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and IL-10 Regulate Lipopolysaccharide-Stimulated Human Choriodecidual Cytokine and Prostaglandin E2 Production1
Liggins Institute and Division of Pharmacology and Clinical Pharmacology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand
Increased production of PGs by gestational membranes is
believed to be a principal initiator of term and preterm labor.
Intrauterine infection is associated with an inflammatory response in
the choriodecidua characterized by elevated production of cytokines and
PGs. The precise physiological significance of enhanced choriodecidual
cytokine production in the mechanism of preterm labor remains
uncertain. These studies were undertaken to dissect the roles and
regulation of endogenous cytokines in regulating PG production by human
choriodecidua. We used LPS treatment of human choriodecidual explants
as our model system. In choriodecidual explant cultures, LPS (5
µg/ml) induced a rapid increase in TNF-
production, peaking at
4 h. In contrast, IL-10, IL-1
, and PGE2 production
rates peaked 8, 12, and 24 h, respectively, after LPS stimulation.
Immunoneutralization studies indicated that TNF- was a primary
regulator of IL-1, IL-10, and PGE2 production, while
IL-1 stimulated only PGE2 production. Neutralization of
endogenous IL-10 resulted in increased TNF- and PGE2
production. IL-10 treatment markedly decreased TNF- and IL-1
production, but had no effect on PGE2 production. Taken
together, these results demonstrate that the effects of LPS on
choriodecidual cytokine and PG production are modulated by both
positive and negative feedback loops. In the setting of an infection of
the intrauterine, TNF- may be a potential target for treatment
intervention; IL-10 could be one such therapeutic.
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