Endothelial cell activation by tumour necrosis factor-alpha (TNF-α and the development of pre-eclampsia

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Abstract
SUMMARY: Pre-eclampsia may develop as a result of an endothelial activation. Tumour necrosis factor-alpha (TNF-α) activates endothelial cells which release soluble E-selectin, a putative circulating marker specific for endothelial damage. A retrospective longitudinal study of maternal blood samples, collected at different gestational ages in pregnancy, was undertaken to determine whether the development of pre-eclampsia is associated with TNF-α-mediated endothelial activation. This study included 19 women who developed pre-eclampsia and 22 women whose pregnancy outcome was normal. Ten women had blood samples taken before pre-eclampsia was clinically detected and, in all these, TNF-α was below the immunoassay limit of detection (< 80 pg/ml). Five had further samples taken after pre-eclampsia was clinically diagnosed and, initially, TNF-α was still below the lower limit of detection in all five pregnancies, but rose later in three (80, 156 and 250 pg/ml). In nine other patients with diagnosed pre-eclampsia, TNF-α was detected in only two (80 and 650 pg/ml). TNF-α was identified in only one of the 22 normal pregnancies (80 pg/ml), this being at term. There was no statistical difference in soluble E-selectin levels between normal and pre-eclamptic pregnancies, neither before nor after pre-eclampsia was diagnosed. Hence, blood TNF-α levels measured by immunoassay can be elevated in approximately 36% of cases of established preeclampsia, but this rise occurs only after the syndrome is detected clinically. Blood concentrations of TNF-α and soluble E-selectin are not related to severity of the disorder. These findings suggest that circulating TNF-α does not contribute to the initiation of endothelial cell activation that may be associated with the development of pre-eclampsia, but may rise as a consequence of the pathological processes of this disorder.