Kristen A Cadden1, Scott W Walsh. 1. Department of Obstetrics and Gynecology, Virginia Commonwealth University Medical Center, Richmond, Virginia 23298-0034, USA.
Abstract
OBJECTIVE: Leukocytes are activated in women with preeclampsia, but the class of leukocytes that infiltrates the maternal vasculature and, therefore, is most likely to cause vascular dysfunction is not known. METHODS: Subcutaneous fat biopsies were obtained at Cesarean section or abdominal surgery from 7 normal non-pregnant women, 7 women with normal pregnancies, and 7 women with preeclampsia. Tissues were immunohistochemically stained for CD14, a monocyte/macrophage antigen, CD99, a lymphocyte antigen, and CD66b, a neutrophil antigen. RESULTS: CD14 stained cells were found infiltrated into fat tissue but were not present in vessels for any of the groups. CD99-stained cells were present in approximately 20% to 30% of vessels with no difference among groups. CD66b-stained cells were present in all groups with a significantly greater percentage of vessels stained for preeclamptic than normal pregnant or normal non-pregnant women (70 +/- 6 vs. 43 +/- 9 vs. 21 +/- 5%, respectively, p < 0.01). CD66b cells were the most abundant cell type that infiltrated vessels of preeclamptic women. CONCLUSIONS: 1) A significantly greater number of neutrophils adhered to endothelium and infiltrated into the intimal space in the maternal systemic vasculature of preeclamptic women than in that of normal pregnant women or normal non-pregnant women; 2) No significant difference in lymphocyte infiltration was observed among the patient groups, and lymphocytes were present in much lower numbers than-neutrophils; 3) Monocytes/macrophages were found in fat tissue but not in vessels. We speculate that neutrophils are the class of leukocytes that cause the majority of vascular cell dysfunction in women with preeclampsia.
OBJECTIVE: Leukocytes are activated in women with preeclampsia, but the class of leukocytes that infiltrates the maternal vasculature and, therefore, is most likely to cause vascular dysfunction is not known. METHODS: Subcutaneous fat biopsies were obtained at Cesarean section or abdominal surgery from 7 normal non-pregnant women, 7 women with normal pregnancies, and 7 women with preeclampsia. Tissues were immunohistochemically stained for CD14, a monocyte/macrophage antigen, CD99, a lymphocyte antigen, and CD66b, a neutrophil antigen. RESULTS:CD14 stained cells were found infiltrated into fat tissue but were not present in vessels for any of the groups. CD99-stained cells were present in approximately 20% to 30% of vessels with no difference among groups. CD66b-stained cells were present in all groups with a significantly greater percentage of vessels stained for preeclamptic than normal pregnant or normal non-pregnant women (70 +/- 6 vs. 43 +/- 9 vs. 21 +/- 5%, respectively, p < 0.01). CD66b cells were the most abundant cell type that infiltrated vessels of preeclamptic women. CONCLUSIONS: 1) A significantly greater number of neutrophils adhered to endothelium and infiltrated into the intimal space in the maternal systemic vasculature of preeclamptic women than in that of normal pregnant women or normal non-pregnant women; 2) No significant difference in lymphocyte infiltration was observed among the patient groups, and lymphocytes were present in much lower numbers than-neutrophils; 3) Monocytes/macrophages were found in fat tissue but not in vessels. We speculate that neutrophils are the class of leukocytes that cause the majority of vascular cell dysfunction in women with preeclampsia.
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