Identification of placental cytokine-producing cells in term and preterm labor

Steinborn, Andrea; Gall, Charlotte von; Hildenbrand, Ralf; Stutte, H. J.; Kaufmann, M.

doi:10.1016/s0029-7844(97)00680-7

Cited by 99 publications

(48 citation statements)

References 22 publications

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“…25,34 Previous studies have shown placental production of cytokines such as IL-1β and adiponectin in normal pregnancy. 8,9,27 In the present study, pregnant women with GDM showed at second trimester (a period of insulin resistance development) higher insulin resistance compared to BMI-and age-matched pregnant women without GDM. Furthermore, pregnant women with GDM presented at 2 nd trimester lower serum adiponectin and higher IL-1β levels than women without GDM.…”

Section: Discussionsupporting

confidence: 49%

“…40,41 Otherwise, the significant decrease of the studied cytokines during the early postpartum period in pregnancies with GDM in this study could be explained by the withdrawal of cytokines produced by the placenta during pregnancy. 8,9,27 The role of the placenta in the production of adiponectin and IL-1β during pregnancy is further reinforced by the non-significant but clear downward trend of these cytokines during third day postpartum found in pregnancies without GDM. The 3 rd day postpartum is a period in which the effect of the placenta on maternal metabolism regarding insulin resistance has just been removed and lactation is started.…”

Section: Discussionmentioning

confidence: 99%

“…4,5 Placenta is involved in the process of insulin resistance and fetal growth in both non-diabetic pregnancies and in pregnancies complicated by GDM through human placental lactogen and placental growth hormone production. 6 Recently, human placenta and adipose tissue have been found to produce various pro-inflammatory factors, including cytokines such as Interleukin-1 beta (IL-1β) and adiponectin [7][8][9] Adiponectin is an adipocytokine with profound insulin sensitizing, anti-inflammatory and antiatherogenic effects. 10,11 It has also been proposed that adiponectin may play a role in regulating fetal growth in pre-term and term infants of non-diabetic pregnancies.…”

Section: I) Anthropometric Measurementsmentioning

confidence: 99%

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Pre- and early post-partum adiponectin and Interleukin-1beta levels in women with and without gestational diabetes

Vitoratos¹,

Valsamakis²,

Mastorakos³

et al. 2008

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OBJECTIVE: To investigate maternal serum adiponectin and Ιnterleukin-1beta (IL-1β) levels during the pre-and post-partum periods in pregnant women with and without Gestational Diabetes Mellitus (GDM). DESIGN: Thirty control pregnant Caucasian women without GDM and thirty Body Mass Index (BMI) and age-matched Caucasian women with GDM examined in the outpatient clinic between the 24 th and 26 th week of their pregnancy and on the 3 rd day postpartum underwent anthropometry and had serum blood taken. Both groups, were monitored by a dietitian and had comparable weight gain during pregnancy. Birth weight was also measured. RESULTS: At the 3 rd day postpartum, compared to the 2 nd trimester of pregnancy, women with GDM had lower serum adiponectin levels, lower serum IL-1β levels and lower Homeostasis Model Assessment for Insulin Resistance (HOMA-IR) values. At the 2 nd trimester of pregnancy, women with GDM had lower serum adiponectin levels, higher IL-1β and higher HOMA-IR values compared to women without GDM. At the 3 rd day postpartum, women with GDM had lower serum adiponectin levels, higher IL-1β and higher HOMA-IR values compared to women without GDM. Second trimester serum adiponectin values of women with GDM correlated negatively with birth weight. CONCLUSIONS: Gestational diabetes is a state of insulin resistance associated with altered levels of proinflammatory cytokines, increased IL-1β and decreased adiponectin values. Both of these alterations might be attributed to placental pathology in pregnancies with GDM.

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Section: Discussionsupporting

confidence: 49%

Section: Discussionmentioning

confidence: 99%

Section: I) Anthropometric Measurementsmentioning

confidence: 99%

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Pre- and early post-partum adiponectin and Interleukin-1beta levels in women with and without gestational diabetes

Vitoratos¹,

Valsamakis²,

Mastorakos³

et al. 2008

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“…The mechanism through which epidural analgesia may trigger cytokine production during labor is not clear. However, the placenta is a rich source of cytokine production, 14 which may explain the unique response to epidural analgesia observed during labor. Increased placental inflammation has been reported in the setting of epidural fever, 15 supporting the placenta as a potential source.…”

Section: Commentmentioning

confidence: 99%

Prophylactic Acetaminophen Does Not Prevent Epidural Fever in Nulliparous Women: A Double-Blind Placebo-Controlled Trial

et al. 2004

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OBJECTIVE:Epidural analgesia is associated with a four-to five-fold increase in noninfectious maternal fever in nulliparous women. Fever prophylaxis may safely reduce both unnecessary neonatal sepsis evaluations and the potential effect of fever on the fetus. STUDY DESIGN:We performed a randomized double-blind placebo-controlled study. Immediately after epidural placement, full-term nulliparas with a temperature of <99.51F received acetaminophen 650 mg or placebo, per rectum, every 4 hours. Tympanic membrane temperatures were measured hourly. Our power to detect an effect of acetaminophen treatment on maternal temperature over time was 90%. RESULTS:In all, 21 subjects were randomized to each arm. Treatment with acetaminophen did not impact maternal temperature curves. Fever >100.41F was identical in the acetaminophen and placebo groups (23.8%, p ¼ 1.0). Neonatal surveillance blood cultures did not reveal occult infection. CONCLUSIONS:Acetaminophen prophylaxis prevented neither maternal hyperthermia nor fever secondary to epidural analgesia, suggesting that the mechanism underlying fever does not include centrally mediated perturbations of maternal thermoregulation.

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“…Placental cytokine production occurs predominantly from resident macrophages (24), the trophoblast (25), and endothelial cells. This system is partially regulated by glucocorticoids via transcriptional regulation of cytokine genes (26,27).…”

mentioning

confidence: 99%

Placental Cytokine Expression Covaries with Maternal Asthma Severity and Fetal Sex

Scott¹,

Hodyl

Murphy

et al. 2009

The Journal of Immunology

120

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In the presence of maternal asthma, we have previously reported reduced placental blood flow, decreased cortisol metabolism, and reductions in fetal growth in response to maternal asthma and asthma exacerbations. We have proposed that these changes in placental function and fetal development may be related to activation of proinflammatory pathways in the placenta in response to maternal asthma. In the present study, we examined the influence of maternal asthma severity, inhaled glucocorticoid treatment, maternal cigarette use, placental macrophage numbers, and fetal sex on placental cytokine mRNA expression from a prospective cohort study of pregnant women with and without asthma. Placental expression of TNF-α, IL-1β, IL-6, IL-8, and IL-5 mRNA were all increased significantly in placentae of female fetuses whose mothers had mild asthma, but no changes were observed in placentae of male fetuses. The proinflammatory cytokines TNF-α, IL-1β, and IL-6 were negatively correlated with female cord blood cortisol, but there were no such correlations in placentae from males. Multivariate analysis indicated the strongest predictor of both cytokine mRNA expression in the placenta and birth weight was fetal cortisol but only in females. Placental cytokine mRNA levels were not significantly altered by inhaled glucocorticoid use, placental macrophage numbers, cigarette use, moderate-severe asthma, or male sex. These data suggest that placental basal cytokine mRNA expression is sex specifically regulated in pregnancies complicated by asthma, and interestingly these changes are more prevalent in mild rather than severe asthma.

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Identification of placental cytokine-producing cells in term and preterm labor

Abstract: The source of labor-associated release of tumor-necrosis-factor-alpha from placental tissues are macrophages, whereas interleukin-1beta and interleukin-6 are released from placental endothelial cells.

Cited by 99 publications

References 22 publications

Pre- and early post-partum adiponectin and Interleukin-1beta levels in women with and without gestational diabetes

Pre- and early post-partum adiponectin and Interleukin-1beta levels in women with and without gestational diabetes

Prophylactic Acetaminophen Does Not Prevent Epidural Fever in Nulliparous Women: A Double-Blind Placebo-Controlled Trial

Placental Cytokine Expression Covaries with Maternal Asthma Severity and Fetal Sex

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