Pn. Rauk et Jp. Chiao, Oxytocin signaling in human myometrium is impaired by prolonged exposure to interleukin-1, BIOL REPROD, 63(3), 2000, pp. 846-850
Intra-amniotic infection leads to preterm labor and is associated with the
local release of inflammatory cytokines by fetal membranes, resulting in th
e production of uterotonic prostaglandins, Oxytocin, however, also plays a
key role in the initiation of labor, Short-term exposure of myometrium to i
nterleukin (IL)-1 enhances oxytocin signaling and contractility, With intra
uterine infection, however, myometrium is exposed to inflammatory cytokines
for prolonged periods. The present study was conducted to demonstrate that
myometrial oxytocin signaling is significantly impaired following prolonge
d exposure to IL-1, Myometrial cells were treated with IL-1 for 24 h. Oxyto
cin-stimulated inositol trisphosphate (IP3) production was measured in trit
iated myoinositol-loaded myometrial cells. Arachidonic acid (AA) release wa
s measured in tritiated AA-loaded myometrial cells. Increases in intracellu
lar calcium were measure with fluo-3. Prostaglandin (PC) F-2 alpha and 6-ke
to-PGF(1 alpha) were measured by ELISA assay, Prolonged exposure of myometr
ial cells to IL-1 resulted in a significant reduction in oxytocin-mediated
signaling as measured by IP3 production and AA release, as well as a decrea
se in intracellular calcium. Prolonged exposure of myometrial cells to IL-1
, however, resulted in enhanced PC release. Oxytocin may not contribute sig
nificantly to the labor-inducing action of IL-1 in the setting of preterm l
abor with prolonged infection.