scholarly journals Sustained Adenosine Caused Endothelial Mitochondrial Dysfunction: Implications for Cigarette Smoke‐Induced Increased Susceptibility to Acute Lung Injury

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Eboni Chambers ◽  
Junsuk Ko ◽  
Diana Borgas ◽  
Julie Newton ◽  
Sharon Rounds ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Mitochondrial Dysfunction ◽  
Cigarette Smoke ◽  
Increased Susceptibility

Gene silencing of receptor-interacting protein 2 protects against cigarette smoke-induced acute lung injury

2019 ◽  
Vol 139 ◽  
pp. 560-568 ◽  
Author(s):  
Jinrui Dong ◽  
Wupeng Liao ◽  
Lay Hong Tan ◽  
Amy Yong ◽  
Wen Yan Peh ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Gene Silencing ◽  
Cigarette Smoke ◽  
Interacting Protein

CRTH2 antagonist, CT‑133, effectively alleviates cigarette smoke-induced acute lung injury

Life Sciences ◽  
2019 ◽  
Vol 216 ◽  
pp. 156-167 ◽  
Author(s):  
Musaddique Hussain ◽  
Chengyun Xu ◽  
Minli Yao ◽  
Qin Zhang ◽  
Junsong Wu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Cigarette Smoke

scholarly journals Mitochondrial Division Inhibitor 1 Attenuates Mitophagy in a Rat Model of Acute Lung Injury

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Xu Luo ◽  
Ruimeng Liu ◽  
Zhihao Zhang ◽  
Zhugui Chen ◽  
Jian He ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Mitochondrial Dysfunction ◽  
Cell Damage ◽  
A549 Cells ◽  
Oxygenation Index ◽  
Lipid Peroxides ◽  
Dry Weight ◽  
Induced Apoptosis

The regulation of intracellular mitochondria degradation is mediated by mitophagy. While studies have shown that mitophagy can lead to mitochondrial dysfunction and cell damage, the role of Mdivi-1 and mitophagy remains unclear in acute lung injury (ALI) pathogenesis. In this study, we demonstrated that Mdivi-1, which is widely used as an inhibitor of mitophagy, ameliorated acute lung injury assessed by HE staining, pulmonary microvascular permeability assay, measurement of wet/dry weight (W/D) ratio, and oxygenation index (PaO2/FiO2) analysis. Then, the mitophagy related proteins were evaluated by western blot. The results indicated that LPS-induced activation of mitophagy was inhibited by Mdivi-1 treatment. In addition, we found that Mdivi-1 protected A549 cells against LPS-induced mitochondrial dysfunction. We also found that Mdivi-1 reduced pulmonary cell apoptosis in the LPS-challenged rats and protected pulmonary tissues from oxidative stress (represented by the content of superoxide dismutase, malondialdehyde and lipid peroxides in lung). Moreover, Mdivi-1 treatment ameliorated LPS-induced lung inflammatory response and cells recruitment. These findings indicate that Mdivi-1 mitigates LPS-induced apoptosis, oxidative stress, and inflammation in ALI, which may be associated with mitophagy inhibition. Thus, the inhibition of mitophagy may represent a potential therapy for treating ALI.

Effects of Eucalyptol in respiratory system mechanics on acute lung injury after exposure to short-term cigarette smoke

2019 ◽  
Vol 266 ◽  
pp. 33-38 ◽  
Author(s):  
Fladimir de Lima Gondim ◽  
Daniel Silveira Serra ◽  
Francisco Sales Ávila Cavalcante
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Cigarette Smoke ◽  
Respiratory System ◽  
Short Term ◽  
Respiratory System Mechanics

Apple polyphenol protects against cigarette smoke-induced acute lung injury

Nutrition ◽  
2013 ◽  
Vol 29 (1) ◽  
pp. 235-243 ◽  
Author(s):  
Meng-Jing Bao ◽  
Jian Shen ◽  
Yong-Liang Jia ◽  
Fen-Fen Li ◽  
Wen-Jiang Ma ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Cigarette Smoke

Transgenic HbS Mouse Neutrophils in Increased Susceptibility to Acute Lung Injury

CHEST Journal ◽  
1999 ◽  
Vol 116 ◽  
pp. 92S ◽  
Author(s):  
L. Hsu ◽  
T. McDermott ◽  
L. Brown ◽  
S.M. Aguayo
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Increased Susceptibility

scholarly journals Cigarette smoke exposure worsens acute lung injury in antibiotic-treated bacterial pneumonia in mice

2018 ◽  
Vol 315 (1) ◽  
pp. L25-L40 ◽  
Author(s):  
Jeffrey E. Gotts ◽  
Lauren Chun ◽  
Jason Abbott ◽  
Xiaohui Fang ◽  
Naoki Takasaka ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Cigarette Smoke ◽  
Clinical Relevance ◽  
Bacterial Pneumonia ◽  
Pneumococcal Infection ◽  
Whole Body ◽  
Cigarette Smoke Exposure ◽  
Surfactant Protein D ◽  
Systemic Spread

Evidence is accumulating that exposure to cigarette smoke (CS) increases the risk of developing acute respiratory distress syndrome (ARDS). Streptococcus pneumoniae is the most common cause of bacterial pneumonia, which in turn is the leading cause of ARDS. Chronic smokers have increased rates of pneumococcal colonization and develop more severe pneumococcal pneumonia than nonsmokers; yet mechanistic connections between CS exposure, bacterial pneumonia, and ARDS pathogenesis remain relatively unexplored. We exposed mice to 3 wk of moderate whole body CS or air, followed by intranasal inoculation with an invasive serotype of S. pneumoniae. CS exposure alone caused no detectable lung injury or bronchoalveolar lavage (BAL) inflammation. During pneumococcal infection, CS-exposed mice had greater survival than air-exposed mice, in association with reduced systemic spread of bacteria from the lungs. However, when mice were treated with antibiotics after infection to improve clinical relevance, the survival benefit was lost, and CS-exposed mice had more pulmonary edema, increased numbers of BAL monocytes, and elevated monocyte and lymphocyte chemokines. CS-exposed antibiotic-treated mice also had higher serum surfactant protein D and angiopoietin-2, consistent with more severe lung epithelial and endothelial injury. The results indicate that acute CS exposure enhances the recruitment of immune cells to the lung during bacterial pneumonia, an effect that may provide microbiological benefit but simultaneously exposes the mice to more severe inflammatory lung injury. The inclusion of antibiotic treatment in preclinical studies of acute lung injury in bacterial pneumonia may enhance clinical relevance, particularly for future studies of current or emerging tobacco products.

scholarly journals Inhalation of ambroxol inhibits cigarette smoke-induced acute lung injury in a mouse model by inhibiting the Erk pathway

2016 ◽  
Vol 33 ◽  
pp. 90-98 ◽  
Author(s):  
Ling-tian Ge ◽  
Ya-nan Liu ◽  
Xi-xi Lin ◽  
Hui-juan Shen ◽  
Yong-liang Jia ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Mouse Model ◽  
Cigarette Smoke ◽  
Erk Pathway
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