scholarly journals Immune Dysfunction in Uremia 2020

Toxins ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 439
Author(s):  
Gerald Cohen
Keyword(s):  
Cardiovascular Disease ◽  
Immune System ◽  
Immune Cells ◽  
Protein Profile ◽  
Density Lipoprotein ◽  
Uremic Toxins ◽  
Water Soluble ◽  
Retinol Binding Protein ◽  
Intestinal Microbiome ◽  
The Impact

Cardiovascular disease and infections are major causes for the high incidence of morbidity and mortality of patients with chronic kidney disease. Both complications are directly or indirectly associated with disturbed functions or altered apoptotic rates of polymorphonuclear leukocytes, monocytes, lymphocytes, and dendritic cells. Normal responses of immune cells can be reduced, leading to infectious diseases or pre-activated/primed, giving rise to inflammation and subsequently to cardiovascular disease. This review summarizes the impact of kidney dysfunction on the immune system. Renal failure results in disturbed renal metabolic activities with reduced renin, erythropoietin, and vitamin D production, which adversely affects the immune system. Decreased kidney function also leads to reduced glomerular filtration and the retention of uremic toxins. A large number of uremic toxins with detrimental effects on immune cells have been identified. Besides small water-soluble and protein-bound compounds originating from the intestinal microbiome, several molecules in the middle molecular range, e.g., immunoglobulin light chains, retinol-binding protein, the neuropeptides Met-enkephalin and neuropeptide Y, endothelin-1, and the adipokines leptin and resistin, adversely affect immune cells. Posttranslational modifications such as carbamoylation, advanced glycation products, and oxidative modifications contribute to uremic toxicity. Furthermore, high-density lipoprotein from uremic patients has an altered protein profile and thereby loses its anti-inflammatory properties.

scholarly journals Immune cells—A curse and a blessing!

2021 ◽  
Vol 218 (6) ◽  
Author(s):  
Valbona Mirakaj
Keyword(s):  
Cardiovascular Disease ◽  
Immune System ◽  
Immune Cells ◽  
Innate Immune System ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
The Impact

Innate immune cells are crucial in the development and regulation of cardiovascular disease. In this issue, two groups, Davis et al. (2021. J. Exp. Med.https://doi.org/10.1084/jem.20201839) and Li et al. (2021. J. Exp. Med.https://doi.org/10.1084/jem.20210008) describe the impact of the innate immune system on the development of cardiovascular disease.

scholarly journals The Effect of Air Pollution on the Immune System

2020 ◽  
Vol 4 (4) ◽  
Author(s):  
Diana Liu
Keyword(s):  
Cardiovascular Disease ◽  
Air Pollution ◽  
Innate Immunity ◽  
Particulate Matter ◽  
Immune System ◽  
Sulfur Dioxide ◽  
Nitrogen Oxide ◽  
Immune Cells ◽  
Cytokine Secretion ◽  
Acquired Immunity

Air pollution has become a serious problem, the pollutant mainly came from industrial and vehicle exhaustion will harm people’s bodies to a different extent, cause lots of diseases like asthma, and cardiovascular disease. The system protects us are also be damaged by pollutant entering the tissue barrier, harm to immune cells and regulate cytokine secretion. This essay is mainly focused on the particulate matter, sulfur dioxide, and nitrogen oxide effect on the immune system from the innate immunity to the acquired immunity, and how the immune system defense.

scholarly journals Nutritional immunity: the impact of metals on lung immune cells and the airway microbiome during chronic respiratory disease

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Claire Healy ◽  
Natalia Munoz-Wolf ◽  
Janné Strydom ◽  
Lynne Faherty ◽  
Niamh C. Williams ◽  
...  
Keyword(s):  
Immune System ◽  
Trace Metals ◽  
Lung Disease ◽  
Chronic Lung Disease ◽  
Immune Cells ◽  
Immune Cell ◽  
Redox Activity ◽  
Nutritional Immunity ◽  
Airway Microbiome ◽  
The Impact

AbstractNutritional immunity is the sequestration of bioavailable trace metals such as iron, zinc and copper by the host to limit pathogenicity by invading microorganisms. As one of the most conserved activities of the innate immune system, limiting the availability of free trace metals by cells of the immune system serves not only to conceal these vital nutrients from invading bacteria but also operates to tightly regulate host immune cell responses and function. In the setting of chronic lung disease, the regulation of trace metals by the host is often disrupted, leading to the altered availability of these nutrients to commensal and invading opportunistic pathogenic microbes. Similarly, alterations in the uptake, secretion, turnover and redox activity of these vitally important metals has significant repercussions for immune cell function including the response to and resolution of infection. This review will discuss the intricate role of nutritional immunity in host immune cells of the lung and how changes in this fundamental process as a result of chronic lung disease may alter the airway microbiome, disease progression and the response to infection.

scholarly journals Low‐Density Lipoprotein Cholesterol Corrected for Lipoprotein(a) Cholesterol, Risk Thresholds, and Cardiovascular Events

2020 ◽  
Vol 9 (23) ◽  
Author(s):  
Peter Willeit ◽  
Calvin Yeang ◽  
Patrick M. Moriarty ◽  
Lena Tschiderer ◽  
Stephen A. Varvel ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Clinical Care ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Cholesterol Content ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Lipoprotein A ◽  
The Impact

Background Conventional "low‐density lipoprotein cholesterol (LDL‐C)" assays measure cholesterol content in both low‐density lipoprotein and lipoprotein(a) particles. To clarify the consequences of this methodological limitation for clinical care, our study aimed to compare associations of “LDL‐C” and corrected LDL‐C with risk of cardiovascular disease and to assess the impact of this correction on the classification of patients into guideline‐recommended LDL‐C categories. Methods and Results Lipoprotein(a) cholesterol content was estimated as 30% of lipoprotein(a) mass and subtracted from “LDL‐C” to obtain corrected LDL‐C values (LDL‐C corr30 ). Hazard ratios for cardiovascular disease (defined as coronary heart disease, stroke, or coronary revascularization) were quantified by individual‐patient‐data meta‐analysis of 5 statin landmark trials from the Lipoprotein(a) Studies Collaboration (18 043 patients; 5390 events; 4.7 years median follow‐up). When comparing top versus bottom quartiles, the multivariable‐adjusted hazard ratio for cardiovascular disease was significant for “LDL‐C” (1.17; 95% CI, 1.05–1.31; P =0.005) but not for LDL‐C corr30 (1.07; 95% CI, 0.93–1.22; P =0.362). In a routine laboratory database involving 531 144 patients, reclassification of patients across guideline‐recommended LDL‐C categories when using LDL‐C corr30 was assessed. In “LDL‐C” categories of 70 to <100, 100 to <130, 130 to <190, and ≥190 mg/dL, significant proportions (95% CI) of participants were reassigned to lower LDL‐C categories when LDL‐C corr30 was used: 30.2% (30.0%–30.4%), 35.1% (34.9%–35.4%), 32.9% (32.6%–33.1%), and 41.1% (40.0%–42.2%), respectively. Conclusions “ LDL‐C” was associated with incident cardiovascular disease only when lipoprotein(a) cholesterol content was included in its measurement. Refinement in techniques to accurately measure LDL‐C, particularly in patients with elevated lipoprotein(a) levels, is warranted to assign risk to the responsible lipoproteins.

scholarly journals Crosstalk between Red Blood Cells and the Immune System and Its Impact on Atherosclerosis

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Brigitta Buttari ◽  
Elisabetta Profumo ◽  
Rachele Riganò
Keyword(s):  
Oxidative Stress ◽  
Immune System ◽  
Red Blood Cells ◽  
Immune Cells ◽  
Blood Cells ◽  
Atherosclerotic Disease ◽  
Intraplaque Hemorrhage ◽  
Immune System Activation ◽  
Adaptive Immune Cells ◽  
The Impact

Atherosclerosis is a chronic multifactorial disease of the arterial wall characterized by inflammation, oxidative stress, and immune system activation. Evidence exists on a pathogenic role of oxidized red blood cells (RBCs) accumulated in the lesion after intraplaque hemorrhage. This review reports current knowledge on the impact of oxidative stress in RBC modifications with the surface appearance of senescent signals characterized by reduced expression of CD47 and glycophorin A and higher externalization of phosphatidylserine. The review summarizes findings indicating that oxidized, senescent, or stored RBCs, due to surface antigen modification and release of prooxidant and proinflammatory molecules, exert an impaired modulatory activity on innate and adaptive immune cells and how this activity contributes to atherosclerotic disease. In particular RBCs from patients with atherosclerosis, unlike those from healthy subjects, fail to control lipopolysaccharide-induced DC maturation and T lymphocyte apoptosis. Stored RBCs, accompanied by shedding of extracellular vesicles, stimulate peripheral blood mononuclear cells to release proinflammatory cytokines, augment mitogen-driven T cell proliferation, and polarize macrophages toward the proinflammatory M1 activation pathway. Collectively, literature data suggest that the crosstalk between RBCs with immune cells represents a novel mechanism by which oxidative stress can contribute to atherosclerotic disease progression and may be exploited for therapeutic interventions.

scholarly journals Real-world use of PCSK9 inhibitors: A single-center experience

2018 ◽  
Vol 47 (1) ◽  
pp. 265-270 ◽  
Author(s):  
Sinan Sarsam ◽  
Abeer Berry ◽  
George Degheim ◽  
Robby Singh ◽  
Marcel Zughaib
Keyword(s):  
Cardiovascular Disease ◽  
Lipid Profile ◽  
Real World ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Atherosclerotic Cardiovascular Disease ◽  
Pcsk9 Inhibitors ◽  
Pcsk9 Inhibitor ◽  
The Impact

Objective Hyperlipidemia is an important risk factor for atherosclerotic cardiovascular disease. Many patients are intolerant to or have limited benefit from statins. Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors have been approved for treating hyperlipidemia in these patients. We sought to investigate the impact of these medications in a real-world cardiology practice. Methods This was a retrospective study of 17 patients with either heterozygous familial hypercholesterolemia or established atherosclerotic cardiovascular disease with low-density lipoprotein cholesterol (LDL-C) levels above the treatment target despite maximally tolerated statins. Baseline lipid profile was compared with a repeat lipid profile obtained 4 to 6 weeks after initiating treatment with a PCSK9 inhibitor. Results The average duration of PCSK9 inhibitor treatment was 10.7 months. Lipid profile comparison showed that total cholesterol decreased from 243 ± 72 to 148 ± 39 (mg/dL) (39% reduction), triglycerides decreased from 185 ± 86 to 149 ± 62 (mg/dL) (19.5% reduction), high-density lipoprotein cholesterol increased from 56 ± 20 to 62 ± 26 (mg/dL) (10.7% increase), and LDL-C decreased from 154 ± 30 to 57 ± 32 (mg/dL) (63% reduction) from baseline. Conclusions PCSK9 inhibitors as add-on therapy to maximally tolerated statins resulted in an approximately 63% reduction in LDL-C.

scholarly journals The impact of host immune cells on the development of neurofibromatosis type 1: The abnormal immune system provides an immune microenvironment for tumorigenesis

2019 ◽  
Vol 2 (Supplement_1) ◽  
pp. i33-i39
Author(s):  
Cheng-Jiang Wei ◽  
Shu-Chen Gu ◽  
Jie-Yi Ren ◽  
Yi-Hui Gu ◽  
Xiang-Wen Xu ◽  
...  
Keyword(s):  
Immune System ◽  
Immune Cells ◽  
Neurofibromatosis Type 1 ◽  
Immune Escape ◽  
Genetic Disorder ◽  
Neurofibromatosis Type ◽  
Complex Interactions ◽  
Nf1 Gene ◽  
The Impact

Abstract AbstractThe immune system plays an essential role in the development of tumors, which has been demonstrated in multiple types of cancers. Consistent with this, immunotherapies with targets that disrupt these mechanisms and turn the immune system against developing cancers have been proven effective. In neurofibromatosis type 1 (NF1), an autosomal dominant genetic disorder, the understanding of the complex interactions of the immune system is incomplete despite the discovery of the pivotal role of immune cells in the tumor microenvironment. Individuals with NF1 show a loss of the NF1 gene in nonneoplastic cells, including immune cells, and the aberrant immune system exhibits intriguing interactions with NF1. This review aims to provide an update on recent studies showing the bilateral influences of NF1 mutations on immune cells and how the abnormal immune system promotes the development of NF1 and NF1-related tumors. We then discuss the immune receptors major histocompatibility complex class I and II and the PD-L1 mechanism that shield NF1 from immunosurveillance and enable the immune escape of tumor tissues. Clarification of the latest understanding of the mechanisms underlying the effects of the abnormal immune system on promoting the development of NF1 will indicate potential future directions for further studies and new immunotherapies.

scholarly journals Atherosclerotic Cardiovascular Disease Risk Profile of Tenofovir Alafenamide Versus Tenofovir Disoproxil Fumarate

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Gregory D Huhn ◽  
David J Shamblaw ◽  
Jean-Guy Baril ◽  
Priscilla Y Hsue ◽  
Brittany L Mills ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Total Cholesterol ◽  
Statin Therapy ◽  
Tenofovir Disoproxil Fumarate ◽  
Density Lipoprotein ◽  
Hiv Care ◽  
Atherosclerotic Cardiovascular Disease ◽  
Ascvd Risk ◽  
Tenofovir Alafenamide ◽  
The Impact

Abstract Background In human immunodeficiency virus (HIV) treatment, tenofovir alafenamide (TAF) is associated with greater increases in all fasting cholesterol subgroups compared with tenofovir disoproxil fumarate (TDF). Because lipid abnormalities may contribute to cardiovascular morbidity and mortality, cardiovascular risk assessment is integral to routine HIV care. This post hoc study evaluates the impact of lipid changes on predicted atherosclerotic cardiovascular disease (ASCVD) risk and statin eligibility in treatment-naive adults living with HIV treated with TAF or TDF. Methods Participants (N = 1744) were randomized (1:1) to initiate TAF or TDF, each coformulated with elvitegravir/cobicistat/emtricitabine (studies GS-US-292-0104 and GS-US-292-0111). Eligibility for statin therapy and estimated 10-year ASCVD risk among adults aged 40–79 years treated with TAF or TDF for 96 weeks (W96) were analyzed based on American College of Cardiology/American Heart Association Pooled Cohort Equations. Categorical shifts in 10-year ASCVD risk from &lt;7.5% to ≥7.5% by W96 on TAF versus TDF were calculated. Results Participants initiating TAF versus TDF in the overall study population showed small but significant increases in median fasting lipid parameters at W96, including total cholesterol (191 vs 177 mg/dL; P &lt; .001), low-density lipoprotein ([LDL] 119 vs 112 mg/dL; P &lt; .001), and high-density lipoprotein ([HDL] 51 vs 48 mg/dL; P &lt; .001), respectively. At baseline, 18% and 23% on TAF versus TDF had a 10-year ASCVD risk score ≥7.5%, with mean risk scores low overall for TAF versus TDF at baseline (4.9% vs 5.4%; P = .35) and W96 (6.1% vs 6.2%; P = .04). Increases in ASCVD risk from baseline to W96 were driven by both increasing age and changes in total cholesterol (TC) and HDL cholesterol. At W96, TC/HDL ratios (median) were 3.7 for both groups (P = .69). There was no difference between shifts in categorical risk for TAF versus TDF (9% vs 5%; P = .19). Eligibility for high-intensity statin therapy were similar for TAF versus TDF groups (19% vs 21%; P = .47). Conclusions Lipid changes with TAF as part of coformulated regimens do not substantively affect CVD risk profiles compared with TDF.

404Impact of cardiovascular risk factors for the development of cardiovascular disease: Results from MORGAM and BiomarCaRE consortia

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C Magnussen
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Cardiovascular Risk ◽  
Substantial Reduction ◽  
Density Lipoprotein ◽  
Daily Smoking ◽  
Cvd Risk ◽  
Coronary Death ◽  
Cardiac Revascularization ◽  
The Impact

Abstract Background Knowledge about the impact of modifiable risk factors for cardiovascular disease (CVD) onset is essential to improve CVD prevention. Purpose We estimated population-attributable fractions (PAFs) of body-mass-index (BMI), systolic blood pressure (SBP), diabetes, blood lipids (non-high-density lipoprotein cholesterol; non-HDL-C) and daily smoking for CVD. Methods Harmonized data from MOnica Risk, Genetics, Archiving and Monograph (MORGAM) and Biomarkers for Cardiovascular Risk Assessment in Europe (BiomaCaRE) consortia were used to calculate hazard ratios (HRs; 95% CI) and PAFs for incident CVD (myocardial infarction or coronary death, unstable angina, cardiac revascularization, ischemic stroke). PAFs for single risk factors or any combination of them were estimated using methods by Laaksonen 2011. Results We included 150,190 participants (77,801 men and 72,389 women) without CVD at baseline. Strongest associations were seen for SBP ≥160 mmHg (HR 1.79, 1.67–1.92 men; HR 1.93, 1.75–2.14 women), diabetes (HR 2.02, 1.86–2.20 men; HR 2.29, 2.06–2.55 women), non-HDL-C ≥220 mg/dL (HR 3.11, 2.49–3.88 men; HR 2.27, 1.68–3.05 women), daily smoking (HR 1.82, 1.73–1,90 men; HR 2.16, 2.0–2.33 women). Table 1 provides PAFs for incident CVD. Overall PAFs for men and women were 73.7% (67.7–79.1) and 73.3% (64.9–80.9). Table 1. PAFs (%) for 5-year incident CVD Risk factor/category PAFs (95% CI), men PAFs (95% CI), women Underweight 0.1 (−0.1, 0.3) 0.2 (−0.1, 0.6) Pre-obesity 6.6 (4.3, 8.9) 4.3 (1.5, 6.9) Obesity 3.9 (2.7, 5.3) 8.0 (5.3, 10.5) SBP 130 to <140 mmHg 2.8 (1.7, 4.0) 2.7 (1.3, 4.0) SBP 140 to <160 mmHg 9.7 (8.1, 11.3) 9.3 (6.7, 11.6) SBP ≥160 mmHg 11.3 (9.7, 12.8) 18.9 (16.2, 21.8) Diabetes 5.2 (4.5, 6.2) 7.8 (6.5, 9.4) non-HDL-C 100 to <145 mg/dL 4.3 (1.8, 6.4) 3.3 (0.5, 6.5) non-HDL-C 145 to <185 mg/dL 13.9 (9.8, 17.5) 11.3 (6.0, 16.2) non-HDL-C 185 to <220 mg/dL 15.8 (12.8, 18.4) 12.8 (8.8, 17.0) non-HDL-C ≥220 mg/dL 16.7 (14.6, 18.5) 17.0 (12.5, 21.1) Daily smoking 16.5 (15.0, 18.3) 12.3 (10.7, 13.7) The N CVD events/N used was 8,302/77,801 for men and 4,071/72,389 for women. Conclusion Uncontrolled risk factors, especially non-HDL-C and SBP in the highest category, daily smoking and diabetes had the highest impact for incident CVD. All risk factors combined accounted for a PAF of 73%. Targeting risk factors would lead to a substantial reduction of CVD onset. Acknowledgement/Funding BiomarCaRE: EU Seventh Framework Programme (FP7/2007-2013), No. HEALTH-F2-2011-278913. MORGAM: EU FP 7 CHANCES (HEALTH-F3-2010-242244).

Sign in / Sign up

Export Citation Format

Share Document