scholarly journals miR-34b-5p inhibition attenuates lung inflammation and apoptosis in an LPS-induced acute lung injury mouse model by targeting progranulin

2018 ◽  
Vol 233 (9) ◽  
pp. 6615-6631 ◽  
Author(s):  
Wang Xie ◽  
Qingchun Lu ◽  
Kailing Wang ◽  
Jingjing Lu ◽  
Xia Gu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Mouse Model ◽  
Lung Inflammation

scholarly journals Inhibition of Pyk2 blocks lung inflammation and injury in a mouse model of acute lung injury

2012 ◽  
Vol 13 (1) ◽  
pp. 4 ◽  
Author(s):  
Yingli Duan ◽  
Jonathan Learoyd ◽  
Angelo Y Meliton ◽  
Alan R Leff ◽  
Xiangdong Zhu
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Mouse Model ◽  
Lung Inflammation

Inhibition Of Pyk2 Blocks Lung Inflammation And Vascular Leakage In A Mouse Model Of Acute Lung Injury

2012 ◽  
Author(s):  
Xiangdong Zhu ◽  
Yingli Duan ◽  
Jonathan Learoyd ◽  
Angelo Y. Meliton ◽  
Alan R. Leff
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Mouse Model ◽  
Lung Inflammation ◽  
Vascular Leakage

Inhibition Of Pyk2 Blocks Lung Inflammation And Injury In A Mouse Model Of Acute Lung Injury

2010 ◽  
Author(s):  
Yingli Duan ◽  
Jonathan Learoyd ◽  
Angelo Y. Meliton ◽  
Alan R. Leff ◽  
Xiangdong Zhu
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Mouse Model ◽  
Lung Inflammation

Abstract 20051: Divergent Actions of Circulating Angiopoietin-2 on Vascular Inflammation and Leak in a Mouse Model of Acute Lung Injury

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Kenny Schlosser ◽  
Mohamad Taha ◽  
Yupu Deng ◽  
Shirley H Mei ◽  
Duncan J Stewart
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Mouse Model ◽  
Lung Inflammation ◽  
Partial Agonist ◽  
Vascular Inflammation ◽  
Vascular Leak ◽  
Angiopoietin 2 ◽  
Circulating Levels

Introduction: Angiopoietin-2 (Angpt2) is a partial agonist/antagonist of the vascular-stabilizing endothelial Tie2 receptor. In both animal models and patients with acute lung injury (ALI), Angpt2 circulating levels are elevated; however, it remains unclear whether these elevated levels contribute to, or protect against, the lung inflammation and vascular leak associated with ALI. Objective: To evaluate the biological consequences of elevated circulating Angpt2 levels in a mouse model of endotoxin-induced ALI. Methods and Results: Transgenic mice (Angpt2OVR) with elevated circulating levels of human (h)Angpt2, via conditional hepatocyte-specific overexpression, were examined at several timepoints (from 3 h to 72 h) following lipopolysaccharide (LPS)-induced ALI (n=7-14 mice/genotype group/timepoint). Bronchoalveolar lavage (BAL) neutrophil and inflammatory cytokine levels were significantly higher (P<0.05) in Angpt2OVR versus littermate controls at 48 h and 6 h post LPS, respectively. In contrast, vascular leak, evidenced by decreased BAL IgM and albumin levels at 24 and 48 h, was attenuated in Angpt2OVR mice. Systemic Angpt2 overexpression showed no net detriment or benefit for survival following LPS-induced injury (n=37-38 mice/group). Tail vein injection of an anti-hAngpt2-neutralizing aptamer (versus non-functional scrambled-sequence control; n=12-13 mice/group), reversed the pro-inflammatory and anti-leak effects observed at 48 h in LPS-injured Angpt2OVR mice. Transcript profiling, via PCR array, was also conducted to probe the effects of Angpt2 neutralization on the lung tissue expression of 84 genes involved in vascular biology. Angpt2 neutralization via aptamer caused alterations in multiple genes linked to angiogenesis, vascular tone, inflammation, apoptosis, cell adhesion, coagulation, and platelet activation (P<0.05 versus scrambled control, n=4/group). Conclusions: Angpt2 exerts differential effects on lung inflammation and permeability under pathological conditions in vivo. These data establish novel context-dependent actions of Angpt2, and suggest elevated circulating levels may help regulate multiple pathways necessary to fine-tune the vascular response to lung injury.

Impaired airway epithelial barrier integrity was mediated by PI3Kδ in a mouse model of lipopolysaccharide-induced acute lung injury

2021 ◽  
Vol 95 ◽  
pp. 107570
Author(s):  
Lihong Yao ◽  
Ying Tang ◽  
Junjie Chen ◽  
Jiahui Li ◽  
Hua Wang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Mouse Model ◽  
Epithelial Barrier ◽  
Airway Epithelial ◽  
Barrier Integrity

scholarly journals Effects of Positive End-expiratory Pressure Titration and Recruitment Maneuver on Lung Inflammation and Hyperinflation in Experimental Acid Aspiration–induced Lung Injury

2012 ◽  
Vol 117 (6) ◽  
pp. 1322-1334 ◽  
Author(s):  
Aline M. Ambrosio ◽  
Rubin Luo ◽  
Denise T. Fantoni ◽  
Claudia Gutierres ◽  
Qin Lu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Lung Inflammation ◽  
Recruitment Maneuver ◽  
Alveolar Wall ◽  
Arterial Oxygenation ◽  
Positive End Expiratory Pressure ◽  
Acid Aspiration ◽  
Recruitment Maneuvers ◽  
Alveolar Area

Background In acute lung injury positive end-expiratory pressure (PEEP) and recruitment maneuver are proposed to optimize arterial oxygenation. The aim of the study was to evaluate the impact of such a strategy on lung histological inflammation and hyperinflation in pigs with acid aspiration-induced lung injury. Methods Forty-seven pigs were randomly allocated in seven groups: (1) controls spontaneously breathing; (2) without lung injury, PEEP 5 cm H2O; (3) without lung injury, PEEP titration; (4) without lung injury, PEEP titration + recruitment maneuver; (5) with lung injury, PEEP 5 cm H2O; (6) with lung injury, PEEP titration; and (7) with lung injury, PEEP titration + recruitment maneuver. Acute lung injury was induced by intratracheal instillation of hydrochloric acid. PEEP titration was performed by incremental and decremental PEEP from 5 to 20 cm H2O for optimizing arterial oxygenation. Three recruitment maneuvers (pressure of 40 cm H2O maintained for 20 s) were applied to the assigned groups at each PEEP level. Proportion of lung inflammation, hemorrhage, edema, and alveolar wall disruption were recorded on each histological field. Mean alveolar area was measured in the aerated lung regions. Results Acid aspiration increased mean alveolar area and produced alveolar wall disruption, lung edema, alveolar hemorrhage, and lung inflammation. PEEP titration significantly improved arterial oxygenation but simultaneously increased lung inflammation in juxta-diaphragmatic lung regions. Recruitment maneuver during PEEP titration did not induce additional increase in lung inflammation and alveolar hyperinflation. Conclusion In a porcine model of acid aspiration-induced lung injury, PEEP titration aimed at optimizing arterial oxygenation, substantially increased lung inflammation. Recruitment maneuvers further improved arterial oxygenation without additional effects on inflammation and hyperinflation.

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