scholarly journals Long noncoding RNA NEAT 1 and its target microRNA‐125a in sepsis: Correlation with acute respiratory distress syndrome risk, biochemical indexes, disease severity, and 28‐day mortality

2020 ◽  
Vol 34 (12) ◽  
Author(s):  
Yongkai Yang ◽  
Liu Yang ◽  
Zhenqing Liu ◽  
Yujun Wang ◽  
Junhui Yang
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Disease Severity ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Distress Syndrome

Long noncoding plasmacytoma variant translocation 1 facilitates the surveillance of acute respiratory distress syndrome and mortality prediction in sepsis

2021 ◽  
Vol 15 (6) ◽  
pp. 401-412
Author(s):  
Yijue Liu ◽  
Huan Peng ◽  
Feng Gui
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Disease Severity ◽  
Noncoding Rna ◽  
Distress Syndrome ◽  
Mortality Prediction ◽  
Prediction Of Mortality ◽  
Failure Assessment ◽  
Variant Translocation

Aim: We aimed to investigate the association of long noncoding RNA plasmacytoma variant translocation 1 (lncRNA PVT1) expression with acute respiratory distress syndrome (ARDS) risk and its prognostic value for 28-day mortality in sepsis patients. Materials & methods: LncRNA PVT1 expression from 109 sepsis patients and 100 health controls was detected. General sepsis severity was assessed using acute physiology and chronic health evaluation II score and sequential organ failure assessment score. Results: LncRNA PVT1 had an acceptable predictive value for higher ARDS risk, then was identified as an independent risk factor for sepsis ARDS; LncRNA PVT1 expression positively correlated with general disease severity in sepsis patients; LncRNA PVT1 was overexpressed in 28-day deaths compared with 28-day survivors in sepsis patients. Conclusion: LncRNA PVT1 may facilitate the surveillance of ARDS, general disease severity and the prediction of mortality in sepsis patients.

scholarly journals Silencing of long noncoding RNA H19 alleviates pulmonary injury, inflammation and fibrosis in acute respiratory distress syndrome rats through regulating MicroRNA-423-5p

2020 ◽  
Author(s):  
Xianyu Mu ◽  
Hongrong Wang ◽  
Haiyong Li
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Distress Syndrome ◽  
Luciferase Reporter ◽  
Pulmonary Injury ◽  
Tnf Α ◽  
Histology Score

Abstract Background: This study aimed to explore the function of long noncoding RNA H19 (H19) on pulmonary injury, inflammation and fibrosis in lipoproteins (LPS)-induced acute respiratory distress syndrome (ARDS) rats. Methods: The LPS-induced ARDS rat model was established by intratracheal instillation with 2 mg/kg LPS. QRT-PCR was performed to detect the expression of H19, miR-423-5p, tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6,, monocyte chemoattractant protein (MCP)-1 and vascular endothelial growth factor (VEGF). Histology score was detected by hematoxylin-eosin (HE) staining. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of proinflammatory cytokines and the concentration of VEGF in bronchoalveolar lavage fluid (BALF). The protein expression of fiber factors was measured by western blot. The degree of fibrosis was observed by masson-trichrome staining. Dual-luciferase reporter assay was used to determine the binding site between miR-423-5p and H19.Results: The expression of H19 was significantly increased, while miR-423-5p was decreased in LPS-induced ARDS rats. Silencing of H19 decreased the mRNA expression of TNF-α, IL-1β, IL-6, MCP-1 and VEGF in LPS-induced ARDS rats, and decreased the levels of TNF-α, IL-1β, IL-6and the concentration of VEGF in BALF, histology score of LPS-induced ARDS rats. H19 inhibition also decreased the fibrosis score and the proteins expression of fiber factors of LPS-induced ARDS rats. Furthermore, miR-423-5p eliminated the effect of H19 on LPS-induced MH-S cells.Conclusions: Silencing of H19 ameliorated the pulmonary injury, inflammation and fibrosis of LPS-induced ARDS through regulating miR-423-5p, which may be a promising therapeutic strategy to treat ARDS.

scholarly journals Cardiovascular biomarkers in patients with COVID-19

2021 ◽  
Author(s):  
Christian Mueller ◽  
Evangelos Giannitsis ◽  
Allan S Jaffe ◽  
Kurt Huber ◽  
Johannes Mair ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Disease Severity ◽  
Natriuretic Peptide ◽  
Cardiac Troponin ◽  
Distress Syndrome ◽  
Risk Of Death ◽  
Cardiovascular Biomarkers

Abstract The coronavirus disease 2019 (COVID-19) pandemic has increased awareness that severe acute respiratory distress syndrome coronavirus-2 (SARS-CoV-2) may have profound effects on the cardiovascular system. COVID-19 often affects patients with pre-existing cardiac disease, and may trigger acute respiratory distress syndrome (ARDS), venous thromboembolism (VTE), acute myocardial infarction (AMI), and acute heart failure (AHF). However, as COVID-19 is primarily a respiratory infectious disease, there remain substantial uncertainty and controversy whether and how cardiovascular biomarkers should be used in patients with suspected COVID-19. To help clinicians understand the possible value as well as the most appropriate interpretation of cardiovascular biomarkers in COVID-19, it is important to highlight that recent findings regarding the prognostic role of cardiovascular biomarkers in patients hospitalized with COVID-19 are similar to those obtained in studies for pneumonia and ARDS in general. Cardiovascular biomarkers reflecting pathophysiological processes involved in COVID-19/pneumonia and its complications have a role evaluating disease severity, cardiac involvement, and risk of death in COVID-19 as well as in pneumonias caused by other pathogens. First, cardiomyocyte injury, as quantified by cardiac troponin concentrations, and haemodynamic cardiac stress, as quantified by natriuretic peptide concentrations, may occur in COVID-19 as in other pneumonias. The level of those biomarkers correlates with disease severity and mortality. Interpretation of cardiac troponin and natriuretic peptide concentrations as quantitative variables may aid in risk stratification in COVID-19/pneumonia and also will ensure that these biomarkers maintain high diagnostic accuracy for AMI and AHF. Second, activated coagulation as quantified by D-dimers seems more prominent in COVID-19 as in other pneumonias. Due to the central role of endothelitis and VTE in COVID-19, serial measurements of D-dimers may help physicians in the selection of patients for VTE imaging and the intensification of the level of anticoagulation from prophylactic to slightly higher or even therapeutic doses.

scholarly journals CD14 Positive Extracellular Vesicles in Broncho-Alveolar Lavage Fluid as a New Biomarker of Acute Respiratory Distress Syndrome

2021 ◽  
Author(s):  
Rahul Y Mahida ◽  
Joshua Price ◽  
Sebastian T. Lugg ◽  
Hui Li ◽  
Dhruv Parekh ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Disease Severity ◽  
Extracellular Vesicles ◽  
Distress Syndrome ◽  
Lavage Fluid ◽  
Cell Of Origin ◽  
Potential Biomarker ◽  
Operative Control

Recent studies have indicated that extracellular vesicles (EV) may play a role in the pathogenesis of Acute Respiratory Distress Syndrome (ARDS). EV have been identified as potential biomarkers of disease severity and prognosis in other pulmonary diseases. We sought to characterize the EV phenotype within ARDS patient broncho-alveolar lavage fluid (BAL), and to determine whether BAL EV could be utilized as a potential biomarker in ARDS. EV from the BAL of sepsis patients with ARDS, sepsis patients without ARDS, and post-operative control patients were characterized with regards to size, number and cell of origin. ARDS patients had significantly higher numbers of CD14+/CD81+ monocyte-derived BAL EV than sepsis patients without ARDS (p=0.022). CD14+/CD81+ BAL EV numbers were significantly higher in those ARDS patients who died during the 30 days following ICU admission (p=0.027). Also, across all sepsis patients there was an association between CD66b+/CD63+ neutrophil-derived BAL EV and increased BAL IL-8 concentration, increased alveolar neutrophil apoptosis and decreased alveolar macrophage efferocytosis. Thus, CD14+/CD81+ BAL EV are a potential biomarker for disease severity and mortality in ARDS. These findings provide the impetus to further elucidate the contribution of these EV to ARDS pathogenesis.

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