Angiopoietin-2 is increased in septic shock: Evidence for the existence of a circulating factor stimulating its release from human monocytes

Angiopoietin-2 Enhances Survival in Experimental Sepsis Induced by Multidrug-ResistantPseudomonas aeruginosa

“…However, evidence from our group suggests that endothelial cells are not the only site of production of Ang-2 and in the event of sepsis circulating monocytes are able to secrete Ang-2 (Kranidioti et al, 2009). More precisely, it was described that a circulating factor existed in patients with .…”

“…Circulating concentrations of Ang-2 are reported to be considerably increased in patients with sepsis, and their levels are related with disease severity (Giuliano et al, 2007;Orfanos et al, 2007;Kranidioti et al, 2009). It is unclear, however, whether this is a circumstantial association or there is a functional consequence of Ang-2 increased levels related to the course of the disease.…”

Biomarkers of endothelial dysfunction: can they help us deciphering systemic inflammation and sepsis?

“…Other small clinical studies demonstrated that circulating Ang-2 levels correlated with the APACHE and SOFA scoring systems as well as with the 28-day mortality reflecting disease severity and prognosis (Fiedler et al 2006;Kranidioti et al 2009;McCarter et al 2007;Orfanos et al 2007;Thurston et al 2000;Thurston et al 1999;Witzenbichler et al 2005).…”

Angiopoietin-2 associations with the underlying infection and sepsis severity

“…Various studies by us and others have shown that circulating Ang-2 (cAng-2) is increased in severe sepsis/septic shock [7][8][9][10][11][12]. In addition our group has recently provided evidence that endothelial cells (EC) are not the only source of Ang-2 during the septic process [7]; its expression was detected in the supernatants of cultured circulating monocytes from septic patients suffering from ventilator-associated pneumonia (VAP), providing thus evidence that Ang-2 is partly secreted by monocytes as well [7].…”

“…In addition our group has recently provided evidence that endothelial cells (EC) are not the only source of Ang-2 during the septic process [7]; its expression was detected in the supernatants of cultured circulating monocytes from septic patients suffering from ventilator-associated pneumonia (VAP), providing thus evidence that Ang-2 is partly secreted by monocytes as well [7]. More recent work has provided evidence for an antiinflammatory-protective role of Ang-2; in a murine septic model pre-treatment with Ang-2 prolonged survival from lethal infection by Pseudomonas aeruginosa [13].…”