Details

Autor(en) / Beteiligte

• Guzeloglu-Kayisli, Ozlem
• Kayisli, Umit A
• Semerci, Nihan
• Basar, Murat
• Buchwalder, Lynn F
• Buhimschi, Catalin S
• Buhimschi, Irina A
• Arcuri, Felice
• Larsen, Kellie
• Huang, Joseph S
• Schatz, Frederick
• Lockwood, Charles J

Titel

Mechanisms of chorioamnionitis-associated preterm birth: interleukin-1[beta] inhibits progesterone receptor expression in decidual cells

Ist Teil von

• The Journal of pathology, 2015-12, Vol.237 (4), p.423

Ort / Verlag

Bognor Regis: Wiley Subscription Services, Inc

Erscheinungsjahr

2015

Link zum Volltext

Quelle

Wiley Online Library - AutoHoldings Journals

Beschreibungen/Notizen

• In chorioamnionitis (CAM), a major cause of preterm birth (PTB), maternal-fetal inflammation of the decidua and amniochorion cause the release of cytokines that elicit cervical ripening, fetal membrane rupture and myometrial activation. We posit that this inflammatory milieu triggers PTB by inhibiting progesterone receptor (PR) expression and increasing decidual prostaglandin (PG) production. Immunohistochemical staining of decidua detected significantly lower PR levels in decidual cells (DCs) from CAM-complicated PTB. Incubation of DCs with IL-1[beta] decreased PR expression and significantly increased PGE2 and PGF2[alpha] production and COX-2 expression. The addition of PGF2[alpha] to DC cultures also suppressed PR expression. However, the COX inhibitor, indomethacin, did not reverse IL-1[beta] suppression of PR expression in DC cultures. Although IL-1[beta] treatment activated the NF-KB, ERK1/2 and p38 MAPK signalling cascades in DCs, inhibition of ERK1/2 MAPK signalling alone was sufficient to completely reverse the suppression of PR levels by IL-1[beta]. These findings suggest that CAM-associated PTB is induced at least in part by IL-1[beta]-mediated functional progesterone withdrawal. Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.