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Regular Article |
a Department of Obstetrics and Gynaecology, Melbourne University, Mercy Hospital for Women, East Melbourne, Victoria 3002, Australia
b Gynaecological Cancer Research Centre, Royal Women's Hospital, Carlton, Victoria 3053, Australia
Proinflammatory cytokines are implicated in the initiation and progression of human labor and delivery, particularly in relation to infection-induced preterm labor. In nongestational tissues, the nuclear factor kappa B (NF-
B) transcription pathway is a key regulator of proinflammatory cytokine release. In these tissues, sulfasalazine (SASP), through its ability to inhibit NF-B activation, inhibits release of interleukin (IL)-2, IL-12, and tumor necrosis factor (TNF)-
. Therefore, the aim of this study was to investigate whether or not NF-B activation regulates the formation of proinflammatory cytokines in human gestational tissues. Human placenta, amnion, and choriodecidua (n = 9 separate placentas) were incubated with 10 µg/ml of lipopolysaccharide (LPS) in the absence (control) or presence of SASP (0.1, 1, 5, or 10 mM). After 6 h of incubation, the tissues were collected, and NF-B DNA binding activity in nuclear extracts was assessed by electromobility shift binding assay. The incubation medium was collected and the release of IL-6, IL-8, and TNF- was quantified by ELISA. Treatment of placenta, amnion, and choriodecidua with SASP at concentrations 5 mM or greater significantly inhibited the release of IL-6, IL-8, and TNF-, and NF-B activation (ANOVA, P < 0.05). The data presented in this study demonstrate that the NF-B transcription pathway is a key regulator of LPS-stimulated IL-6, IL-8, and TNF- release from human gestational tissues. The control of NF-B activation may therefore provide an alternative therapeutic strategy for reducing the release of proinflammatory mediators in infection associated preterm labor.
1 This work was funded by National Health and Medical Research Council (NHMRC) grant 960232 and the 3AW Community Trust Foundation. G.E.R. was in receipt of a Principal Research Fellowship from NHMRC.
2 Correspondence: Martha Lappas, Department of Obstetrics and Gynecology, University of Melbourne, Mercy Hospital for Women, 126 Clarendon Street, East Melbourne, Victoria 3002, Australia. FAX: 61 3 9417 5406; mlappas{at}unimelb.edu.au
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