Clark C J, Boswell F, Greer I A, Lyall F
Department of Obstetrics and Gynaecology, Glasgow Royal Infirmary, Scotland.
J Soc Gynecol Investig. 1997 Jan-Feb;4(1):27-33. doi: 10.1016/S1071-5576(96)00057-3.
The purpose of our study was to determine whether the previously reported neutrophil activation that occurs in the maternal circulation of women with preeclampsia is due to a factor (or factors) in serum that increases neutrophil adhesion to endothelial cells.
The extent of neutrophil adhesion to endothelial cells incubated with serum from women with preeclampsia (n = 12) was compared with serum from normal, pregnant women matched for maternal age and gestational age at blood sampling (n = 12). Preeclampsia was defined as persistent diastolic blood pressure above 90 mmHg, with proteinuria greater than 0.3 g per 24 hours, in patients who were normotensive before 20 weeks' gestation. The ability of serum (with and without heat inactivation of the complement system) from both groups of patients to stimulate neutrophil adhesion to endothelial monolayers was tested in a 15-minute quantitative assay using fluorescence-labeled neutrophils. The extent of neutrophil adhesion was quantified indirectly from fluorescence counts.
No significant differences were found regarding neutrophil-endothelial cell adhesion in response to media alone, serum from women with preeclampsia, and serum from normal, pregnant women. This was also the case when the serum was heat inactivated to destroy the complement system. However, heat inactivated serum produced a significantly greater extent of adhesion compared with serum containing an intact complement system, regardless of whether the patient had preeclampsia.
This study found no evidence of a factor in serum from women with preeclampsia that could alter neutrophil-endothelial cell adhesion via a direct effect on the endothelium. However, our data suggest that adhesion may be regulated in an inhibitory manner by the complement system.
