Tumor Necrosis Factor‐α in the Placenta is not Elevated in Pre‐eclamptic Patients Despite its Elevation in Peripheral Blood

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Abstract
Problem: Tumor necrosis factor-α (TNF-α) is present in human placental and uterine cells at the early and late stages of gestation and promotes the regulation of trophoblast growth and invasion. We evaluated whether TNF-α levels in the placenta and blood of pre-eclamptic women differed from those with normal pregnancies. Method of study: The subjects were 39 pregnant women carrying single fetuses (21 normal-pregnant and 18 pre-eclamptic patients). Their average gestational age at entry was 38–39 weeks. Peripheral blood was collected before the onset of labor and separated serum was stored at −20°C. A tissue segment of the placenta was cut and frozen in liquid nitrogen immediately after delivery at −80°C. The frozen placental tissue was added to phosphate-buffered saline. The tissue was fully homogenized and centrifuged. Separated supernatant was stored at −80°C. TNF-α levels in separated serum and TNF-α and total protein (TP) levels in separated supernatant were measured. The presence of TNF-α in the placenta was evaluated by immunohistochemistry in five pre-eclamptic and five normal-pregnant patients. Results: Serum TNF-α levels were higher in pre-eclampsia than in normal pregnancies. However, TNF-α/TP levels in the placenta did not differ significantly between the two groups. As for TNF-α immunostaining of trophoblastic cells in the placenta, it was weak in three and moderate in two of the normal pregnancies, while it was absent in two, weak in one, and moderate in two in the pre-eclampsia group. Conclusions: We demonstrated no significant increase in TNF-α/TP levels in the placenta in pre-eclampsia despite a significant increase in serum TNF-α levels. There was no strong immunostaining for TNF-α detected by immunohistochemistry in the pre-eclampsia group. These findings suggest that TNF-α in the placenta is not a key cytokine to interfere with normal trophoblast invasion into the myometrium in pre-eclampsia, and that sources other than the placenta may contribute to the elevated levels of TNF-α found in the circulation of pre-eclamptic patients.

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