The blockade of neddylation alleviates ventilator-induced lung injury by reducing stretch-induced damage to pulmonary epithelial cells.

Ventilator-induced lung injury is a serious complication in mechanically ventilated patients. Neddylation, the post-translational modification of neural precursor cell-expressed developmentally down-regulated 8 (NEDD8) conjugation, regulates numerous biological functions. However, its involvement and therapeutic significance in ventilator-induced lung injury remains unknown.

N-acetylcysteine alleviates fine particulate matter (PM2.5)-induced lung injury by attenuation of ROS-mediated recruitment of neutrophils and Ly6C monocytes and lung inflammation.

Background: Exposure to particulate matter (PM) may contribute to lung inflammation and injury. The therapeutic effect of N-acetylcysteine (NAC), a well-known antioxidant, with regards to the prevention and treatment of fine PM (PM2.5)-induced lung injury is poorly understood.

Roles of lung-recruited monocytes and pulmonary Vascular Endothelial Growth Factor (VEGF) in resolving Ventilator-Induced Lung Injury (VILI).

Monocytes and vascular endothelial growth factor (VEGF) have profound effects on tissue injury and repair. In ventilator-induced lung injury (VILI), monocytes, the majority of which are Ly6C+high, and VEGF are known to initiate lung injury. However, their roles in post-VILI lung repair remain unclear.

Cyclooxygenase-2 Activity Regulates Recruitment of VEGF-Secreting Ly6C Monocytes in Ventilator-Induced Lung Injury.

Mechanical ventilation is usually required for saving lives in critically ill patients; however, it can cause ventilator-induced lung injury (VILI). As VEGF-secreting Ly6C monocytes are involved in VILI pathogenesis, we investigated whether cyclooxygenase-2 (COX-2) activity regulates the recruitment of VEGF-secreting Ly6C monocytes during VILI. The clinically relevant two-hit mouse model of VILI, which involves the intravenous injection of lipopolysaccharide prior to high tidal volume (HTV)-mechanical ventilation, was used in this study.

VEGF Production by Ly6C+high Monocytes Contributes to Ventilator-Induced Lung Injury.

Background: Mechanical ventilation is a life-saving procedure for patients with acute respiratory failure, although it may cause pulmonary vascular inflammation and leakage, leading to ventilator-induced lung injury (VILI). Ly6C+high monocytes are involved in the pathogenesis of VILI. In this study, we investigated whether pulmonary infiltrated Ly6C+high monocytes produce vascular endothelial growth factor (VEGF) and contribute to VILI.