Preeclampsia is a potentially life-threatening disease for both mother and
fetus. Endothelial dysfunction is pivotal in the pathogenesis of this disor
der, possibly reflecting a state of persistent inflammation. In the present
study, we examined whether signs of inflammation with production of chemok
ines and leukocyte activation were present in the fetal circulation during
preeclampsia. Venous cord blood was sampled during cesarean sections from 3
6 neonates born after uncomplicated pregnancies and from 35 born after seve
re preeclamptic pregnancies with premature newborns. The expression of adhe
sion molecules on neutrophils and monocytes was analyzed by flow cytometry,
and plasma levels of chemokines and soluble adhesion molecules were analyz
ed by enzyme immunoassay. Newborns of preeclamptic mothers had increased ex
pression of CD15s (P=0.003), CD49d/CD29 (P=0.01/0.005), and CD31 (P=0.007)
on neutrophils and CD15s (P<0.001), CD11c (P=0.009), and CD54 (P=0.001) on
monocytes. This activation of neutrophils and monocytes was accompanied by
raised plasma levels of the CXC chemokines interleukin-8 (P=0.007) and grow
th-related oncogene-a (P=0.01) and decreased plasma levels of soluble E-sel
ectin (P=0.001) and L-selectin (P=0.002). Although raised levels of adhesio
n molecules on leukocytes or decreased levels of soluble adhesion molecules
in plasma were not related to prematurity or the degree of preeclampsia, r
aised interleukin-8 levels were found only in neonates of preeclamptic moth
ers with the highest blood pressures. Our findings suggest the activation o
f neutrophils and monocytes in the fetus during preeclampsia involving enha
nced chemokine activation, possibly contributing to the fetal morbidity of
this disorder.