Inflammatory Cytokines, Immune Cells, and Organ Interactions in Heart Failure.
Ontology highlight
ABSTRACT:
SUBMITTER: Li H
PROVIDER: S-EPMC8281681 | biostudies-literature | 2021
REPOSITORIES: biostudies-literature
Publications
Inflammatory Cytokines, Immune Cells, and Organ Interactions in Heart Failure.
Li Huihui H Chen Chen C Wang Dao Wen DW
Frontiers in physiology 20210701
Despite mounting evidence demonstrating the significance of inflammation in the pathophysiological mechanisms of heart failure (HF), most large clinical trials that target the inflammatory responses in HF yielded neutral or even worsening outcomes. Further in-depth understanding about the roles of inflammation in the pathogenesis of HF is eagerly needed. This review summarizes cytokines, cardiac infiltrating immune cells, and extracardiac organs that orchestrate the complex inflammatory response ...[more]
Similar Datasets
Project description:BackgroundDistinct monocyte subsets predict cardiovascular risk and contribute to heart failure progression in murine models, but they have not been examined in clinical acute decompensated heart failure (ADHF).Methods and resultsBlood samples were obtained from 11 healthy control subjects (HCs) and at admission and discharge from 19 ADHF patients. Serologic markers of inflammation were assessed at admission and discharge. Monocyte populations were defined with the use of flow cytometry for cell-surface expression of CD14 and CD16: CD14++CD16- (classic), CD14++CD16+ (intermediate), and CD14+CD16++ (nonclassic). In ADHF patients, C-reactive protein (CRP) and interleukin-6 (IL-6) were higher compared with HCs (both P < .001) and decreased from admission to discharge (CRP: 12.1 ± 10.1 to 8.6 ± 8.4 mg/L [P = .005]; IL-6: 19.8 ± 34.5 to 7.1 ± 4.7 pg/mL [P = .08]). In ADHF patients, the admission proportion of CD14++CD16- monocytes was lower (68% vs 85%; P < .001) and that of CD14++CD16+ (15% vs 8%; P = .002) and CD14+CD16++ (17% vs 7%, P = .07) monocytes higher compared with HCs. Additionally, the proportion of CD14++CD16- monocytes increased (68% to 79%, P = .04) and the CD14+CD16++ monocytes decreased (17% to 7%, P = .049) between admission and discharge.ConclusionsFollowing standard treatment of ADHF, the monocyte profile and circulating inflammatory markers shifts to more closely resemble those of HC, suggesting a resolution of the acute inflammatory state. Functional studies are warranted to understand how specific monocyte subsets and systemic inflammation may contribute to ADHF pathophysiology.
| S-EPMC4861694 | biostudies-literature
Project description:Patients with chronic inflammatory diseases are at increased risk for heart failure due to ischemic heart disease and other causes including heart failure with preserved ejection fraction. Using rheumatoid arthritis and treated HIV infection as two prototypical examples, we review the epidemiology and potential therapies to prevent heart failure in these populations. Particular focus is given to anti-inflammatory therapies including statins and biologic disease modifying drugs. There is also limited evidence for lifestyle changes and blockade of the renin-angiotensin-aldosterone system. We conclude by proposing how a strategy for heart failure prevention, such as the model tested in the Screening To Prevent Heart Failure (STOP-HF) trial, may be adapted to chronic inflammatory disease.
| S-EPMC4548924 | biostudies-literature
Project description:Heart failure-either with reduced or preserved ejection fraction (HFrEF/HFpEF)-is a clinical syndrome of multifactorial and gender-dependent aetiology, indicating the insufficiency of the heart to pump blood adequately to maintain blood flow to meet the body's needs. Typical symptoms commonly include shortness of breath, excessive fatigue with impaired exercise capacity, and peripheral oedema, thereby alluding to the fact that heart failure is a syndrome that affects multiple organ systems. Patients suffering from progressed heart failure have a very limited life expectancy, lower than that of numerous cancer types. In this position paper, we provide an overview regarding interactions between the heart and other organ systems, the clinical evidence, underlying mechanisms, potential available or yet-to-establish animal models to study such interactions and finally discuss potential new drug interventions to be developed in the future. Our working group suggests that more experimental research is required to understand the individual molecular mechanisms underlying heart failure and reinforces the urgency for tailored therapeutic interventions that target not only the heart but also other related affected organ systems to effectively treat heart failure as a clinical syndrome that affects and involves multiple organs.
| S-EPMC8562335 | biostudies-literature
Project description:Heart failure is the end stage of cardiovascular disease, with high morbidity and mortality rates worldwide. Heart failure is associated with long-term and insufficient inhibition of inflammatory response. miRNA is a class of endogenous, non-coding, single-stranded small RNA molecules, that can regulate gene expression through translational inhibition or degradation of targeted mRNA, widely regulate myocardial remodeling, inflammatory response, and other pathological processes, and play an important regulatory role in the occurrence and development of cardiovascular diseases. This article reviews the role of miRNA in the inflammatory response in heart failure.
| S-EPMC11646975 | biostudies-literature
Project description:ObjectivesPrevious studies have reported that immunoinflammatory responses have associations with mastitis. Here, we aimed to further figure out whether circulating inflammatory cytokines and immune cells causally impact mastitis liability.MethodsThe two-sample Mendelian randomization made use of genetic variances of 91 inflammatory cytokines from a large publicly available genome-wide association study (GWAS) containing 14,824 participants, 731 immunophenotypes data from 3,757 individuals as exposures separately, and mastitis from a GWAS summary (1880 cases and 211699 controls of European ancestry) as outcome. The primary analysis applied the inverse-variance weighted (IVW) method to estimate causal influences, with MR-Egger, weighted median, weighted mode and simple mode as supplementary approaches. Heterogeneity and pleiotropy were evaluated by the Cochrane Q test, MR-Egger intercept test, and MR-PRESSO global test.ResultsThe results indicated that CX3CL1 may be suggestively relevant to the risk of mastitis (odds ratio, OR = 1.434, 95% CI = 1.142~1.800, p = 0.002). Moreover, three immunophenotypes were identified as having a potential causal link to mastitis (p < 0.05). Significantly, CD28- CD8dim %CD8dim (OR = 1.058, 95% CI = 1.024 ~ 1.093, p = 0.0006) and CD45 on CD33br HLA DR+ (OR = 1.097, 95% CI = 1.039 ~ 1.157, p = 0.0008) were found to induce mastitis possibly. Conversely, CD39+ secreting Treg AC (OR = 0.929, 95% CI = 0.884~ 0.978, p = 0.005) pertained to protective factors of mastitis. Cochran's Q test and MR-Egger intercept test indicated no significant heterogeneity (p > 0.05) or pleiotropy (p > 0.05), supporting the robustness and reliability of our findings.ConclusionOur study adds to current knowledge on the causal roles of inflammatory cytokines and immune cells on mastitis by genetic means, thus guiding future clinical research.
| S-EPMC11466835 | biostudies-literature
Project description:Betel nut consumption has significant implications for the public health globally, as the wide-spread habit of Areca chewing throughout Asia and the Pacific is associated with a high prevalence of oral carcinoma and other diseases. Despite a clear causal association of betel nut chewing and oral mucosal diseases, the biological mechanisms that link Areca nut-contained molecules, inflammation and cancer remain underexplored. In this study we show that the whole Areca nut extract (ANE) is capable of mobilizing Ca2+ in various immune cell lines. Interestingly, none of the four major alkaloids or a range of other known constituents of Areca nut were able to induce such Ca2+ signals, suggesting that the active components might represent novel or so far unappreciated chemical structures. The separation of ANE into aqueous and organic fractions has further revealed that the calcium-mobilizing molecules are exclusively present in the aqueous extract. In addition, we found that these calcium signals are associated with the activation of several immune cell lines as shown by the release of pro-inflammatory cytokines and increased cell proliferation. These results indicate that calcium-mobilizing molecules present in the aqueous fraction of the Areca nut may critically contribute to the inflammatory disorders affecting betel nut chewers.
| S-EPMC5773534 | biostudies-literature
Project description:BackgroundHeart failure (HF)-related skeletal muscle wasting inversely affects the prognosis of HF, in which systemic inflammation may be involved. The relationships among skeletal muscle mass (SMM), systemic inflammation, and cardiovascular outcomes have not been clarified.ObjectivesThis study evaluated the associations of SMM with cardiovascular outcomes, systemic immune-inflammatory index (SII) with cardiovascular outcomes, and the mediation role of SII in the relationship between SMM and outcomes.MethodsWe included inpatients from the RED-CARPET trial (Real-world Data of Cardiometabolic ProtEcTion trial) with a definitive diagnosis of HF. We explored the associations of SMM with prognosis and SII with prognosis stratified by sex. Mediation analysis was applied for the role of SII in the association of SMM and the prognosis.ResultsWith a median follow-up of 4.9 years, 1402 patients with HF had 208 all-cause deaths and 106 cardiovascular deaths. Each 1-SD decrement in SMM was significantly associated with an increased risk of all-cause death (HR: 2.17; 95% CI: 1.20-3.91; P = 0.01 in males and HR: 2.90; 95% CI: 1.27-6.67; P = 0.012 in females). For cardiovascular death, the HR was 3.61 (95% CI: 1.56-8.40; P = 0.003) in males and 6.67 (95% CI: [2.33, 18.9]; P < 0.001) in females. Higher SII was associated with adverse outcomes. In the mediation analyses, SII was partially mediated in the relationship between SMM and cardiovascular death (7.1% [proportion-mediated 95% CI: 0.5%-26%]; P = 0.036 for males, and 5.4% [proportion mediated 95% CI: 0%-18.8%]; P = 0.064 for females).ConclusionsBoth low SMM and increased SII were significantly associated with unfavorable outcomes in HF. SII was partially mediated in the relationship between low SMM and cardiovascular death in HF.
| S-EPMC11877227 | biostudies-literature
Project description:Heart failure (HF) is accompanied by the upregulation of bioactive signaling molecules, known as cytokines, and a family of downstream proteases, matrix metalloproteinases (MMPs). It is now apparent that these molecules contribute to adverse myocardial remodeling during HF. Elevated levels of cytokines and MMPs exist in the myocardium and can subsequently spill over into the systemic circulation. The purpose of this article is to examine clinical studies of HF that have quantified levels of different types of cytokines, MMPs and endogenous tissue inhibitors of MMPs in relation to this disease process. HF is a complex syndrome that can develop from various etiologies and can be characterized into two distinct phenotypes: systolic and diastolic. This article will present recent clinical studies that have identified significant differences between the cytokine and MMP circulating profile of systolic and diastolic HF patients. In general, elevated levels of cytokines and MMPs exist in systolic HF patients when compared with diastolic HF patients, whereas diastolic HF patients have elevated levels of cytokines and MMPs when compared with controls. Therefore, future studies distinguishing between HF phenotypes may provide more consistent results in determining possible analytes to be used as biomarkers. Furthermore, this article will emphasize why standardization of analytical techniques and establishment of referent cytokine and MMP levels are necessary if these analytes are to be used as biomarkers for the diagnosis, prognosis and evaluation of treatment in the context of HF.
| S-EPMC2794436 | biostudies-literature
Project description:Recurrent implantation failure (RIF) is a leading impediment to assisted reproductive technology, yet the underlying pathogenesis of RIF remains elusive. Recent studies have sought to uncover novel biomarkers and etiological factors of RIF by profiling transcriptomes of endometrial samples. Nonetheless, the inherent heterogeneity among published studies and a scarcity of experimental validations hinder the identification of robust markers of RIF. Hence, we integrated six publicly accessible datasets with 209 samples, including microarray profiles of endometrial samples in the secretory phase. After removing batch effects, we identified 175 differentially expressed genes. Gene set enrichment analysis identified dysregulation of immunological pathways in RIF. We also observed altered immune infiltration and pro-inflammatory cytokines in RIF. Protein-protein interaction network analysis identified ten hub genes, representing two co-expression modules significantly related to RIF. Knockdown of ENTPD3, one of the hub genes, promoted the epithelial-mesenchymal transition process and resulted in elevated levels of pro-inflammatory cytokines. Collectively, our study reveals abnormal gene expressions involving the regulation of epithelial-mesenchymal transition and immune status in RIF, providing valuable insights into its pathogenesis.
| S-EPMC11749484 | biostudies-literature
Project description:AimsThe value of the systemic immune-inflammatory index (SII) in assessing adverse outcomes in various cardiovascular diseases has been extensively discussed. This study aims to evaluate the predictive value and risk stratification ability of SII for 30 day mortality in patients with acute decompensated heart failure (ADHF).MethodsThis analysis included 1452 patients hospitalized for ADHF, all the participants being part of the China Jiangxi-acute decompensated heart failure1 project. The risk stratification capability of the SII in patients with ADHF, as well as its correlation with the 30 day mortality risk among ADHF patients, was evaluated utilizing Kaplan-Meier survival analysis and multivariable Cox regression models. A restricted cubic spline was employed to model the dose-response relationship between the two, and the receiver operating characteristic curve was utilized to assess the predictive ability of SII for 30 day mortality.ResultsThe Kaplan-Meier analysis revealed that the risk of mortality in the high SII group (SII ≥ 980 × 109/L) was significantly greater than that in the low SII group (SII < 980 × 109/L, log-rank P < 0.001). After adjusting for various confounding factors, a higher SII was associated with an increased risk of 30 day mortality in ADHF patients [hazard ratio (HR) = 2.03, 95% confidence interval (CI): 1.34-3.08]. Further restricted cubic spline analysis revealed a non-linear dose-response relationship between the two (P for non-linear = 0.006). Receiver operating characteristic analysis demonstrated that SII had a high accuracy in predicting 30 day mortality events in ADHF patients (AUC = 0.7479), and the optimal predictive threshold was calculated to be 980 × 109/L, a sensitivity of 0.7547 and a specificity of 0.7234.ConclusionsThis study found a significant positive association between SII and 30 day all-cause mortality in ADHF patients. We determined the SII cut-off point for predicting 30 day all-cause mortality in patients with ADHF to be 980 × 109/L.
| S-EPMC11424332 | biostudies-literature