Study of plasma factors associated with neutrophil activation and lipid peroxidation in preeclampsia

Neutrophil activation occurs in women with preeclampsia and is resolved aft er delivery. The present study examined whether circulating factors in plas ma of women with preeclampsia caused neutrophil activation and lipid peroxi dation. Twenty-one women with proteinuric preeclampsia were matched for age and gestational age with 19 normal pregnant women. Plasma was collected fr om all subjects before delivery and at 6 weeks postpartum and incubated wit h autologous white-cell buffy coat collected at the postpartum visit. Neutr ophil activation was assessed by level of CD11b and CD18 expression after i ncubation with autologous antepartum or postpartum plasma. Lipid peroxidati on was assessed by measurement of F-2-isoprostanes in plasma, plasma-white cell incubates, and urine. Neutrophil CD11b and CD18 expression was not dif ferentially altered by incubation with plasma from either women with preecl ampsia or normal pregnant women and was similar between groups when incubat ion was performed with plasma collected after delivery. In preeclampsia, pl asma F-2-isoprostanes were significantly increased before and after deliver y compared with controls. Plasma F-2-isoprostanes were increased 2-fold aft er incubation of plasma with buffy coat, but preeclamptic women had higher levels compared with those of controls when either pregnant or postpartum p lasma was used. In pregnant preeclamptics, plasma F-2-isoprostanes were pos itively correlated with lymphocyte count. Six weeks after delivery, plasma F-2-isoprostanes in the preeclamptic Women were significantly positively as sociated with lymphocyte count and cholesterol and negatively associated wi th albumin. In conclusion, the present study does not suggest that a stable circulating factor causes neutrophil activation in preeclampsia. However, lipid peroxidation is elevated before and after delivery in women with pree clampsia, which suggests that these women may have an underlying predisposi tion to increased oxidative stress that may be driven by or contribute to a persistent low-grade inflammatory response.