Both the innate and adaptive immune responses depend on the migration of leukocytes across endothelial cells. Inhibition of leukocyte migration into the target organs may be an effective
therapeutic approach for diseases in which inflammation has noxious effects. ICAM-1, which controls the firm adhesion of neutrophils on endothelium and consequently transendothelial neutrophil migration response to sites of infection, has been studied in relation to sepsis severity and outcome. However, the results of these investigations are inconsistent and occasionally contradictory, possibly due to the precise time point in illness at which they were measured. ICAM-1 production is induced by endotoxins and has been shown to be associated with increasing sepsis sever-
ity or mortality , while sICAM-1 appears to be a reliable biomarker for classifying patients with infectious SIRS, i.e.sepsis, from those with non-infectious SIRS. Data from a very
recent study, suggested that serum levels of sICAM-1 may serve as indicators of the current and subsequent respiratory dysfunction in patients with systemic sclerosis. In our study, sICAM-admission levels did not show any differentiation between patients who subsequently became septic and those who did not.The selectin family is an early mediator of the adhesion of activated neutrophils to endothelia in inflammatory states before their firm adhesion and diapedesis at sites of tissue injury and inflammation; a phenomenon that has been implicated in the pathogenesis of sepsis and organ failure. Soluble E-selectin is present at very low levels in healthy humans. Its concentration increases in various inflammatory pathologies while other investigations have shown higher levels in non survivors than survivors. A recent publication by de Pablo et al. showed that particularly attractive candidate as a target in the treatment of patients with SIRS, especially in septic shock. Moreover,sE-selectin has also been proposed as a predictor of bacteremia in severe sepsis patients. P-selectin has a similar function,but is constitutively expressed in lung ECs, and correlates with
lung endothelial injury.
Both the innate and adaptive immune responses depend on the migration of leukocytes across endothelial cells. Inhibition of leukocyte migration into the target organs may be an effectivetherapeutic approach for diseases in which inflammation has noxious effects. ICAM-1, which controls the firm adhesion of neutrophils on endothelium and consequently transendothelial neutrophil migration response to sites of infection, has been studied in relation to sepsis severity and outcome. However, the results of these investigations are inconsistent and occasionally contradictory, possibly due to the precise time point in illness at which they were measured. ICAM-1 production is induced by endotoxins and has been shown to be associated with increasing sepsis sever-ity or mortality , while sICAM-1 appears to be a reliable biomarker for classifying patients with infectious SIRS, i.e.sepsis, from those with non-infectious SIRS. Data from a veryrecent study, suggested that serum levels of sICAM-1 may serve as indicators of the current and subsequent respiratory dysfunction in patients with systemic sclerosis. In our study, sICAM-admission levels did not show any differentiation between patients who subsequently became septic and those who did not.The selectin family is an early mediator of the adhesion of activated neutrophils to endothelia in inflammatory states before their firm adhesion and diapedesis at sites of tissue injury and inflammation; a phenomenon that has been implicated in the pathogenesis of sepsis and organ failure. Soluble E-selectin is present at very low levels in healthy humans. Its concentration increases in various inflammatory pathologies while other investigations have shown higher levels in non survivors than survivors. A recent publication by de Pablo et al. showed that particularly attractive candidate as a target in the treatment of patients with SIRS, especially in septic shock. Moreover,sE-selectin has also been proposed as a predictor of bacteremia in severe sepsis patients. P-selectin has a similar function,but is constitutively expressed in lung ECs, and correlates withlung endothelial injury.
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