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Elevated IL‐6 in Midtrimester Amniotic Fluid Is Involved with the Onset of Preeclampsia
Author(s) -
Nakabayashi Masao,
Sakura Mari,
Takeda Yoshihiko,
Sato Kodo
Publication year - 1998
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.1998.tb00526.x
Subject(s) - preeclampsia , amniotic fluid , medicine , thrombomodulin , cytokine , gestation , pathogenesis , interleukin 6 , tumor necrosis factor alpha , pregnancy , immunology , endocrinology , andrology , fetus , biology , thrombin , genetics , platelet
PROBLEM: The primary defect of placental development in preeclampsia is speculated to occur at midtrimester gestation. Abnormal feto‐maternal immune reactions have been considered as factors in such defective placentation. METHOD OF STUDY: Midtrimester amniotic fluid specimens were retrospectively identified as coming from gestations that later had severe preeclampsia develop, gestations with normal outcomes, and gestations measured for cytokines tumor necrosis factor‐α (TNF‐α), interleukin (IL‐1β, IL‐6, and IL‐8). The effect of each cytokine on thrombomodulin levels was tested in cultured trophoblast cells. RESULTS: Among the measured cytokines, IL‐6 and IL‐8 were significantly elevated in the midtrimester amniotic fluid of the future preeclamptic group. Trophoblasts stimulated with TNF‐α plus IL‐6 had significantly decreased levels of cellular thrombomodulin compared to those without cytokine addition. CONCLUSIONS: Elevated cytokines in midtrimester amniotic fluid suggest an abnormal fetomaternal immune response occurring before the clinical manifestation of preeclampsia. Cytokine‐induced suppression of thrombomodulin in trophoblasts may be directly involved in the pathogenesis of preeclampsia.