Abstract
Endothelial injury is common to all pathological features of preeclampsia. Neutrophil
activation has been implicated in the pathophysiology of preeclampsia and requires
binding and transmigration of neutrophils through the endothelium. This occurs via
an interaction of endothelial adhesion molecules and surface receptors on neutrophils.
Upon activation, neutrophil granules are released, the contents of which are capable
of mediating vascular damage. In addition, leukotrienes are synthesized, and superoxide
is generated in a respiratory burst. These products also provoke vascular damage.
Neutrophil recruitment to the endothelium involves expression of P-selectin and release
of platelet activating factor from the endothelium. In preeclampsia there is evidence
of an increase in neutrophil activation with up-regulation of neutrophil integrin
expression and increased release of the protease elastase. Furthermore, these markers
neutrophil activation correlate with established markers of disease severity. The
primary mechanism of neutrophil activation is unknown, but neutrophils in preeclampsia
appear to have normal motor activity. Several potential mechanisms of neutrophil activation
have been identified. They include up-regulation of cellular adhesion molecules on
the endothelial surface, increased generation of tumor necrosis factor-α, and endothelial
activation from hyperlipidemia. In addition to activation of neutrophils in preeclampsia,
there may be involvement of interleukin-6 and endothelin-1 in “priming” neutrophils
for subsequent superoxide production. Activated neutrophils are likely to play a large
part in the arteriopathy and endothelial damage associated with preeclampsia, but
it is unclear whether neutrophil activation is the cause or the consequence of endothelial
damage.
Keywords:
Neutrophil - preeclampsia - pregnancy
