Tristetraprolin Mediates Anti-Inflammatory Effects of Carbon Monoxide on Lipopolysaccharide-Induced Acute Lung Injury

2015 ◽  
Vol 185 (11) ◽  
pp. 2867-2874 ◽  
Author(s):  
Yeonsoo Joe ◽  
Seul-Ki Kim ◽  
Yingqing Chen ◽  
Jung Wook Yang ◽  
Jeong-Hee Lee ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Anti Inflammatory

Class B Scavenger Receptors BI and BII Protect Against LPS-induced Acute Lung Injury in Mice by Mediating LPS Clearance

2021 ◽  
Author(s):  
Irina N. Baranova ◽  
Alexander V. Bocharov ◽  
Tatyana G. Vishnyakova ◽  
Zhigang Chen ◽  
Anna A. Birukova ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Transgenic Mice ◽  
Neutrophil Infiltration ◽  
Lavage Fluid ◽  
Protective Role ◽  
Lung Damage ◽  
Wild Type ◽  
Class B ◽  
Anti Inflammatory

Recent studies suggest an anti-inflammatory protective role for class B scavenger receptor BI (SR-BI) in endotoxin-induced inflammation and sepsis. Other data, including ours, provide evidence for an alternative role of SR-BI, facilitating bacterial and endotoxin uptake, and contributing to inflammation and bacterial infection. Enhanced endotoxin susceptibility of SR-BI deficient mice due to their anti-inflammatory glucocorticoid deficiency complicates understanding SR-BI’s role in endotoxemia/sepsis, calling for use of alternative models. In this study, using hSR-BI and hSR-BII transgenic mice, we found that SR-BI and to a lesser extent its splicing variant SR-BII, protects against LPS-induced lung damage. At 20 hours after intratracheal LPS instillation the extent of pulmonary inflammation and vascular leakage was significantly lower in hSR-BI and hSR-BII transgenic mice compared to wild type mice. Higher bronchoalveolar lavage fluid (BALF) inflammatory cell count and protein content as well as lung tissue neutrophil infiltration found in wild type mice was associated with markedly (2-3 times) increased pro-inflammatory cytokine production as compared to transgenic mice following LPS administration. Markedly lower endotoxin levels detected in BALF of transgenic vs. wild type mice along with the significantly increased BODIPY-LPS uptake observed in lungs of hSR-BI and hSR-BII mice 20 hours after the IT LPS injection suggest that hSR-BI and hSR-BII-mediated enhanced LPS clearance in the airways could represent the mechanism of their protective role against LPS-induced acute lung injury.

Bilobalide, a bioactive compound on sepsis-induced acute lung injury through its anti-inflammatory and antioxidative activity

2021 ◽  
Vol 17 (73) ◽  
pp. 163
Author(s):  
Yi Zhu ◽  
Feng Wang ◽  
Jian Huang ◽  
Jun Li ◽  
Kang Chen ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Antioxidative Activity ◽  
Bioactive Compound ◽  
Anti Inflammatory

Vanillin protects lipopolysaccharide-induced acute lung injury by inhibiting ERK1/2, p38 and NF-κB pathway

2019 ◽  
Vol 11 (16) ◽  
pp. 2081-2094 ◽  
Author(s):  
Tingting Guo ◽  
Zhenzhong Su ◽  
Qi Wang ◽  
Wei Hou ◽  
Junyao Li ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Western Blot ◽  
Lung Inflammation ◽  
Macrophage Activation ◽  
Myeloperoxidase Activity ◽  
Histopathological Changes ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Inflammatory Effect

Aim: Thus far, the anti-inflammatory effect of vanillin in acute lung injury (ALI) has not been studied. This study aimed to investigate the effect of vanillin in lipopolysaccharide (LPS)-induced ALI. Results & methodology: Our study detected the anti-inflammatory effects of vanillin by ELISA and western blot, respectively. Pretreatment of mice with vanillin significantly attenuated LPS-stimulated lung histopathological changes, myeloperoxidase activity and expression levels of proinflammatory cytokines by inhibiting the phosphorylation activities of ERK1/2, p38, AKT and NF-κB p65. In addition, vanillin inhibited LPS-induced TNF-α and IL-6 expression in RAW264.7 cells via ERK1/2, p38 and NF-κB signaling. Conclusion: Vanillin can inhibit macrophage activation and lung inflammation, which suggests new insights for clinical treatment of ALI.

Obeticholic acid alleviate lipopolysaccharide-induced acute lung injury via its anti-inflammatory effects in mice

2019 ◽  
Vol 66 ◽  
pp. 177-184 ◽  
Author(s):  
Jun Fei ◽  
Lin Fu ◽  
Biao Hu ◽  
Yuan-Hua Chen ◽  
Hui Zhao ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Obeticholic Acid ◽  
Anti Inflammatory

scholarly journals Emodin alleviates LPS-induced inflammatory response in lung injury rat by affecting the function of neutrophils

2020 ◽  
Author(s):  
Hongxia Mei ◽  
Ying Tao ◽  
Tianhao Zhang ◽  
Feng Qi
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Rat Model ◽  
Neutrophil Function ◽  
Life Threatening ◽  
Pulmonary Inflammatory Response ◽  
Anti Inflammatory ◽  
Factor Α ◽  
The Impact

Abstract Background: Acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS) are critical life-threatening syndromes characterized by the infiltration of a large number of neutrophils that lead to an excessive inflammatory response. Emodin (Emo) is a naturally occurring anthraquinone derivative and an active ingredient of Chinese medicine. It is believed to have anti-inflammatory effects. In this study, we examined the impact of Emo on the pulmonary inflammatory response and the neutrophil function in a rat model of lipopolysaccharide (LPS)-induced ALI.Results: Treatment with Emo protected rat against LPS-induced ALI. Compared to untreated rat, Emo-treated rat exhibited significantly ameliorated lung pathological changes and decreased tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). However, Emo has no protective effect on the rat model of acute lung injury with neutrophil deficiency. In addition, treatment with Emo enhanced the bactericidal capacity of LPS-induced neutrophils via the up-regulation of the ability of neutrophils to phagocytize bacteria and generate neutrophil extracellular traps (NETs). Emo also downregulated the neutrophil respiratory burst and the expression of reactive oxygen species (ROS) in LPS-stimulated neutrophils, alleviating the damage of neutrophils to surrounding tissues. Finally, Emo can accelerate the resolution of inflammation by promoting apoptosis of neutrophils. Conclusion: Our results provide the evidence that Emo could ameliorates LPS-induced ALI via its anti-inflammatory action by modulating the function of neutrophils. Emo may be a promising preventive and therapeutic agent in the treatment of ALI.

scholarly journals Exhaled carbon monoxide and inducible heme oxygenase expression in a rat model of postperfusion acute lung injury

2003 ◽  
Vol 126 (6) ◽  
pp. 1867-1874 ◽  
Author(s):  
Rachid Zegdi ◽  
Olivier Fabre ◽  
Nermine Lila ◽  
Paul Fornès ◽  
Michèle Cambillau ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Heme Oxygenase ◽  
Rat Model ◽  
Exhaled Carbon Monoxide

Effects of an Intratracheally Delivered Anti-Inflammatory Protein (rhCC10) on Physiological and Lung Structural Indices in a Juvenile Model of Acute Lung Injury

Neonatology ◽  
2006 ◽  
Vol 89 (3) ◽  
pp. 159-170 ◽  
Author(s):  
Thomas L. Miller ◽  
Beth N. Shashikant ◽  
Aprile L. Pilon ◽  
Richard A. Pierce ◽  
Thomas H. Shaffer ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Protein ◽  
Anti Inflammatory ◽  
Structural Indices
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