scholarly journals Soluble programmed cell death receptor-1 (sPD-1): a potential biomarker with anti-inflammatory properties in human and experimental acute respiratory distress syndrome (ARDS)

2016 ◽  
Vol 14 (1) ◽  
Author(s):  
Sean F. Monaghan ◽  
Chun-Shiang Chung ◽  
Yaping Chen ◽  
Joanne Lomas-Neira ◽  
William G. Fairbrother ◽  
...  
Keyword(s):  
Cell Death ◽  
Acute Respiratory Distress Syndrome ◽  
Programmed Cell Death ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Death Receptor ◽  
Potential Biomarker ◽  
Anti Inflammatory ◽  
Cell Death Receptor

scholarly journals Respiratory and Systemic Effects of LASSBio596 Plus Surfactant in Experimental Acute Respiratory Distress Syndrome

2016 ◽  
Vol 38 (2) ◽  
pp. 821-835 ◽  
Author(s):  
Johnatas Dutra Silva ◽  
Gisele Pena de Oliveira ◽  
Cynthia dos Santos Samary ◽  
Carla Cristina Araujo ◽  
Gisele de Araujo Padilha ◽  
...  
Keyword(s):  
Surface Tension ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Cecal Ligation ◽  
Exogenous Surfactant ◽  
Experimental Sepsis ◽  
Apoptosis Protein ◽  
Anti Inflammatory

Background/Aims: Exogenous surfactant has been proposed as adjunctive therapy for acute respiratory distress syndrome (ARDS), but it is inactivated by different factors present in the alveolar space. We hypothesized that co-administration of LASSBio596, a molecule with significant anti-inflammatory properties, and exogenous surfactant could reduce lung inflammation, thus enabling the surfactant to reduce edema and improve lung function, in experimental ARDS. Methods: ARDS was induced by cecal ligation and puncture surgery in BALB/c mice. A sham-operated group was used as control (CTRL). After surgery (6 hours), CTRL and ARDS animals were assigned to receive: (1) sterile saline solution; (2) LASSBio596; (3) exogenous surfactant or (4) LASSBio596 plus exogenous surfactant (n = 22/group). Results: Regardless of exogenous surfactant administration, LASSBio596 improved survival rate and reduced collagen fiber content, total number of cells and neutrophils in PLF and blood, cell apoptosis, protein content in BALF, and urea and creatinine levels. LASSBio596 plus surfactant yielded all of the aforementioned beneficial effects, as well as increased BALF lipid content and reduced surface tension. Conclusion: LASSBio596 exhibited major anti-inflammatory and anti-fibrogenic effects in experimental sepsis-induced ARDS. Its association with surfactant may provide further advantages, potentially by reducing surface tension.

scholarly journals Oleic acid-based nanosystems for mitigating acute respiratory distress syndrome in mice through neutrophil suppression: how the particulate size affects therapeutic efficiency

2020 ◽  
Author(s):  
Huang-Ping Yu ◽  
Fu-Chao Liu ◽  
Ani Umoro ◽  
Zih-Chan Lin ◽  
Ahmed O. Elzoghby ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Oleic Acid ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Inflammatory Activity ◽  
Human Neutrophils ◽  
Essential Property ◽  
Anti Inflammatory

Abstract Background: Oleic acid (OA) is reported to show anti-inflammatory activity toward activated neutrophils. It is also an important material in nanoparticles for increased stability and cellular internalization. We aimed to evaluate the anti-inflammatory activity of injectable OA-based nanoparticles for treating lung injury. Different sizes of nanocarriers were prepared to explore the effect of nanoparticulate size on inflammation inhibition. Results: The nanoparticles were fabricated with the mean diameters of 105, 153, and 225 nm. The nanocarriers were ingested by isolated human neutrophils during a 5-min period, with the smaller sizes exhibiting greater uptake. The size reduction led to the decrease of cell viability and the intracellular calcium level. The OA-loaded nanosystems dose-dependently suppressed the superoxide anion and elastase produced by the stimulated neutrophils. The inhibition level was comparable for the nanoparticles of different sizes. In the ex vivo biodistribution study, the pulmonary accumulation of nanoparticles increased following the increase of particle size. The nanocarriers were mainly excreted by the liver and bile clearance. Mice were exposed to intratracheal lipopolysaccharide (LPS) to induce acute respiratory distress syndrome (ARDS), like lung damage. The lipid-based nanocarriers mitigated myeloperoxidase (MPO) and cytokines more effectively as compared to OA solution. The larger nanoparticles displayed greater reduction on MPO, TNF-α, and IL-6 than the smaller ones. The histology confirmed the decreased pulmonary neutrophil recruitment and lung-architecture damage after intravenous administration of larger nanoparticles. Conclusions: Nanoparticulate size, an essential property governing the anti-inflammatory effect and lung-injury therapy, had different effects on activated neutrophil inhibition and in vivo therapeutic efficacy.

Novel anti-inflammatory mechanism in critically ill: Soluble programmed cell death receptor-1 (sPD-1)

2011 ◽  
Vol 213 (3) ◽  
pp. S54-S55
Author(s):  
Sean F. Monaghan ◽  
Rajan K. Thakkar ◽  
Chun S. Chung ◽  
Yaping Chen ◽  
Daithi S. Heffernan ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Critically Ill ◽  
Death Receptor ◽  
Inflammatory Mechanism ◽  
Anti Inflammatory ◽  
Cell Death Receptor

scholarly journals SARS-CoV-2 envelope protein causes acute respiratory distress syndrome (ARDS)-like pathological damages and constitutes an antiviral target

Cell Research ◽  
2021 ◽  
Author(s):  
Bingqing Xia ◽  
Xurui Shen ◽  
Yang He ◽  
Xiaoyan Pan ◽  
Feng-Liang Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Dominant Negative ◽  
Dominant Negative Mutation ◽  
E Protein

AbstractCytokine storm and multi-organ failure are the main causes of SARS-CoV-2-related death. However, the origin of excessive damages caused by SARS-CoV-2 remains largely unknown. Here we show that the SARS-CoV-2 envelope (2-E) protein alone is able to cause acute respiratory distress syndrome (ARDS)-like damages in vitro and in vivo. 2-E proteins were found to form a type of pH-sensitive cation channels in bilayer lipid membranes. As observed in SARS-CoV-2-infected cells, heterologous expression of 2-E channels induced rapid cell death in various susceptible cell types and robust secretion of cytokines and chemokines in macrophages. Intravenous administration of purified 2-E protein into mice caused ARDS-like pathological damages in lung and spleen. A dominant negative mutation lowering 2-E channel activity attenuated cell death and SARS-CoV-2 production. Newly identified channel inhibitors exhibited potent anti-SARS-CoV-2 activity and excellent cell protective activity in vitro and these activities were positively correlated with inhibition of 2-E channel. Importantly, prophylactic and therapeutic administration of the channel inhibitor effectively reduced both the viral load and secretion of inflammation cytokines in lungs of SARS-CoV-2-infected transgenic mice expressing human angiotensin-converting enzyme 2 (hACE-2). Our study supports that 2-E is a promising drug target against SARS-CoV-2.

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