Changes in TNF-α, IL-6, IL-10 and VEGF in rats with ARDS and the effects of dexamethasone

Qin, Momei; Qiu, Zhongpeng

doi:10.3892/etm.2018.6926

Cited by 35 publications

(38 citation statements)

References 28 publications

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“…In this study, DEX administration decreased levels of pro-inflammatory cytokines in the lung and plasma compared to the ARDS group, while the higher dose DEX-1.0 had slightly stronger impact on these changes. The effectiveness of dexamethasone in reducing levels of cytokines was observed also by other authors (Xinmin et al 2006, Qin andQiu 2019).…”

Section: Nt Tbarssupporting

confidence: 76%

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Effect of Different Dosages of Dexamethasone Therapy on Lung Function and Inflammation in an Early Phase of Acute Respiratory Distress Syndrome Model

Mikolka

Kosutova²,

M³

et al. 2019

Physiol Res

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Inflammation associated with acute respiratory distress syndrome (ARDS) can damage the alveolar epithelium and surfactant and worsen the respiratory failure. Glucocorticoids (GC) appear to be a rational therapeutic approach, but the effect is still unclear, especially for early administration and low-dose. In this study we compared two low doses of dexamethasone in early phase of surfactant-depleted model of acute respiratory distress syndrome (ARDS). In the study, lung-lavaged New Zealand rabbits with respiratory failure (PaO2<26.7 kPa in FiO2 1.0) were treated with intravenous dexamethasone (DEX): 0.5 mg/kg (DEX-0.5) and 1.0 mg/kg (DEX-1.0), or were untreated (ARDS). Animals without ARDS served as controls. Respiratory parameters, lung edema, leukocyte shifts, markers of inflammation and oxidative damage in the plasma and lung were evaluated. Both doses of DEX improved the lung function vs. untreated animals. DEX-1.0 had faster onset with significant improvement in gas exchange and ventilation efficiency vs. DEX-0.5. DEX-1.0 showed a trend to reduce lung neutrophils, local oxidative damage, and levels of TNFα, IL-6, IL-8 more effectively than DEX-0.5 vs. ARDS group. Both dosages of dexamethasone significantly improved the lung function and suppressed inflammation in early phase ARDS, while some additional enhancement was observed for higher dose (1 mg/kg) of DEX.

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Section: Nt Tbarssupporting

confidence: 76%

“…, Beck et al 2009, Newton et al 2010 and their role was found in favor of treatment of ARDS (Peter et al 2008). There are evidences for the beneficial role of dexamethasone (DEX) in ARDS condition (Villar et al 2016, Qin andQiu 2019), particularly for low dose of DEX (Lee et al 2005, Xinmin et al 2006, Wang et al 2008.…”

Section: Discussionmentioning

confidence: 99%

Effect of Different Dosages of Dexamethasone Therapy on Lung Function and Inflammation in an Early Phase of Acute Respiratory Distress Syndrome Model

Mikolka

Kosutova²,

M³

et al. 2019

Physiol Res

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“…MPO expressed in neutrophil granules is a major mediator of lung injury. Neutrophils also secrete some cytokines such as TNF-α, IL-1β, and IL-6 to deteriorate ARDS [51]. An attenuation of ARDS by nanoparticulate OA was found, based on the reduction of MPO and cytokines.…”

Section: Discussionmentioning

confidence: 94%

“…Cytokines can be produced by different immune cells. For instance, IL-6 is a key proinflammatory mediator secreted by neutrophils, macrophages, and T cells to induce an inflammatory cascade in ARDS [51]. Alveolar macrophages are important phagocytic cells in the lung for nanoparticle internalization.…”

Section: Discussionmentioning

confidence: 99%

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

Liu

Umoro

et al. 2020

J Nanobiotechnol

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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 antiinflammatory 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.

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“…After PBLI, the alveolar epithelium and alveolar capillaries are exposed to high concentrations of VEGF, which increase the vascular permeability, resulting in an increased inflammatory response during the exudation period and exacerbating the condition of PBLI [ 102 ]. Qin et al [ 103 ] found that in the ARDS model, levels of TNF-α, IL-6, and VEGF in bronchoalveolar lavage fluid (BALF) were significantly higher than those of the control group, resulting in an imbalance between pro-inflammatory and anti-inflammatory responses. In addition, Lin et al [ 98 ] suggested that VEGF participates in fat embolism (FE)-induced ALI via VEGFR-2 and MAPK cascade, which induce IL-1β release and inducible nitric oxide synthase (iNOS) upregulation ( Figure 3 ).…”

Section: Damps and Their Signaling Pathways Related To Pblimentioning

confidence: 99%

Damage-Associated Molecular Patterns and Their Signaling Pathways in Primary Blast Lung Injury: New Research Progress and Future Directions

Geng

Hou

et al. 2020

IJMS

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Primary blast lung injury (PBLI) is a common cause of casualties in wars, terrorist attacks, and explosions. It can exist in the absence of any other outward signs of trauma, and further develop into acute lung injury (ALI) or a more severe acute respiratory distress syndrome (ARDS). The pathogenesis of PBLI at the cellular and molecular level has not been clear. Damage-associated molecular pattern (DAMP) is a general term for endogenous danger signals released by the body after injury, including intracellular protein molecules (HMGB1, histones, s100s, heat shock proteins, eCIRP, etc.), secretory protein factors (IL-1β, IL-6, IL-10, TNF-α, VEGF, complements, etc.), purines and pyrimidines and their derived degradation products (nucleic acids, ATP, ADP, UDPG, uric acid, etc.), and extracellular matrix components (hyaluronic acid, fibronectin, heparin sulfate, biglycan, etc.). DAMPs can be detected by multiple receptors including pattern recognition receptors (PRRs). The study of DAMPs and their related signaling pathways, such as the mtDNA-triggered cGAS-YAP pathway, contributes to revealing the molecular mechanism of PBLI, and provides new therapeutic targets for controlling inflammatory diseases and alleviating their symptoms. In this review, we focus on the recent progress of research on DAMPs and their signaling pathways, as well as the potential therapeutic targets and future research directions in PBLI.

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Changes in TNF-α, IL-6, IL-10 and VEGF in rats with ARDS and the effects of dexamethasone

Cited by 35 publications

References 28 publications

Effect of Different Dosages of Dexamethasone Therapy on Lung Function and Inflammation in an Early Phase of Acute Respiratory Distress Syndrome Model

Effect of Different Dosages of Dexamethasone Therapy on Lung Function and Inflammation in an Early Phase of Acute Respiratory Distress Syndrome Model

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

Damage-Associated Molecular Patterns and Their Signaling Pathways in Primary Blast Lung Injury: New Research Progress and Future Directions

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