Pulmonary endothelium in acute lung injury: from basic science to the critically ill

Abstract

We highlight pathogenic mechanisms of pulmonary endothelial injury and their clinical implications in ALI/ARDS patients.

Angiopoietin-2 is increased in severe sepsis: Correlation with inflammatory mediators

“…Sepsis is characterized by a generalized overwhelming inflammatory process and a widespread endothelial dysfunction, leading to thrombosis and increased vascular leak (21)(22)(23). Because Ang-2 is up-regulated by diverse proinflammatory stimuli and promotes inflammation and vascular leakage, it might participate in the ongoing inflammatory process during sepsis.…”

Lipopolysaccharide Impaired the Functional Activity of Endothelial Colony-Forming Cells

“…Although LPS is often used as a stimulus for lung injury in several species [2,3,4], the pathophysiology of LPS-induced lung injury is not thoroughly well known. Recent studies have demonstrated that destruction of pulmonary endothelium is one of the main histological changes in the lung tissue in ALI during the acute exudative phase [5]. Activation and damage of pulmonary endothelium is the hallmark of ALI, so endothelial repair after vascular injury is important for the prevention and treatment of ALI.…”

Role of endothelial injury in disease mechanisms and contribution of progenitor cells in mediating endothelial repair

“…Inflammation also induces upregulation of adhesion molecules on the cell surface of endothelial cells which significantly contribute to the local recruitment of leukocytes. Some of these adhesion molecules such as the leukocyte adhesion molecule Pselectin, which is stored preformed within endothelial cells, can appear on the endothelial surface within minutes after stimulation by histamine, thrombin, bradykinin, leukotriene, compliment component C4 or free radicals (Orfanos et al 2004). Others such as E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular cellular adhesion molecule-1 (VCAM-1) are upregulated through transcriptional gene regulation in endothelial cells and appear hours after inflammation (Granger and Kubes 1994).…”