CHORIOAMNIONITIS REDUCES PLACENTAL ENDOCRINE FUNCTIONS - THE ROLE OF BACTERIAL LIPOPOLYSACCHARIDE AND SUPEROXIDE ANION

Chorioamnionitis has been shown to be one of the most important factor s in inducing preterm delivery. The present study was undertaken to ex amine the effects oi chorioamnionitis on placental endocrine functions . Preterm placentas with histologic chorioamnionitis produced smaller amounts of human chorionic gonadotropin (hCG) and human placental lact ogen (hPL) than those without chorioamnionitis (P<0.001). To examine t he mechanism involved in tile suppression of placental endocrine funct ions induced by chorioamnionitis, we initially confirmed the expressio n of lipopolysaccharide (LPS) receptor, i.e. the CD14 molecule, on tro phoblasts by Northern blot analysis and immunohistochemistry. We then stimulated purified trophoblasts with LPS, which is the major agent wh ich induces inflammatory responses in the host via the LPS receptor. T he trophoblasts stimulated with LPS produced reduced amounts of hCG, h PL, and progesterone in a time-and dose-dependent fashion in spite of the induced manganese-superoxide dismutase (SOD) synthesis. Stimulatio n of trophoblasts with hypoxanthine and xanthine oxidase resulted in s uppressed hCG production, while the simultaneous addition of SOD into the culture medium, reversed the suppression of hCG production. LPS in the placenta with chorioamnionitis might directly stimulate trophobla sts through the LPS receptor (CD14), thus reducing placental endocrine functions. Superoxide anions which exogenously act on trophoblasts mi ght be generated by simultaneous stimulation of neutrophils and monocy tes at the feto-maternal interface by LPS, and additively reduce place ntal endocrine functions.