Modulation of the prostaglandin e receptor: a possible mechanism for infection-induced preterm labor

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Abstract
Objective: To evaluate the modulatory effects of interleukin (IL)-1β and prostaglandin (PG)E2 on the PGE2 receptor subtype EP1 in amnion cell cultures. Methods: Amnion cell cultures were incubated in increasing concentrations of (IL)-1β or PGE2. Cultures were also incubated in high concentrations of IL-1β and PGE2 in combination. Changes in EP1 receptor levels were evaluated by western and northern blot analysis. Culture fluid PGE2 levels were measured by enzyme-linked immunosorbent assay. Results: EP1 receptor protein levels decreased with increasing levels of PGE2 (r = −0.82, P < .05). EP1 receptor protein (r = 0.95, P < .05), EP1 mRNA (r = 0.95, P < .01), and culture fluid PGE2 levels (P < .01) were all increased after IL-1β administration. EP1 receptor levels also increased approximately fourfold in response to IL-1β incubation even in the presence of high agonist (PGE2) concentrations (P < .01). Conclusion: The results of this study show that IL-1β might be involved in infection-induced preterm labor by interfering with the normal regulation of EP1 receptor levels and with the promotion of increased PGE2 production in amnion tissue.

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