In preeclampsia, poor placentation is an important predisposing factor and endothelial damage underlies disease manifestations. Although the processes leading to endothelial damage are not fully understood, the maternal innate immune system, particularly neutrophils, has been identified as key players. In preeclampsia there is evidence of increased neutrophil activation, marked by up-regulation of neutrophil integrin expression, and increased production of the protease elastase and reactive oxygen species. Direct evidence of neutrophil mediated endothelial cell damage is also reported. The placenta may release various factors that stimulate neutrophil activation in response to reduced perfusion due to poor placentation. They include increased production of pro-inflammatory cytokines, oxidative damage products, and syncytiotrophoblast microvesicles. The relationship between neutrophil activation and endothelial damage argues for a role for neutrophils in the pathogenesis of preeclampsia. In this review, we focus on the phenotypic and metabolic characteristics of neutrophils in normal pregnancy and preeclampsia in order to identify the potential cellular and molecular processes that contribute to the maternal endothelial damage seen in preeclampsia.