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

Abstract

OBJECTIVE:

To evaluate the modulatory effects of interleukin (IL)-1beta 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)-1beta or PGE2. Cultures were also incubated in high concentrations of IL-1beta 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-1beta administration. EP1 receptor levels also increased approximately fourfold in response to IL-1beta incubation even in the presence of high agonist (PGE2) concentrations (P < .01).

CONCLUSION:

The results of this study show that IL-1beta 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.

• Authors: E P Spaziani, W F O'Brien, J C Tsibris, R R Benoit, S F Gould
• Journal: Obstetrics and gynecology (Obstet Gynecol) Vol. 93 Issue 1 Pg. 84-8 (Jan 1999) ISSN: 0029-7844 [Print] United States
• PMID: 9916962 (Publication Type: Journal Article)

Chemical References

• Interleukin-1
• Receptors, Prostaglandin E
• Dinoprostone

Topics

• Cells, Cultured
• Dinoprostone (physiology)
• Female
• Humans
• Interleukin-1 (physiology)
• Obstetric Labor, Premature (microbiology)
• Pregnancy
• Pregnancy Complications, Infectious
• Receptors, Prostaglandin E (metabolism)