[A biochemical study on the effects of interleukin-6 for premature rupture of membranes].

Chorioamnionitis was thought to be a cause of premature rupture of membranes (PROM). Recently it has been accepted that IL-6 is one of the important cytokines in inflammation. To investigate the correlation between PROM and IL-6, IL-6 production in chorionic cells and amniotic cells was examined. Moreover, the response of these cells to IL-6 was also examined. The results were as follows. 1. Chorionic cells and amniotic cells obtained from human membranes were cultured. 2. Comparing IL-6 production, chorionic cells produced a larger amount of IL-6 (425pg/ml/24 hrs) than amniotic cells (4pg/ml/24 hrs). 3. IL-1 treatment (10U/ml) caused a significant increase in IL-6 release from both chorionic and amniotic cells (43.2ng/ml/24hrs vs. 50.3pg/ml/24hrs, respectively). 4. Lipopolysaccharide (LPS) (10 micrograms/ml) stimulated the release of IL-6 in chorionic cells, but did not affect it in amniotic cells at all. 5. By staining with F actin, it was demonstrated that IL-6 expanded the cellular gap in amniotic cells. 6. After amniotic cells were co-cultured with chorionic cells, IL-1 treatment caused actin-polymerization in amniotic cells. These results suggest that chorionic cells produce a large amount of IL-6 as a result of stimulation by IL-1 or LPS, and the IL-6 produced constricts the amniotic cells. The phenomena may participate in the mechanism of PROM.