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Human Reproduction, Vol. 15, No. 10, 2234-2240, October 2000
© 2000 European Society of Human Reproduction and Embryology

Chorioamnionitis decreased incidence of respiratory distress syndrome by elevating fetal interleukin-6 serum concentration

Koichiro Shimoya1,2,7, Takeshi Taniguchi3, Noboru Matsuzaki4, Akihiro Moriyama1, Yuji Murata1, Hiroyuki Kitajima5, Masanori Fujimura5 and Masahiro Nakayama6

1 Department of Obstetrics and Gynecology, Faculty of Medicine Osaka University, 2 Department of Obstetrics and Gynecology, Osaka Police Hospital, 3 Department of Obstetrics and Gynecology, Taniguchi Hospital, 4 Department of Obstetrics and Gynecology, Ikeda City Hospital, 5 Department of Neonatal Medicine and 6 Pathology, Osaka Medical Center and Research Institute for Maternal and Child Health, Osaka, Japan

Respiratory distress syndrome (RDS) of newborns is one of the most important factors determining neonatal morbidity and mortality. The interleukin-6 (IL-6) titre in cord sera of RDS-free neonates born to mothers with histological chorioamnionitis was significantly higher than that in RDS-complicated neonates without chorioamnionitis. Maternal administration of glucocorticoid suppressed the IL-6 concentrations in the cord sera of fetuses with chorioamnionitis. The fetuses without chorioamnionitis who suffered from RDS even after maternal glucocorticoid administration showed a similar IL-6 titre to that of RDS-affected neonates without chorioamnionitis. Examination of the mechanism by which IL-6 decreased the incidence of fetal RDS revealed that H441-4, a human pulmonary adenocarcinoma cell line, stimulated with recombinant (r)-IL-6 started the synthesis of mRNA and protein of pulmonary surfactant protein (SP)-A. The present study shows that IL-6 elevation in fetuses with chorioamnionitis promotes fetal lung maturation by inducing SP-A synthesis, thereby decreasing the incidence of RDS in the preterm neonates.

Key words: chorioamnionitis/interleukin-6/respiratory distress syndrome/surfactant protein

7 To whom correspondence should be addressed at: Department of Obstetrics and Gynecology, Faculty of Medicine, Osaka University, 2–2 Yamada-oka, Suita City, Osaka 565-0871, Japan.E-mail: shimoya{at}gyne.med.osaka-u.ac.jp


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