Neutrophil-derived reactive oxygen species can modulate neutrophil adhesion to endothelial cells in preeclampsia

Neutrophil activation has been implicated in the pathophysiology of preeclampsia. The aim of this study was to investigate whether neutrophil-derived reactive oxygen species (ROS) modulate adhesion to endothelial cells in preeclampsia.

We first assessed neutrophil superoxide production and neutrophil-endothelial cell adhesion in normal nonpregnant women (n = 8), normal pregnant women (n = 10), and preeclamptic pregnant women (n = 8). We then examined the effects of neutrophil-derived ROS on neutrophil-endothelial adhesion. The release of neutrophil superoxide was measured using cytochrome C reduction.

N-formyl-methionyl-leucyl-phenylalanine (FMLP)-stimulated superoxide production by neutrophils was significantly increased in women with preeclampsia when compared with the other two groups. Neutrophils from women with preeclampsia were more likely to adhere to endothelial cells, than were those from the other two groups (mean adhesion rate +/- s.d. (%); 20.6 +/- 2.7 in preeclampsia, 10.2 +/- 1.2 in normal pregnancy, 11.0 +/- 0.9 in normal nonpregnancy, P < 0.01). Superoxide dismutase (SOD), which dismutates the excess superoxide to hydrogen peroxide, did not affect neutrophil-endothelial adhesion. In contrast, catalase, which catalyzes the conversion of hydrogen peroxide to oxygen and water, inhibited neutrophil-endothelial adhesion in the preeclamptic group (8.1 +/- 0.5%, P < 0.01).

Neutrophils from women with preeclampsia demonstrate increased CD11b expression and adhesion to endothelial cells. This is likely caused by elevations in superoxide and its derivative, hydrogen peroxide.