particularly attractive candidate as a target in the treatment of
patients with SIRS, especially in septic shock [33]. Moreover,
sE-selectin has also been proposed as a predictor of bacteremia
in severe sepsis patients [44]. P-selectin has a similar function,
but is constitutively expressed in lung ECs, and correlates with
lung endothelial injury [45].
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
[46]. 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 [47].
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 [48].
A recent study by Wang et al. [49] demonstrated in patients
hospitalized for infections that higher baseline levels of interleukin-
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. [49]; 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 [50].