Plasma long noncoding RNA IL‐7R as a prognostic biomarker for clinical outcomes in patients with acute respiratory distress syndrome

2017 ◽  
Vol 12 (4) ◽  
pp. 1607-1614 ◽  
Author(s):  
Bing Wan ◽  
Wu‐Jian Xu ◽  
Wei‐Nan Xu ◽  
Ping Zhan ◽  
Guan‐Nan Wu ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Clinical Outcomes ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Distress Syndrome ◽  
Prognostic Biomarker

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.

Acute respiratory distress syndrome phenotypes with distinct clinical outcomes in PHARLA trial cohort

2021 ◽  
Vol 23 (2) ◽  
pp. 163-170
Author(s):  
Shailesh Bihari ◽  
◽  
Andrew Bersten ◽  
Eldho Paul ◽  
Shay McGuinness ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Clinical Outcomes ◽  
Distress Syndrome ◽  
Lung Ventilation ◽  
Tumour Necrosis Factor Receptor ◽  
Open Lung ◽  
Inflammatory Phenotype ◽  
Parsimonious Model

Background: The Permissive Hypercapnia, Alveolar Recruitment and Low Airway Pressure (PHARLAP) randomised controlled trial compared an open lung ventilation strategy with control ventilation, and found that open lung ventilation did not reduce the number of ventilator-free days (VFDs) or mortality in patients with moderate-to-severe acute respiratory distress syndrome (ARDS). Parsimonious models can identify distinct phenotypes of ARDS (hypo-inflammatory and hyperinflammatory) which are associated with different outcomes and treatment responses. Objective: To test the hypothesis that a parsimonious model would identify patients with distinctly different clinical outcomes in the PHARLAP study. Design, setting and participants: Blood and lung lavage samples were collected in a subset of PHARLAP patients who were recruited in Australian and New Zealand centres. A previously validated parsimonious model (interleukin-8, soluble tumour necrosis factor receptor-1 and bicarbonate) was used to classify patients with blood samples into hypo-inflammatory and hyperinflammatory groups. Generalised linear modelling was used to examine the interaction between inflammatory phenotype and treatment group (intervention or control). Main outcome measure: The primary outcome was number of VFDs at Day 28. Results: Data for the parsimonious model were available for 56 of 115 patients (49%). Within this subset, 38 patients (68%) and 18 patients (32%) were classified as having hypo-inflammatory and hyperinflammatory phenotypes, respectively. Patients with the hypo-inflammatory phenotype had more VFDs at Day 28 when compared with those with the hyperinflammatory phenotype (median [IQR], 19.5 [11–24] versus 8 [0–21]; P = 0.03). Patients with the hyperinflammatory phenotype had numerically fewer VFDs when managed with an open lung strategy than when managed with control “protective” ventilation (median [IQR], 0 [0–19] versus 16 [8–22]). Conclusion: In the PHARLAP trial, ARDS patients classified as having a hyperinflammatory phenotype, with a parsimonious three-variable model, had fewer VFDs at Day 28 compared with patients classified as having a hypo-inflammatory phenotype. Future clinical studies of ventilatory strategies should consider incorporating distinct ARDS phenotypes into their trial design.

scholarly journals Cholestenoic acid is a prognostic biomarker in acute respiratory distress syndrome

2019 ◽  
Vol 143 (1) ◽  
pp. 440-442.e8
Author(s):  
Jennifer H. Madenspacher ◽  
Renee D. Stapleton ◽  
Benjamin T. Suratt ◽  
Anne E. Dixon ◽  
Fred B. Lih ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Prognostic Biomarker ◽  
Cholestenoic Acid

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.

Alveolar MMP28 is Associated With Clinical Outcomes and Measures of Lung Injury in Acute Respiratory Distress Syndrome

2020 ◽  
Author(s):  
Eric Morrell ◽  
Carmen Mikacenic ◽  
Ke-Qin Gong ◽  
Susanna Kosamo ◽  
Renee D. Stapleton ◽  
...  
Keyword(s):  
Gene Expression ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Clinical Outcomes ◽  
Peripheral Blood ◽  
Distress Syndrome ◽  
Lavage Fluid ◽  
Peripheral Blood Monocyte ◽  
Omega 3

Abstract Background Excessive inflammation leading to increased alveolar-capillary barrier permeability remains the pathogenic model for acute respiratory distress syndrome (ARDS). Alveolar macrophage (AM) polarization has been shown to modify the activity of various matrix metalloproteinases (MMPs) that have downstream effects on key ARDS cytokines/chemokines, however the relationship between AMs, MMP28 (the newest member of the MMP family), and ARDS clinical outcomes is unknown.Methods We analyzed bronchoalveolar lavage fluid (BALF) and peripheral blood from subjects previously enrolled in a phase-II trial of omega-3 fatty acids for the treatment of ARDS ( n = 76). In a subset of these patients ( n = 25), we tested for assocations between AM- and peripheral blood monocyte (PBM)-specific MMP28 gene expression and clincal outcomes [ventilator-free days (VFDs), P a O 2 /F i O 2 ratio (P/F ratio), and sequential organ failure assessment score (SOFA)]. We tested for assocations between soluble BALF or plasma MMP28 concentrations and ARDS clinical outcomes and inflammatory mediator concentrations in the entire cohort.Results Increased AM MMP28 gene expression was significantly associated with worse VFDs and P/F ratio ( p < 0.05). Higher BALF MMP28 concentrations were associated with worse P/F, but not VFDs. Increased BALF MMP28 concentrations were associated with increased % neutrophils as well as BALF total protein, IL-6, IL-17A, and MCP-1 concentrations (all p < 0.05). Plasma MMP28 concentrations were not associated with any clinical outcome. Increased PBM MMP28 gene expression was associated with worse P/F ratio but not VFDs.Conclusions Higher AM MMP28 gene expression and BALF MMP28 concentrations are associated with poor clinical outcomes and with increased alveolar inflammatory mediators in patients with ARDS.

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