Serum levels of IL-32 in patients with coronary artery disease and its relationship with the serum levels of IL-6 and TNF-α

Abstract Coronary Artery Disease (CAD) is a chronic inflammatory disease caused by atherosclerosis and arteries become clogged due to plaque formation, fat accumulation, and various sorts of immune cells. IL-32 is a new proinflammatory cytokine, which enhances inflammation through inducing different inflammatory cytokines. The purpose of current research was to assess IL-32 serum levels in coronary artery disease subjects and its relationship with serum levels of IL-6 and TNF-α. Forty-two subjects diagnosed with CAD and thirty-nine control subjects were enrolled in the research. Serum levels of IL-6, TNF-α, and IL-32 were measured using the enzyme-linked immunosorbent assay (ELISA). IL-32, TNF-α, and IL-6 serum levels were significantly higher by 2.7, 3.48, and 3.2-fold in the CAD subjects than in control subjects, respectively. Moreover, no significant difference was found in TNF-α, IL-6 and IL-32 serum levels with the clogged arteries number in the CAD group. TNF-α and IL-32 serum levels in the CAD subjects with cardiac arterial stenosis in one major vessel were significantly increased than CAD subjects with cardiac arterial stenosis in more than one major vessels. ROC curve analysis revealed that serum levels of IL-32, TNF-α, and IL-6 showed good abilities in predicting CAD. Also, Multiple logistic regression analyses suggested that TNF-α, IL-6, and IL-32, serum levels of LDL and ox-LDL were independently related to the presence of CAD, while HDL serum levels were not. TNF-α, IL-32, and IL-6 showed an increase in CAD group and serum levels of these cytokines showed good abilities in predicting CAD. Our data suggested the involvement of TNF-α and IL-32 in the early stage of CAD.

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Serum levels of Asprosin in patients diagnosed with coronary artery disease (CAD): a case-control study

Lipids in Health and Disease ◽

10.1186/s12944-021-01514-9 ◽

2021 ◽

Vol 20 (1) ◽

Author(s):

Nariman Moradi ◽

Fatima Zahraa Fouani ◽

Akram Vatannejad ◽

Abbas Bakhti Arani ◽

Soraya Shahrzad ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Polycystic Ovary ◽

Serum Levels ◽

Type Ii Diabetes Mellitus ◽

Chronic Inflammatory Disease ◽

Increased Risk ◽

Tnf Α ◽

Artery Disease ◽

Control Study

Abstract Background Coronary artery disease (CAD) is considered as a multi-faceted chronic inflammatory disease involving reduced blood supply to the myocardium as a result of accumulating lipids in the atrial walls. Visceral adiposity with disrupted release of adipokines play a key role in its pathogenesis. Asprosin is a newly identified fasting-induced glucogenic adipokine that has been related with metabolic disorders such as type II diabetes mellitus and polycystic ovary syndrome. The preset study sought to assess circulating asprosin in context of CAD. Methods In this study, serum levels of asprosin were determined in 88 CAD patients and 88 non-CAD healthy controls. Serum IL-6, TNF-α, asprosin and adiponectin were assessed using ELISA kits. Results: Serum asprosin was found to be higher in CAD patients when compared to non-CAD subjects (7.84 ± 2.08 versus 5.02 ± 1.29 μg/mL, p < 0.001). Similarly, serum TNF-α, and IL-6 elevated in CAD group significantly (p < 0.001). However, circulating adiponectin diminished in CAD group when compared with non-CAD subjects (p < 0.001). Moreover, serum asprosin levels directly correlated with BMI, FBG, HOMA-IR, TG and TC. Logistic regression analyses showed that asprosin levels were associated with increased risk of developing CAD (odds ratio: 3.01, 95% CI: 2.16, 4.20 and p < 0.001), after adjusting for potential confounders (age, sex and BMI). Conclusions The present study findings suggested a possible relation of serum asprosin with the pathogenesis of CAD, in particular through insulin resistance and dyslipidemia.

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Elevated level of circulatory sTLT1 induces inflammation through SYK/MEK/ERK signalling in coronary artery disease

Clinical Science ◽

10.1042/cs20190999 ◽

2019 ◽

Vol 133 (22) ◽

pp. 2283-2299

Author(s):

Apabrita Ayan Das ◽

Devasmita Chakravarty ◽

Debmalya Bhunia ◽

Surajit Ghosh ◽

Prakash C. Mandal ◽

...

Keyword(s):

Risk Factors ◽

Coronary Artery Disease ◽

Coronary Artery ◽

Chronic Inflammation ◽

Ex Vivo ◽

Human Subjects ◽

Critical Role ◽

Atherosclerotic Cardiovascular Disease ◽

Tnf Α ◽

Artery Disease

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.

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Osteoprotegerin and Osteopontin Serum Levels are Associated with Vascular Function and Inflammation in Coronary Artery Disease Patients

Current Vascular Pharmacology ◽

10.2174/1570161117666191022095246 ◽

2020 ◽

Vol 18 (5) ◽

pp. 523-530 ◽

Cited By ~ 2

Author(s):

Konstantinos Maniatis ◽

Gerasimos Siasos ◽

Evangelos Oikonomou ◽

Manolis Vavuranakis ◽

Marina Zaromytidou ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Endothelial Function ◽

Vascular Function ◽

Serum Levels ◽

Atherosclerosis Progression ◽

Control Subjects ◽

Significant Difference ◽

Artery Disease ◽

Stable Cad

Background: Osteoprotegerin and osteopontin have recently emerged as key factors in both vascular remodelling and atherosclerosis progression. Interleukin-6 (IL-6) is an inflammatory cytokine with a key role in atherosclerosis. The relationship of osteoprotegerin, osteopontin, and IL-6 serum levels with endothelial function and arterial stiffness was evaluated in patients with coronary artery disease (CAD). Methods: We enrolled 219 patients with stable CAD and 112 control subjects. Osteoprotegerin, osteopontin and IL-6 serum levels were measured using an ELISA assay. Endothelial function was evaluated by flow-mediated dilation (FMD) in the brachial artery and carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness. Results: There was no significant difference between control subjects and CAD patients according to age and sex. Compared with control subjects, CAD patients had significantly impaired FMD (p<0.001) and increased PWV (p=0.009). CAD patients also had significantly higher levels of osteoprotegerin (p<0.001), osteopontin (p<0.001) and IL-6 (p=0.03), compared with control subjects. Moreover, IL-6 levels were correlated with osteoprotegerin (r=0.17, p=0.01) and osteopontin (r=0.30, p<0.001) levels. FMD was correlated with osteoprotegerin levels independent of possible confounders [b coefficient= - 0.79, 95% CI (-1.54, -0.05), p=0.04]. Conclusion: CAD patients have increased osteoprotegerin, osteopontin and IL-6 levels. Moreover, there is a consistent association between osteoprotegerin and osteopontin serum levels, vascular function and inflammation in CAD patients. These findings suggest another possible mechanism linking osteoprotegerin and osteopontin serum levels with CAD progression through arterial wall stiffening and inflammation.

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Implications of cardiac markers in risk-stratification and management for COVID-19 patients

Critical Care ◽

10.1186/s13054-021-03555-z ◽

2021 ◽

Vol 25 (1) ◽

Author(s):

Pengping Li ◽

Wei Wu ◽

Tingting Zhang ◽

Ziyu Wang ◽

Jie Li ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Risk Stratification ◽

Rna Sequencing ◽

High Mortality ◽

Admission Rate ◽

Serum Levels ◽

Receptor Expression ◽

Cardiac Markers ◽

Artery Disease

Abstract Background COVID-19 has resulted in high mortality worldwide. Information regarding cardiac markers for precise risk-stratification is limited. We aim to discover sensitive and reliable early-warning biomarkers for optimizing management and improving the prognosis of COVID-19 patients. Methods A total of 2954 consecutive COVID-19 patients who were receiving treatment from the Wuhan Huoshenshan Hospital in China from February 4 to April 10 were included in this retrospective cohort. Serum levels of cardiac markers were collected after admission. Coronary artery disease diagnosis and survival status were recorded. Single-cell RNA-sequencing and bulk RNA-sequencing from different cohorts of non-COVID-19 were performed to analyze SARS-CoV-2 receptor expression. Results Among 2954 COVID-19 patients in the analysis, the median age was 60 years (50–68 years), 1461 (49.5%) were female, and 1515 (51.3%) were severe/critical. Compared to mild/moderate (1439, 48.7%) patients, severe/critical patients showed significantly higher levels of cardiac markers within the first week after admission. In severe/critical COVID-19 patients, those with abnormal serum levels of BNP (42 [24.6%] vs 7 [1.1%]), hs-TNI (38 [48.1%] vs 6 [1.0%]), α- HBDH (55 [10.4%] vs 2 [0.2%]), CK-MB (45 [36.3%] vs 12 [0.9%]), and LDH (56 [12.5%] vs 1 [0.1%]) had a significantly higher mortality rate compared to patients with normal levels. The same trend was observed in the ICU admission rate. Severe/critical COVID-19 patients with pre-existing coronary artery disease (165/1,155 [10.9%]) had more cases of BNP (52 [46.5%] vs 119 [16.5%]), hs-TNI (24 [26.7%] vs 9.6 [%], α- HBDH (86 [55.5%] vs 443 [34.4%]), CK-MB (27 [17.4%] vs 97 [7.5%]), and LDH (65 [41.9%] vs 382 [29.7%]), when compared with those without coronary artery disease. There was enhanced SARS-CoV-2 receptor expression in coronary artery disease compared with healthy controls. From regression analysis, patients with five elevated cardiac markers were at a higher risk of death (hazards ratio 3.4 [95% CI 2.4–4.8]). Conclusions COVID-19 patients with pre-existing coronary artery disease represented a higher abnormal percentage of cardiac markers, accompanied by high mortality and ICU admission rate. BNP together with hs-TNI, α- HBDH, CK-MB and LDH act as a prognostic biomarker in COVID-19 patients with or without pre-existing coronary artery disease.

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Effect of probiotic supplementation along with calorie restriction on metabolic endotoxemia, and inflammation markers in coronary artery disease patients: a double blind placebo controlled randomized clinical trial

Nutrition Journal ◽

10.1186/s12937-021-00703-7 ◽

2021 ◽

Vol 20 (1) ◽

Author(s):

Jalal Moludi ◽

Hossein Samadi Kafil ◽

Shaimaa A. Qaisar ◽

Pourya Gholizadeh ◽

Mohammad Alizadeh ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Lactobacillus Rhamnosus ◽

Serum Levels ◽

Interleukin 10 ◽

Probiotic Supplementation ◽

Related Factors ◽

Double Blind ◽

Artery Disease ◽

Metabolic Endotoxemia

Abstract Purpose Alterations in the gut microbiome (dysbiosis) has been associated with increased microbial translocation, leading to chronic inflammation in coronary artery disease (CAD). It has been proposed that modulation of gut microbiota by probiotic might modify metabolic endotoxemia. Therefore, the purpose of this study was to examine the effects of Lactobacillus rhamnosus GG (LGG) on endotoxin level, and biomarkers of inflammation in CAD participants. Methods This study was a 12-weeks randomized, double-blind, and intervention on 44 patients with CAD. Patients were randomly allocated to receive either one LGG capsule 1.6 × 109 colony-forming unit (CFU) or the placebo capsules for 12 weeks. In addition, all the participants were also prescribed a calorie-restricted diet. Serum levels of interleukin-1β (IL-1β), Toll-like receptor 4 (TLR4), interleukin-10 (IL-10), and lipopolysaccharide (LPS), were assessed before and after the intervention. Results A significant decrease in IL1-Beta concentration (− 1.88 ± 2.25, vs. 0.50 ± 1.58 mmol/L, P = 0.027), and LPS levels (− 5.88 ± 2.70 vs. 2.96+ 5.27 mg/L, P = 0.016), was observed after the probiotic supplementation compared with the placebo. Participants who had ≥2.5 kg weight loss showed significantly improved cardiovascular-related factors, compared to patients with < 2.5 kg weight reduction, regardless of the supplement they took. Conclusion These data provide preliminary evidence that probiotic supplementation has beneficial effects on metabolic endotoxemia, and mega inflammation in participants with CAD.

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Association of TNF-α (-308G/A) Gene Polymorphism with Circulating TNF-α Levels and Excessive Daytime Sleepiness in Adults with Coronary Artery Disease and Concomitant Obstructive Sleep Apnea

Journal of Clinical Medicine ◽

10.3390/jcm10153413 ◽

2021 ◽

Vol 10 (15) ◽

pp. 3413

Author(s):

Afrouz Behboudi ◽

Tilia Thelander ◽

Duygu Yazici ◽

Yeliz Celik ◽

Tülay Yucel-Lindberg ◽

...

Keyword(s):

Coronary Artery Disease ◽

Obstructive Sleep Apnea ◽

Coronary Artery ◽

Sleep Apnea ◽

Gene Polymorphism ◽

Excessive Daytime Sleepiness ◽

Daytime Sleepiness ◽

Obstructive Sleep ◽

Tnf Α ◽

Artery Disease

Obstructive sleep apnea (OSA) is common in patients with coronary artery disease (CAD), in which inflammatory activity has a crucial role. The manifestation of OSA varies significantly between individuals in clinical cohorts; not all adults with OSA demonstrate the same set of symptoms; i.e., excessive daytime sleepiness (EDS) and/or increased levels of inflammatory biomarkers. The further exploration of the molecular basis of these differences is therefore essential for a better understanding of the OSA phenotypes in cardiac patients. In this current secondary analysis of the Randomized Intervention with Continuous Positive Airway Pressure in CAD and OSA (RICCADSA) trial (Trial Registry: ClinicalTrials.gov; No: NCT 00519597), we aimed to address the association of tumor necrosis factor alpha (TNF-α)-308G/A gene polymorphism with circulating TNF-α levels and EDS among 326 participants. CAD patients with OSA (apnea–hypopnea-index (AHI) ≥ 15 events/h; n = 256) were categorized as having EDS (n = 100) or no-EDS (n = 156) based on the Epworth Sleepiness Scale score with a cut-off of 10. CAD patients with no-OSA (AHI < 5 events/h; n = 70) were included as a control group. The results demonstrated no significant differences regarding the distribution of the TNF-α alleles and genotypes between CAD patients with vs. without OSA. In a multivariate analysis, the oxygen desaturation index and TNF-α genotypes from GG to GA and GA to AA as well as the TNF-α-308A allele carriage were significantly associated with the circulating TNF-α levels. Moreover, the TNF-α-308A allele was associated with a decreased risk for EDS (odds ratio 0.64, 95% confidence interval 0.41–0.99; p = 0.043) independent of age, sex, obesity, OSA severity and the circulating TNF-α levels. We conclude that the TNF-α-308A allele appears to modulate circulatory TNF-α levels and mitigate EDS in adults with CAD and concomitant OSA.

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Abstract P354: Circulating Interleukin 17 A In Patients With Acute And Chronic Coronary Syndrome

Circulation Research ◽

10.1161/res.129.suppl_1.p354 ◽

2021 ◽

Vol 129 (Suppl_1) ◽

Author(s):

Dinaldo C Oliveira ◽

Edivaldo Mendes Filho ◽

Mariana Barros ◽

Carolina Oliveira ◽

Joao Vitor Cabral ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Healthy Volunteers ◽

Clinical Characteristics ◽

Serum Levels ◽

Cross Sectional Study ◽

Interleukin 17 ◽

Cross Sectional ◽

Coronary Syndrome ◽

Artery Disease

Introduction: Interleukin L-17 is produced by Th 17 cells and other cells. There is a debate if IL 17 is atherogenic or atheroprotective. The true role of this interleukin during the development and progression of the coronary artery disease is not known. Objective: To evaluate if there are differences between the IL17 A serum levels according to clinical presentation of the coronary artery disease. Methods: This is a cross sectional study which enrolled 101 patients with acute coronary syndrome (ACS), 100 patients with chronic coronary syndrome (CCS) and 100 healthy volunteers. Blood samples were taken from patients ( at admission) and controls to analysis the level of IL17A. Clinical characteristics were collected through questionnaires. This research was approved by ethical committee. Results: Comparisons of the clinical characteristics between patients with ACS and CCS revealed: mean age ( 62 ± 12.4 vs 63.3 ± 9.8, p = 0.4 ), male (63.4% vs 58%, p = 0.4) hypertension (85.1% vs 79%, p = 0.1) , disyipidemia (48% vs 31%, p =0.01), Diabetes Mellitus (47.5% vs 41%, p = 0.3), previous myocardial infarction (57.4% vs 40%, p = 0,01), smoking (29.7% vs 38%, p = 1). The peripheral concentrations of IL17A according to ACS, CCS and controls were: 5.36 ± 8.83 vs 6.69 ± 17.92 vs 6.26 ± 11.13, p = 0.6. Besides, the comparison between ACS and CCS showed: 5.36 ± 8.83 vs 6.69 ± 17.92, p = 0.3. Conclusion: The main finding os this study was that the circulating IL 17 concentrations were similar in patients with ACS, CCS and healthy volunteers). Besides, there was no difference between patients with ACS and CCS. Therefore, our hypothesis is that in patients with ACS and CCS the circulating IL 17 A concentrations are low or undetectable.

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Increased serum levels of fetuin B in patients with coronary artery disease

Endocrine ◽

10.1007/s12020-017-1387-1 ◽

2017 ◽

Vol 58 (1) ◽

pp. 97-105 ◽

Cited By ~ 6

Author(s):

Kefu Zhu ◽

Yuming Wang ◽

Pengqin Shu ◽

Qinyi Zhou ◽

Jinzhou Zhu ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Serum Levels ◽

Artery Disease

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CD14+CD16+ monocytes in coronary artery disease and their relationship to serum TNF-α levels

Thrombosis and Haemostasis ◽

10.1160/th04-02-0095 ◽

2004 ◽

Vol 92 (08) ◽

pp. 419-424 ◽

Cited By ~ 164

Author(s):

Stefan Blankenberg ◽

Christine Espinola-Klein ◽

Joern Dopheide ◽

Christoph Bickel ◽

Karl Lackner ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Animal Studies ◽

Inflammatory Diseases ◽

Serum Concentrations ◽

Tnf Α ◽

Hs Crp ◽

Artery Disease ◽

Fourth Quartile

SummaryMonocytes play a central role in the inflammatory disease atherosclerosis. CD14+CD16+ monocytes are considered proinflammatory monocytes, as they have an increased capacity to produce proinflammatory cytokines, such as TNF-α, and are elevated in various inflammatory diseases. We hypothesized that patients with coronary artery disease (CAD) have increased levels of CD14+CD16+ monocytes, and that CD14+CD16+ monocytes are associated with inflammation markers. We investigated CD14+CD16+ monocytes in 247 patients with CAD and 61 control subjects using flow cytometry. In addition serum concentrations of TNF-α, IL-6, and Hs-CRP were assessed. Patients with CAD had higher levels of CD14+CD16+ monocytes than controls (13.6% versus 11.4%; p<0.001). Logistic regression analysis including quartiles of CD14+CD16+ monocytes showed that CD14+CD16+ monocytes were associated with prevalence of CAD (OR 4.9, 95% CI 2.5–19.1, for subjects in the fourth quartile in comparison to subjects in the first quartile). The association between CD14+CD16+ monocytes and CAD remained independently significant after adjustment for most potential confounders (OR 5.0, 95% CI 1.2-20.0). Serum concentrations of TNF-α were elevated in subjects within the highest quartiles of CD14+CD16+ monocytes (p=0.018). Our study showed that increased numbers of CD14+CD16+ monocytes are associated with coronary atherosclerosis and TNF-α. In accordance, recent animal studies suggest a possibly important role of these monocytes in the development of atherosclerosis.

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