Abstract:Summary. The rate of prostaglandin E (PGE) production was measured in collagenase‐dispersed amniotic cells obtained from 14 women after spontaneous labour at term—seven after spontaneous preterm labour, nine after delivery by elective caesarean section at term and six after induction of labour at term. Cells were incubated with and without arachidonic acid and PGE was estimated by specific radioimmunoassay. Basal PGE output (pmol/106 cells per 3 h) was highest in the spontaneous labour group, 27·5 (SEM 5·5) a… Show more
“…There were a few incongruent findings for PGE 2 . Lopez-Bernal et al 1987 found that PGE 2 was produced by chorion and decidual cells and that the production was increased by arachidonic acid treatment, but found no significant change in PGE 2 protein level in labor versus no labor 73 . Similarly, Satoh et al 1981 found that the PGE 2 protein production was the same between labor and non-labor amnion, decidua, and myometrium.…”
Section: Discussionmentioning
confidence: 99%
“…The majority of articles reviewed found an increase in PGE 2 protein at term labor or with in vitro simulated labor. 21, 30, 36, 39, 62, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83…”
Parturition at term is characterized by inflammatory overload in both feto-maternal tissues. Despite the large number of individual studies on changes in inflammatory biomarkers linked to labor, a comprehensive profile of them in each of the uterine compartments is not available to better understand their mechanistic contributions to labor. This systematic review investigated the pro- and anti-inflammatory biomarkers reported in intra-uterine tissues (amnion, chorion, decidua, placenta, and myometrium) at term labor. We conducted a systematic review of studies on pro- and anti-inflammatory biomarkers (mRNA and/or protein) reported in feto-maternal tissues during normal human term labor, published in English (1980-2016), in 3 electronic data bases. From a total of 3712 citations, 172 were included for final review. Each tissue expresses a unique set of biomarkers at the time of term labor, but there is significant overlap between tissues. All tissues had IL-6, IL-8, IL-1β, COX-2, PGE-2, TNF-α, and hCAP18 in common at term labor. Common and unique inflammatory biomarkers are expressed in various feto-maternal compartments at term labor. Increase in pro-inflammatory markers in all gestational tissue signifies their harmonious functional role in promoting labor. Anti-inflammatory markers at term labor are hardly reported.
“…There were a few incongruent findings for PGE 2 . Lopez-Bernal et al 1987 found that PGE 2 was produced by chorion and decidual cells and that the production was increased by arachidonic acid treatment, but found no significant change in PGE 2 protein level in labor versus no labor 73 . Similarly, Satoh et al 1981 found that the PGE 2 protein production was the same between labor and non-labor amnion, decidua, and myometrium.…”
Section: Discussionmentioning
confidence: 99%
“…The majority of articles reviewed found an increase in PGE 2 protein at term labor or with in vitro simulated labor. 21, 30, 36, 39, 62, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83…”
Parturition at term is characterized by inflammatory overload in both feto-maternal tissues. Despite the large number of individual studies on changes in inflammatory biomarkers linked to labor, a comprehensive profile of them in each of the uterine compartments is not available to better understand their mechanistic contributions to labor. This systematic review investigated the pro- and anti-inflammatory biomarkers reported in intra-uterine tissues (amnion, chorion, decidua, placenta, and myometrium) at term labor. We conducted a systematic review of studies on pro- and anti-inflammatory biomarkers (mRNA and/or protein) reported in feto-maternal tissues during normal human term labor, published in English (1980-2016), in 3 electronic data bases. From a total of 3712 citations, 172 were included for final review. Each tissue expresses a unique set of biomarkers at the time of term labor, but there is significant overlap between tissues. All tissues had IL-6, IL-8, IL-1β, COX-2, PGE-2, TNF-α, and hCAP18 in common at term labor. Common and unique inflammatory biomarkers are expressed in various feto-maternal compartments at term labor. Increase in pro-inflammatory markers in all gestational tissue signifies their harmonious functional role in promoting labor. Anti-inflammatory markers at term labor are hardly reported.
“…A number of studies have shown that the fetal membranes are a major source of intrauterine prostaglandins in labour (Kierse & Turnbull 1976, Skinner & Challis 1985. The amnion and decidua are the main synthetic tissues (Okazaki et al 1981, Lopez-Bernal et al 1987, whereas chorionic trophoblast cells have high levels of prostaglandin dehydrogenase to convert the primary prostaglandins to inactive metabolites (Sangha et al 1994). Expression of prostaglandin pathway synthetic enzymes has been clearly demonstrated in both amnion and decidual cells (Mitchell 1987, Romero et al 1988, with increased levels of these enzymes found in the latter stages of pregnancy (Slater et al 1995, and in association with labour (Khan et al 1992, Fuentes et al 1996.…”
Fetal membranes from term human pregnancies produce prostaglandins, and may respond to bacterial endotoxin or interleukin-1ß (IL-1ß) with increased prostaglandin E2 (PGE2) production. The effects of endotoxin persisted for up to 24 h, whereas those of IL-1ß were maximal 4-8 h after addition. The maximum levels of PGE2 (200-350 pg/ml) were similar in all experiments, and were independent of the stimulus used. Not all tissues responded to these stimuli; those which did not had basal levels of PGE2 production of 200-350 pg/ml, which was not further increased by endotoxin or IL-1ß. The basal production from these tissues was therefore similar to the maximal production from those tissues which responded to endotoxin or IL-1ß. The high basal production of PGE2 was attributed to prior in vivo activation of the membranes such that PGE2 synthesis could not be further stimulated in vitro. Overnight pretreatment with aspirin decreased basal PGE2 production from these activated membranes to <100 pg/ml/4 h during subsequent culture in aspirin-free medium. Both endotoxin and IL-1ß increased PGE2 production from the activated aspirin-pretreated membranes during this culture time, but this was transient as after 12 h of culture basal PGE2 production rose to over 200 pg/ml despite aspirin pretreatment.
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