polymorphisms (BsmI, Taq1) can serve as important markers for CAD.
... BAFF are up-regulated in RA synovial joints as well as early stages of PD [33,34]. IL-27 s enhancement of TNF-α mediated upregulation of adhesion molecules and pro-inflammatory IL-6 in blood monocytes of patients with acute myocardial infarction (MI) makes it high CVD risk associated [35]. The TGM2 levels in RA without PD correlate inversely with the total sum of MBL which aligns with previous findings that TGM2 correlates with RANKL production in human periodontal ligament cells as part of the inflammatory response in PD [36]. ...
Objectives:
Periodontal disease (PD) and rheumatoid arthritis (RA) are known chronic conditions with sustained inflammation leading to osteolysis. Cardiovascular diseases (CVD) are frequent comorbidities that may arise from sustained inflammation associated with both PD and RA. In order to determine CVD risk, alterations at the molecular level need to be identified. The objective of this study, therefore, was to assess the relationship of CVD associated biomarkers in RA patients and how it is influenced by PD.
Methods:
The study consisted of patient (26 RA with PD, 21 RA without PD, 51 patients with PD only) and systemically and periodontally healthy control (n = 20) groups. Periodontal parameters bleeding on probing, probing pocket depth, and marginal bone loss were determined to characterize the patient groups. Proteomic analysis of 92 CVD-related protein biomarkers was performed using a multiplex proximity extension assay. Biomarkers were clustered using the search tool for retrieval of interacting genes (STRING) to determine protein-protein interaction (PPI) networks.
Results:
RA patients with PD had higher detection levels for 47% of the measured markers (ANGPT1, BOC, CCL17, CCL3, CD4, CD84, CTRC, FGF-21, FGF-23, GLO1, HAOX1, HB-EGF, hOSCAR, HSP 27, IL16, IL-17D, IL18, IL-27, IL6, LEP, LPL, MERTK, MMP12, MMP7, NEMO, PAPPA, PAR-1, PARP-1, PD-L2, PGF, PIgR, PRELP, RAGE, SCF, SLAMF7, SRC, THBS2, THPO, TNFRSF13B, TRAIL-R2, VEGFD, VSIG2, and XCL1) as compared to RA without PD. Furthermore, a strong biological network was identified amongst these proteins (clustering coefficient = 0.52, PPI enrichment p-value < 0.0001). Coefficients for protein clusters involved in CVD (0.59), metabolic (0.53), and skeletal (0.51) diseases were strongest in the PD group.
Conclusion:
Periodontal disease augments CVD-related biomarkers in RA through shared pathological clusters, concurrently enhancing metabolic and skeletal disease protein interactions, independent of autoimmune status.
... Because single nucleotide polymorphisms in the IL-6 gene promoter can change IL-6 expression and secretion, altering circulating levels may result in significant biological responses (68). Through circulation level variation, IL-6 might be regarded as a crucial regulator of cardiovascular disease beginning and progression (56,69). carried performed research on 20 patients with acute coronary syndrome and 50 individuals with stable coronary artery disease They observed that greater IL-6 levels in the blood were linked to the development of atherosclerosis. ...
... In the past, the inflammatory mediators involved in ACS mainly included CRP, IL-6, and other factors [12,13]. However, with the deepening of medical research, it has been found that IL-37 is also an inflammatory factor related to ACS [14]. ...
Objective:
To explore the level of serum interleukin-37 in patients with acute coronary syndrome (ACS) and its prognostic value.
Methods:
Altogether, 121 continuous ACS cases from September 2017 to June 2020 were selected as the research group (RG), and 107 healthy individuals during the same period were obtained as the control group (CG). ELISA was applied to test IL-37 in the serum of the CG and the RG. Chemiluminescence immunoassay was applied to test NT-pro BNP and hs-cTnI in each group and immune scattering turbidimetry to test hs-CRP. The correlation of IL-37 with serum NT-pro BNP, hs-cTnI, and CRP was analyzed, and the value of IL-37 in diagnosis and prognosis prediction of patients with ACS was tested. Logistic regression was applied to test the independent risk factors affecting poor prognosis of patients with ACS.
Results:
IL-37 was poorly expressed in patients with ACS, which had a high diagnostic value for ACS (sensitivity: 94.39%, specificity: 74.38%, and area under curve: 0.945). There was a negative correlation of IL-37 with serum NT-pro BNP, hs-cTnI, and CRP. IL-37 in patients with poor prognosis was markedly declined compared with that of patients with good prognosis, and the predicted AUC was 0.965. Logistic regression revealed that low IL-37, diabetes, high CRP, NT-pro BNP, and hs-cTnI in the blood were independent risk factors for poor prognosis in patients with ACS.
Conclusion:
IL-37 is low expressed in patients with ACS, which has a good diagnostic and prognostic value for ACS, and may be applied as an important marker for the prediction of patients with ACS.
... Patients with stable angina have significantly higher levels of cytokines, such as IL-6 and TNF-a, than do patients with normal coronary arteries (17,18). Moreover, IL-6 levels are significantly higher in patients with ACS than in patients with stable angina (19). ...
This study aimed to explore the relationship between plasma interleukin 6 (IL-6) levels, adverse cardiovascular events, and the severity of acute coronary syndrome (ACS). A literature review was performed of studies regarding IL-6 and ACS extracted from databases including EMBASE, Cqvip, MEDLINE, Web of Knowledge, PubMed, Cochrane Library, China National Knowledge Infrastructure, and Wanfang data. The Newcastle-Ottawa scale (NOS) was used to evaluate the quality of the literature. The literature was screened, its quality was evaluated, and relevant data were extracted for performing meta-analysis using RevMan software (version 5.3). A total of 524 studies were included in the initial survey. After several rounds of screening and analysis, six studies met the inclusion criteria and underwent meta-analysis using a fixed-effect model. Patients were divided into non-severe and severe groups based on the concentration of high-sensitivity C-reactive protein. Meta-analysis of the relationship between IL-6 and the severity of ACS showed that the plasma IL-6 level of patients in the severe group was significantly higher than that of patients in the non-severe group (p<0.00001). Additionally, patients with experience of major adverse cardiovascular events had significantly higher plasma IL-6 levels than did patients without experience of such events (p<0.00001). In summary, patients with ACS and high IL-6 levels tended to be in a critical condition, with a higher risk of adverse cardiovascular events and worse prognosis. Thus, IL-6 levels could indicate whether patients with ACS may have adverse cardiovascular events and determine the severity of ACS.
