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Maternal leukocyte CD markers, apoptosis and band forms in preeclampsia Fuchisawa, Akiko


INTRODUCTION: Preeclampsia is a pregnancy-specific condition, and it still remains one of the most common causes of maternal mortality in the developed world. Although the exact cause of preeclampsia has not been identified, it is most widely accepted that preeclampsia results from incomplete placentation. Interestingly, normotensive intrauterine growth restriction also shows the same defect of placentation. In preeclampsia, the maternal syndrome develops from a number of alternative pathways leading to uteroplacental mismatch and, consequently, the release of endothelium-activating factors. This research is focused on neutrophil activation and the hypothesis for this research was that maternal neutrophils and monocytes are inappropriately activated in preeclampsia but not in normotensive intrauterine growth restriction. METHODS: This was a prospective controlled cohort study in a tertiary center. Subjects consisted of cases: women with early-onset preeclampsia (<34+0wk; EOPET), late-onset preeclampsia (≧34+0wk; LOPET), normotensive intrauterine growth restriction and controls: normal pregnancy controls (NPC) and non-pregnant controls (non-preg). Peripheral blood leukocytes were analyzed immediately after phlebotomy for CD11b, CD18, CD14 and band forms (marrow production). Neutrophils were cultured for 18-24h and apoptosis was assessed by Annexin V binding and hypodiploid PI. All analyses were by flow cytometry. Kruskal Wallis, Mann Whitney U and Dunn's post test were used for statistical analysis (significance at p<0.05). RESULTS: CD11b/CD18 monocyte expression was increased in pregnancy (all groups). CD18 expression was reduced on preeclampsia lymphocytes. CD14 expression was reduced on preeclampsia granulocytes. Gestational age-dependent decrease was noted for apoptosis in normal pregnancy. Band forms were increased in all pregnancy groups, with no difference seen between normal and abnormal pregnancy. CONCLUSIONS: Normal pregnancy is a state of Th1-to-Th2 switch. In preeclampsia, some findings noted by ourselves and others were not reproduced, probably due to steroid effects. Decreased CD18 on preeclampsia lymphocytes implies excess Th1 activity in preeclampsia. Preeclampsia granulocytes shed CD14, probably in response to prior activation. There was a gestational age effect on neutrophil apoptosis, as previously noted. However, neutrophil apoptosis was not inappropriately delayed in preeclampsia, probably due to steroid effects. Marrow production of neutrophils is similarly increased in all pregnancy groups.

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