Acute respiratory distress syndrome

Dostalova, Vlasta; Dostál, Pavel

doi:10.36290/vnl.2019.036

Cited by 12 publications

(11 citation statements)

References 106 publications

(95 reference statements)

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“…The main pathology is that in sepsis, a large number of inflammatory mediators and lipid metabolites enter the blood circulation, which stimulates the accumulation and activation of inflammatory cells in the lung tissue of patients, thus producing more chemokines and oxygen free radical cytokines, which aggravate the inflammatory response and form a chain reaction (5,6). At this point, the balance between anti-inflammatory and pro-inflammatory mediators cannot be reached, resulting in anti-inflammatory response syndrome, thus resulting in damage to capillary endothelial cells and alveolar epithelial cells in lung tissue, increased permeability of pulmonary capillaries to protein, obstruction of fluid exchange between blood vessels and vascular interstitium in lung tissue, and ultimately leading to the occurrence of permeable pulmonary edema (7)(8)(9). If not treated promptly and effectively, acute lung injury often develops into acute respiratory distress syndrome.…”

Section: Introductionmentioning

confidence: 99%

Puerarin Inhibits Ferroptosis and Inflammation of Lung Injury Caused by Sepsis in LPS Induced Lung Epithelial Cells

Wang

Chen

2021

Front. Pediatr.

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Background: Ferroptosis is a new type of programmed cell death, which plays an important role in lung injury caused by sepsis. Studies have reported that Puerarin (Pue) can treat lung injury caused by sepsis in children, but whether it plays a role by regulating iron death has not been reported.Methods: LPS induced human alveolar epithelial cell A549 to form a model of lung injury caused by sepsis. MTT detected the effect of Pue on A549 cell viability and the effect of Pue on LPS-induced A549 cell viability. The effects of Pue on LPS-induced inflammatory cytokines TNF-α, IL-8, IL-1β in A549 cells were determined by ELISA assay. The expression level of MDA was detected by TBARS colorimetric quantitative detection kit. GSH kit was used to detect the expression of GSH in cells. The iron kit detected the total iron level and the expression level of ferric divalent ions in the cells. DCFH-DA fluorescent probe was used to detect ROS levels. Western blot was used to detect the expression of ferroptosis-related proteins in cells.Results: Pue alleviated LPS-induced injury and inflammatory response in A549 cells, and Pue reduced the expression of ROS, MDA and GSH in LPS-induced A549 cells. In addition, Pue reduced total iron levels and ferrous ion levels in LPS-induced A549 cells, and decreased the expression of iron ferroptosis-related proteins.Conclusion: Puerarin inhibited ferroptosis and inflammation of lung injury caused by sepsis in children in LPS induced lung epithelial cells.

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Section: Introductionmentioning

confidence: 99%

Puerarin Inhibits Ferroptosis and Inflammation of Lung Injury Caused by Sepsis in LPS Induced Lung Epithelial Cells

Wang

Chen

2021

Front. Pediatr.

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“…ARDS may be induced by other infections (sepsis, influenza), major traumatic injury, or inhalation of toxic chemicals [2]. Clinical presentations and pathological manifestations of COVID-19 ARDS overlap with non-COVID-19 ARDS, including decreased static lung compliance, hypoxemia, hypercarbia, inflammation, thrombosis, and endothelial injury [3][4][5][6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

“…Previously, ARDS groups have been studied in comparison to non-ARDS reference groups, such as healthy controls or hospitalized patients without ARDS [5][6][7][8][9][14][15][16]. Here, we present the first detailed comparative multi-omic analysis between COVID-19 ARDS (n=43) and bacterial sepsisinduced (non-COVID-19) ARDS (n=24).…”

Section: Introductionmentioning

confidence: 99%

Multi-omic comparative analysis of COVID-19 and bacterial sepsis-induced ARDS

Batra

Whalen

Alvarez-Mulett

et al. 2022

Preprint

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BackgroundAcute respiratory distress syndrome (ARDS), a life-threatening condition characterized by hypoxemia and poor lung compliance, is associated with high mortality. ARDS induced by COVID-19 has similar clinical presentations and pathological manifestations as non-COVID-19 ARDS. However, COVID-19 ARDS is associated with a more protracted inflammatory respiratory failure compared to traditional ARDS. Therefore, a comprehensive molecular comparison of ARDS of different etiologies groups may pave the way for more specific clinical interventions.Methods and FindingsIn this study, we compared COVID-19 ARDS (n=43) and bacterial sepsis-induced (non-COVID-19) ARDS (n=24) using multi-omic plasma profiles covering 663 metabolites, 1,051 lipids, and 266 proteins. To address both between- and within-ARDS group variabilities we followed two approaches. First, we identified 706 molecules differently abundant between the two ARDS etiologies, revealing more than 40 biological processes differently regulated between the two groups. From these processes, we assembled a cascade of therapeutically relevant pathways downstream of sphingosine metabolism. The analysis suggests a possible overactivation of arginine metabolism involved in long-term sequelae of ARDS and highlights the potential of JAK inhibitors to improve outcomes in bacterial sepsis-induced ARDS. The second part of our study involved the comparison of the two ARDS groups with respect to clinical manifestations. Using a data-driven multi-omic network, we identified signatures of acute kidney injury (AKI) and thrombocytosis within each ARDS group. The AKI-associated network implicated mitochondrial dysregulation which might lead to post-ARDS renal-sequalae. The thrombocytosis-associated network hinted at a synergy between prothrombotic processes, namely IL-17, MAPK, TNF signaling pathways, and cell adhesion molecules. Thus, we speculate that combination therapy targeting two or more of these processes may ameliorate thrombocytosis-mediated hypercoagulation.ConclusionWe present a first comprehensive molecular characterization of differences between two ARDS etiologies – COVID-19 and bacterial sepsis. Further investigation into the identified pathways will lead to a better understanding of the pathophysiological processes, potentially enabling novel therapeutic interventions.

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“…ARDS is a common presentation of critical illnesses, including severe infections, major injury, or inhalation of irritants 3 . While COVID-19-related ARDS and ARDS originating from other pathologies (hereby referred to as non-COVID-19 ARDS) have overlapping clinical features, COVID-19 ARDS is characterized by a protracted hyperinflammatory state and higher rates of thrombosis [4][5][6][7][8][9][10][11][12][13] . The field currently lacks etiologyspecific therapies and reliable predictors of heterogeneous patient outcomes 14 .…”

Section: Introductionmentioning

confidence: 99%

Urine-based multi-omic comparative analysis of COVID-19 and bacterial sepsis-induced ARDS

Batra

Uni²,

Akchurin

et al. 2022

Preprint

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Acute respiratory distress syndrome (ARDS), a life-threatening condition during critical illness, is a common complication of COVID-19. It can originate from various disease etiologies, including severe infections, major injury, or inhalation of irritants. ARDS poses substantial clinical challenges due to a lack of etiology-specific therapies, multisystem involvement, and heterogeneous, poor patient outcomes. A molecular comparison of ARDS groups holds the potential to reveal common and distinct mechanisms underlying ARDS pathogenesis. In this study, we performed a comparative analysis of urine-based metabolomics and proteomics profiles from COVID-19 ARDS patients (n = 42) and bacterial sepsis-induced ARDS patients (n = 17). The comparison of these ARDS etiologies identified 150 metabolites and 70 proteins that were differentially abundant between the two groups. Based on these findings, we interrogated the interplay of cell adhesion/extracellular matrix molecules, inflammation, and mitochondrial dysfunction in ARDS pathogenesis through a multi-omic network approach. Moreover, we identified a proteomic signature associated with mortality in COVID-19 ARDS patients, which contained several proteins that had previously been implicated in clinical manifestations frequently linked with ARDS pathogenesis. In summary, our results provide evidence for significant molecular differences in ARDS patients from different etiologies and a potential synergy of extracellular matrix molecules, inflammation, and mitochondrial dysfunction in ARDS pathogenesis. The proteomic mortality signature should be further investigated in future studies to develop prediction models for COVID-19 patient outcomes.

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Acute respiratory distress syndrome

Cited by 12 publications

References 106 publications

Puerarin Inhibits Ferroptosis and Inflammation of Lung Injury Caused by Sepsis in LPS Induced Lung Epithelial Cells

Puerarin Inhibits Ferroptosis and Inflammation of Lung Injury Caused by Sepsis in LPS Induced Lung Epithelial Cells

Multi-omic comparative analysis of COVID-19 and bacterial sepsis-induced ARDS

Urine-based multi-omic comparative analysis of COVID-19 and bacterial sepsis-induced ARDS

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