Vascular endothelial growth factor (VEGF) is a potent angiogenic and endothelial survival factor, which is abundantly expressed in the normal lung. Conceivably, VEGF may be released by numerous cell types found around the airspaces, including alveolar type 2 cells, alveolar macrophages, and polymorphonuclear neutrophils. Using a bacteria-induced lung injury model in rats, VEGF expression in lun...

Vascular endothelial cells regulate the passage of fluids, solutes, and cells from the vascular space to the tissues. Disruption of vascular integrity is involved in the pathogenesis of inflammatory diseases including transfusionrelated acute lung injury (TRALI), a most severe nonhemolytic transfusion reaction with symptoms such as dyspnea and/or hypotension and fever. Pulmonary edema, due to i...

The endothelium lining blood vessels serves as a barrier against vascular hyperpermeability, and its maintenance is critical to organ health. Inflammatory mediators evoke tissue edema by disrupting the expression of membrane junctional proteins, which mediate binding between endothelial cell membranes. Endothelial cell-cell junctions form a diffusion barrier between the intravascular and inters...

Aggressive treatment with antibiotics in patients infected with Streptococcus pneumoniae induces release of the bacterial virulence factor pneumolysin (PLY). Days after lungs are sterile, this pore-forming toxin can still induce pulmonary permeability edema in patients, characterized by alveolar/capillary barrier dysfunction and impaired alveolar liquid clearance (ALC). ALC is mainly regulated ...

BACKGROUND Interleukin (IL)-17F is involved in lung inflammation, but the effect of IL-17F on endothelial permeability and its signaling pathway remain ill-defined. The current study sought to investigate the effect of IL-17F on endothelium and assess the role of protein kinase C (PKC) and src-suppressed C kinase substrate (SSeCKS) in this process. METHODS Rat pulmonary microvascular endothel...

Previously, in vivo studies showed that neuropeptide Y (NPY) elevates vascular permeability in isolated lung perfusion preparations, possibly through binding to the NPY Y(3) receptor. The present study used monolayers in a double-chamber culture method under conditions of normoxia (5% CO(2)-20% O(2)-75% N(2)) or hypoxia (5% CO(2)-5% O(2)-90% N(2)) to test the hypothesis that NPY directly affect...

In addition to its effects on vascular tone, nitric oxide (NO) has been suggested to function as a participant in fluid homeostasis affecting interactions between the endothelium and circulating inflammatory cells. The role of NO in the increased microvascular permeability of acute lung injury, however, remains controversial. We investigated the hypothesis that NO opposes increases in pulmonary...

One of the most widely recognized mechanisms to initiate an inflammatory response is calcium entry into endothelial cells.1–3 Recent investigations have demonstrated that there are multiple mechanisms which determine calcium flux into endothelial cells (including ligand gated calcium channels, store operated calcium channels and mechanosensitive channels), and that these different mechanisms ar...