The induction of cyclooxygenase-2 (COX-2) in intact human amnion tissue by interleukin-4

Eric P. Spaziani, Michael E. Lantz, Raymond R. Benoit, William F. O'Brien

Research output: Contribution to journalArticlepeer-review

Abstract

Infection is a major cause of preterm labor. Amniotic fluid from women in preterm labor associated with intrauterine infection contains increased concentrations of cytokines. The mechanism underlying this association may be a cytokine-mediated stimulation of amnion cell prostaglandin production. The biosynthesis of prostaglandins from arachidonic acid is regulated by the enzyme cyclooxygenase which exists in two forms; the constitutive form (COX- 1) and the other mitogen inducible (COX-2). The purpose of this study was to evaluate the effect of the cytokine interleukin-4 (IL-4) on cyclooxygenase activity and PGE2 production in amnion. Amnion tissue was taken at caesarean section from term women not in labor and immediately incubated for 2 hours in media containing concentrations of IL-4 ranging from 1 to 100 ng/ml. An increase in both COX-2 enzyme and prostaglandin E2 (PGE2) production was observed for all concentrations of IL-4 greater than 25 ng/ml (P < 0.05, n = 8). No change in COX-1 was observed. Our data suggest that the cytokine IL-4 may be involved in the pathogenesis of premature labor by inducing COX-2 in amnion tissue resulting in increased production of PGE2 and subsequent myometrial activity.

Original languageEnglish (US)
Pages (from-to)215-223
Number of pages9
JournalProstaglandins
Volume51
Issue number3
DOIs
StatePublished - Jan 1 1996
Externally publishedYes

Keywords

  • Interleukin-4
  • amnion
  • cyclooxygenase
  • premature labor

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology

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