Interaction of paracrine factors during labour: interleukin-1 beta causes amplification of decidua cell prostaglandin F2 alpha production in response to bradykinin and epidermal growth factor.

Inflammatory mediators have been implicated in the stimulation of decidual prostaglandin (PG) production during infection-driven preterm labour. The aim of the present study is to investigate a potential interaction between interleukin-1 beta (IL-1) and bradykinin (BK) in the regulation of decidual PGF2 alpha production and PG precursor release. Pretreatment of primary decidua cell cultures with IL-1 significantly enhanced PGF2 alpha production in response to BK. This effect was accompanied by an increase in unesterified arachidonic acid and an enhanced turnover of arachidonoyl phosphatidate. Bradykinin also stimulated arachidonic acid release in decidual fibroblasts, an effect which was potentiated in the presence of epidermal growth factor (EGF), but which was not accompanied by an increase in PGF2 alpha production. Decidual fibroblasts pretreated with IL-1 manifest a 10-fold increase in PGF2 alpha production in response to BK and EGF. These observations provide the first description of synergism between cytokine, kinin and growth factor in the uterine decidua which may partly mediate the in vivo increase in prostaglandin production associated with decidual activation and infection-driven labour.