Modulation of the prostaglandin E receptor: A possible mechanism for infection-induced preterm labor

Objective: To evaluate the modulatory effects of interleukin (IL)-1 beta an d prostaglandin (PG)E-2 on the PGE(2) receptor subtype EP1 in amnion cell c ultures. Methods: Amnion cell cultures were incubated in increasing concentrations o f (IL)-1 beta or PGE,. Cultures were also incubated in high concentrations of IL-1 beta and PGE(2) in combination. Changes in EP1 receptor levels were evaluated by western and northern blot analysis. Culture fluid PGE(2) leve ls were measured by enzyme-linked immunosorbent assay. Results: EP1 receptor protein levels decreased with increasing levels of PG E(2) (v = -0.82, P < .05). EP1 receptor protein (r = 0.95, P < .05), EP1 mR NA (v = 0.95, P < .01), and culture fluid PGE(2) levels (P < .01) were all increased after IL-1 beta administration. EP1 receptor levels also increase d approximately fourfold in response to IL-1 beta incubation even in the pr esence of high agonist (PGE(2)) concentrations (P < .01). Conclusion: The results of this study show that IL-1 beta might be involved in infection-induced preterm labor by interfering with the normal regulati on of EP1 receptor levels and with the promotion of increased PGE(2) produc tion in amnion tissue. (C) 1999 by The American College of Obstetricians an d Gynecologists.