Preeclamptic women are deficient of interleukin-10 as assessed by cytokine release of trophoblast cells in vitro

Background: It is well known that the acceptance of the fetoplacental unit in human pregnancy requires maternal immune tolerance, which is thought to be regulated locally by the placenta. Therefore an anti-inflammatory cytokine such as IL-10 plays a critical role in different pregnancy disorders inc...

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Veröffentlicht in:Cytokine (Philadelphia, Pa.) Pa.), 2003-08, Vol.23 (4), p.119-125
Hauptverfasser: Rein, D.T., Breidenbach, M., Hönscheid, B., Friebe-Hoffmann, U., Engel, H., Göhring, U.-J., Uekermann, L., Kurbacher, C.M., Schöndorf, T.
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Sprache:eng
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Zusammenfassung:Background: It is well known that the acceptance of the fetoplacental unit in human pregnancy requires maternal immune tolerance, which is thought to be regulated locally by the placenta. Therefore an anti-inflammatory cytokine such as IL-10 plays a critical role in different pregnancy disorders including preeclampsia. In the present study, we examined the expression of both proinflammatory (TNF-α, IL-1β, IL-2) and immunoregulatory (IL-6, IL-10) cytokines from normal term and preeclamptic patients in human trophoblast cultures. Methods: Eleven patients with preeclampsia and 11 patients with a normal pregnancy at term were included in the study. Trophoblast cells isolated from placentas were cultured up to 48 h under standard tissue culture conditions and cytokine release was determined by ELISA. IL-10 synthesis was significantly decreased in the third trimester in preeclamptic patients in comparison with the control group. Results: There were no significant differences in IL-1β, IL-2, IL-6 or TNF-α expression but a significant alteration in IL-10 release in trophoblast cultures in vitro in term placentas from preeclamptic patients compared with normal pregnancy. Conclusions: Because IL-10 is a potent regulator of anti-inflammatory immune response these abnormalities may be associated with the inadequate placental development in preeclampsia.
ISSN:1043-4666
1096-0023
DOI:10.1016/S1043-4666(03)00220-5