The Production of IL-1beta and PGE2by Human Decidual Cells aftr Incubation with LPS

Kim, Young Ju; Lee, Kyung Eun; Lee, Eun Hee; Son, Young Soo; Kim, Jong Il; Ahn, Jung Ja; Woo, Bock Hi

Abstract

The mechanisms responsible for the onset of preterm labor in women are poorly understood. It is widely accepted that increased biosynthesis of PGE2 by intrauterine tissues seems to be a key event in the initiation of preterm parturition.However, the mechanisms for the increased PG formation during parturition have not yet been explained.Growing evidednce suggesis an association between intraamniotic infection and preterm labor. It is suggested that bacterial products can signal the increased PG biosynthesis associated with parturition, and that decidua can induce the onset of preterm labor by using inflammatory mediators(for example, IL-1beta) produced in response to bacterial invasion. The purposes of this study were to determine the effect of LPS on the production of IL-1beta and PGE2 and to determine the inhibitory effect of anti-IL-1beta and TGF-beta2 on the production of IL-1beta and PGE2 BY HUMAN DECIDUAL CELLS. The results were as follows : 1. The production of PGE2 AND IL-beta by decidual cells after incubation with LPS for 24 hours culture significantly increased in comparison with controls, respectively. 2. The production of PGE2 by decidual cells after incubation with il-1beta for 24 hours culture significantly increased in comparision with controls. 3. The production of PGE2 by decidual cells after incubation with LPS and anti-IL-1beta for 24 hours culture significantly decreased in comparision with LPS treated groups, respectively. 4. The production of PGE2 by decidual cells after incubation with LPS and TGF-beta2 for 24 hours culture significantly decreased, but IL-1beta production significantly increased in comparision with LPS treated groups. In conclusion, LPS may induce the formation PGE2 through IL-1beta, and LPS induced preterm labor may be prevented by anti-IL-1beta and TGF-beta2.