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The production of interleukin‐1β from human fetal membranes is not obligatory for increased prostaglandin output

Bacterial endotoxin increased the expression of mRNA (maximal after 4 hr) for interleukin‐1β (IL‐1β) and the release of mature protein from intact human fetal membranes. In contrast, the change in expression of mRNA for type 2 cyclo‐oxygenase (COX‐2) was biphasic, with peaks after 0·5–1 hr and after 8 hr of culture. An antibody to IL‐1β was without effect after 4 hr of culture, inhibited endotoxin‐stimulated prostaglandin E2 (PGE2) production after 8 hr of culture, and caused a parallel decrease in the expression of mRNA for COX‐2. We conclude that endotoxin induced the expression of COX‐2 through IL‐1β‐independent and IL‐1β‐dependent mechanisms, and these differences are time dependent. Corticotrophin‐releasing hormone (CRH) or platelet‐activating factor (PAF) also increased the expression of mRNA for IL‐1β and the release of IL‐1β from some, but not all, fetal membranes. The antibody to IL‐1β did not affect CRH‐stimulated or PAF‐stimulated PGE2 production or COX‐2 expression. We conclude that CRH and PAF can induce the expression of IL‐1β, but this is not obligatory for increased PGE2 release, and the effect of these stimuli on COX‐2 expression is a direct, IL‐1β‐independent effect.