The role of membrane-bound E-selectin in pathology is well understood, but that of the soluble form is a subject of ongoing controversy, as are the mechanisms of increased concentrations
of plasma soluble adhesion molecules during inflammation, which probably involve the proteolytic cleavage of transmembrane proteins. E-selectin is exclusively expressed on activated ECs,
hence the levels of its soluble form may provide a circulating surrogate for measurement of endothelial damage or activation.Soluble E-selectin levels in vivo are endotoxin dose dependent,
thus the interest of this soluble molecule as a quantitative marker of inflammation-induced endothelial activation.A recent study by Wang et al. demonstrated in patients hospitalized for infections that higher baseline levels of interleu-kin-6, sE-selectin and sICAM-1 may differentiate those patients who will develop a mild response to infection from those who will
develop full blown sepsis. The authors raised the question whether blocking the production of these cytokines could attenuate sepsis risk. Our study differs from the one by Wang et al.; further to some disparity in terminology, their cohort contained African Americans and Whites with no information on ICU hospitalization. Our group consisted of Caucasian critically ill patients who were studied at a very specific time-point, i.e. at ICU admission, suffering from various conditions not necessarily related to infections. In addition, genetic polymorphisms have been identified for the
secretion of E-selectin and these may also account for discrepancies between studies.
The role of membrane-bound E-selectin in pathology is well understood, but that of the soluble form is a subject of ongoing controversy, as are the mechanisms of increased concentrations
of plasma soluble adhesion molecules during inflammation, which probably involve the proteolytic cleavage of transmembrane proteins. E-selectin is exclusively expressed on activated ECs,
hence the levels of its soluble form may provide a circulating surrogate for measurement of endothelial damage or activation.Soluble E-selectin levels in vivo are endotoxin dose dependent,
thus the interest of this soluble molecule as a quantitative marker of inflammation-induced endothelial activation.A recent study by Wang et al. demonstrated in patients hospitalized for infections that higher baseline levels of interleu-kin-6, sE-selectin and sICAM-1 may differentiate those patients who will develop a mild response to infection from those who will
develop full blown sepsis. The authors raised the question whether blocking the production of these cytokines could attenuate sepsis risk. Our study differs from the one by Wang et al.; further to some disparity in terminology, their cohort contained African Americans and Whites with no information on ICU hospitalization. Our group consisted of Caucasian critically ill patients who were studied at a very specific time-point, i.e. at ICU admission, suffering from various conditions not necessarily related to infections. In addition, genetic polymorphisms have been identified for the
secretion of E-selectin and these may also account for discrepancies between studies.
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