Macrophage inhibitory cytokine 1 in fetal membranes and amniotic fluid from pregnancies with and without preterm labour and premature rupture of membranes

Keelan, Jeffrey

doi:10.1093/molehr/gag068

Cited by 25 publications

(17 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…IL-1β was the first cytokine discovered to play a role in preterm labor associated with intra-amniotic infection 79, 82, 242 . We and other investigators have reported that amniotic fluid concentrations of IL-1β 79, 81, 94, 109, 243, 244 , IL-6 14, 86-88, 94, 95, 109, 189, 244, 245 , MIP-1α 113, 138, 140, 246 , and IL-1α 81, 83, 242, 247 were significantly higher in women with preterm labor who had intra-amniotic infection than in those who did not.…”

Section: Discussionmentioning

confidence: 70%

Evidence of perturbations of the cytokine network in preterm labor

Romero

Grivel

Tarca

et al. 2015

American Journal of Obstetrics and Gynecology

137

131

View full text Add to dashboard Cite

Objective Intra-amniotic infection/inflammation is the only mechanism of disease with persuasive evidence of causality for spontaneous preterm labor/delivery. Previous studies about the behavior of cytokines in preterm labor have been largely based on the analysis of the behavior of each protein independently. Emerging evidence indicates that the study of biological networks can provide insight into the pathobiology of disease, and improve biomarker discovery. The goal of this study is to characterize the inflammatory-related proteins network in the amniotic fluid in patients with preterm labor. Materials and Methods A retrospective cohort study was conducted, and included women with singleton pregnancies who presented with spontaneous preterm labor and intact membranes (n=135). These patients were classified according to the results of amniotic fluid culture, broad-range polymerase chain reaction coupled with electrospray ionization mass spectrometry (PCR/ESI-MS), and amniotic fluid concentration of interleukin (IL)-6 into the following groups: 1) those without intra-amniotic inflammation (n=85); 2) those with microbial-associated intra-amniotic inflammation (n=15); and 3) those with intra-amniotic inflammation without detectable bacteria (n=35). Amniotic fluid concentrations of 33 inflammatory-related proteins were determined using a multiplex bead array assay. Results 1) Patients with preterm labor and intact membranes who had microbial-associated intra-amniotic inflammation had a higher amniotic fluid inflammatory-related protein concentration correlation than those without intra-amniotic inflammation (113 perturbed correlations). IL-1β, IL-6, MIP-1α, and IL-1α were the most connected nodes (highest degree) in this differential correlation network (degree of 20, 16, 12, and 12, respectively); 2) patients with sterile intra-amniotic inflammation had correlation patterns of inflammatory-related proteins that were both increased and decreased when compared to those without intra-amniotic inflammation (50 perturbed correlations). IL-1α, MIP-1α, and IL-1β were the most connected nodes in this differential correlation network (degrees of 12, 10, and 7, respectively); and 3) there were more coordinated inflammatory-related protein concentrations in the amniotic fluid of women with microbial-associated intra-amniotic inflammation than in those with sterile intra-amniotic inflammation (60 perturbed correlations), with IL-4 and IL-33 having the largest number of perturbed correlations (degree of 15 and 13, respectively). Conclusion We report for the first time an analysis of the inflammatory-related protein network in spontaneous preterm labor. Patients with preterm labor who had microbial-associated intra-amniotic inflammation had more coordinated amniotic fluid inflammatory-related proteins than either those with sterile intra-amniotic inflammation or those without intra-amniotic inflammation. The correlations were also stronger in patients with sterile intra-amniotic inflammation than in those without intra-...

show abstract

Section: Discussionmentioning

confidence: 70%

Evidence of perturbations of the cytokine network in preterm labor

Romero

Grivel

Tarca

et al. 2015

American Journal of Obstetrics and Gynecology

137

131

View full text Add to dashboard Cite

show abstract

“…IL-8, also known as neutrophil activating peptide, and CXCL6 – granulocyte chemotactic protein) 215, 216, 296 . Intra-amniotic inflammation due to microorganisms or “danger signals” can result in the production of the following chemokines: IL-8 26, 187-189, 196, 199, 200, 202, 206-210 , Macrophage inhibitory cytokine 297, 298 , MCP 27, 299-302 , MCP-2, MCP-3 303 , MIP-1α 29, 196, 302, 304 , CXCL6 212 , CXCL10 281 , CXCL13 305 , ENA-78 306 , RANTES 307 and GRO-α 28, 208 . Therefore, amniotic fluid chemokine concentrations are elevated and establish a chemotactic gradient favoring migration of neutrophils.…”

Section: Pathogenesis: Chemotactic Signals In the Amniotic Cavity mentioning

confidence: 99%

Acute chorioamnionitis and funisitis: definition, pathologic features, and clinical significance

Kim

Romero

Chaemsaithong

et al. 2015

American Journal of Obstetrics and Gynecology

752

652

View full text Add to dashboard Cite

Acute inflammatory lesions of the placenta consist of diffuse infiltration of neutrophils at different sites in the organ. These lesions include acute chorioamnionitis, funisitis, and chorionic vasculitis, and represent a host response (maternal or fetal) to a chemotactic gradient in the amniotic cavity. While acute chorioamnionitis is evidence of a maternal host response, funisitis and chorionic vasculitis represent fetal inflammatory responses. Intra-amniotic infection has been generally considered to be the cause of acute histologic chorioamnionitis and funisitis; however, recent evidence indicates that “sterile” intra-amniotic inflammation, which occurs in the absence of demonstrable microorganisms but can be induced by “danger signals”, is frequently associated with these lesions. In the context of intra-amniotic infection, chemokines (such as interleukin-8 and granulocyte chemotactic protein) establish a gradient favoring the migration of neutrophils from maternal or fetal circulation into the chorioamniotic membranes or umbilical cord, respectively. Danger signals released during the course of cellular stress or cell death can also induce the release of neutrophil chemokines. The prevalence of chorioamnionitis is a function of gestational age at birth, and is present in 3-5% of placentas delivered at term, but in 94% of placentas delivered between 21-24 weeks of gestation. The frequency is higher in patients with spontaneous labor, preterm labor, clinical chorioamnionitis (preterm or term), or ruptured membranes. Funisitis and chorionic vasculitis are the hallmarks for the fetal inflammatory response syndrome, a condition characterized by an elevation in fetal plasma concentrations of interleukin-6, associated with the impending onset of preterm labor, a higher rate of neonatal morbidity (after adjustment for gestational age), and multi-organ fetal involvement. This syndrome is the counterpart of the systemic inflammatory response syndrome in adults; however, in fetuses, it is a risk factor for short- and long-term complications (i.e. neonatal sepsis, bronchopulmonary dysplasia, periventricular leukomalacia, and cerebral palsy). This article reviews the definition, pathogenesis, grading and staging, and clinical significance of the most common lesions in placental pathology. Illustrations of the lesions and diagrams of the mechanisms of disease are provided.

show abstract

“…via stimulation of decidual prostaglandinendoperoxide synthase 2 production (25), then the suppression of REN mRNA if the fetus is female would counterbalance this action. Alternatively, it is possible that withdrawal of the decidual RAS could affect the integrity of the fetal membranes through a reduction in production of TGF-␤ (32), which stimulates the formation of profibrotic molecules such as plasminogen activator inhibitor type 1, fibronectin, and collagens (33), or through reduced activation of proinflammatory cytokines (34). These possibilities need to be tested in future studies.…”

Section: Figmentioning

confidence: 99%

Fetal Sex Affects Expression of Renin-Angiotensin System Components in Term Human Decidua

et al. 2012

View full text Add to dashboard Cite

The maternal decidua expresses the genes of the renin-angiotensin system (RAS). Human decidua was collected at term either before labor (i.e. cesarean delivery) or after spontaneous labor. The mRNA for prorenin (REN), prorenin receptor (ATP6AP2), angiotensinogen (AGT), angiotensin-converting enzymes 1 and 2 (ACE1 and ACE2), angiotensin II type 1 receptor (AGTR1), and angiotensin 1-7 receptor (MAS1) were measured by quantitative real-time RT-PCR. Decidual explants were cultured in duplicate for 24 and 48 h, and all RAS mRNA, and the secretion of prorenin, angiotensin II, and angiotensin 1-7 was measured using quantitative real-time RT-PCR, ELISA, and radioimmunoassay, respectively. In the decidua collected before labor, REN mRNA levels were higher if the fetus was female. In addition, REN, ATP6AP2, AGT, and MAS1 mRNA abundance was greater in decidual explants collected from women carrying a female fetus, as was prorenin protein. After 24 h, ACE1 mRNA was higher in the decidual explants from women with a male fetus, whereas after 48 h, both ACE1 and ACE2 mRNA was higher in decidual explants from women with a female fetus. Angiotensin II was present in all explants, but angiotensin 1-7 levels often registered below the lower limits of sensitivity for the assay. After labor, decidua, when compared with nonlaboring decidua, demonstrated lower REN expression when the fetus was female. Therefore, the maternal decidual RAS is regulated in a sex-specific manner, suggesting that it may function differently when the fetus is male than when it is female.

show abstract

Macrophage inhibitory cytokine 1 in fetal membranes and amniotic fluid from pregnancies with and without preterm labour and premature rupture of membranes

Cited by 25 publications

References 22 publications

Evidence of perturbations of the cytokine network in preterm labor

Evidence of perturbations of the cytokine network in preterm labor

Acute chorioamnionitis and funisitis: definition, pathologic features, and clinical significance

Fetal Sex Affects Expression of Renin-Angiotensin System Components in Term Human Decidua

Contact Info

Product

Resources

About