Further observations on the fetal inflammatory response syndrome: A potential homeostatic role for the soluble receptors of tumor necrosis factor α

Romero, Roberto; Maymon, Eli; Pacora, Percy; Gomez, Ricardo; Mazor, Moshe; Yoon, Bo Hyun; Berry, Stanley M.

doi:10.1067/mob.2000.108885

Cited by 67 publications

(38 citation statements)

References 24 publications

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“…Evidence exists that the neonatal period is characterized by a TH2-dominated immune response with a hyporesponsive inflammatory component (1,2). In contrast, clinical observation reveals a more severe parainfectious systemic inflammatory response in neonates than in children and adults, often with detrimental sequelae (3). Consistent with these findings, neonates show an enhanced capacity to produce proinflammatory cytokines during infections (4) and inflammatory diseases, e.g.…”

supporting

confidence: 76%

Diminished Response to Interleukin-10 and Reduced Antibody-Dependent Cellular Cytotoxicity of Cord Blood Monocyte-Derived Macrophages

et al. 2006

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Monocyte-derived macrophage (M⌽) subsets are generated by antagonistic induction pathways. A helper M⌽-type (Mh-M⌽) is induced by interferon gamma (IFN-␥), whereas a cytotoxic M⌽-type (Mc-M⌽), induced by interleukin-10 (IL-10), is a potent mediator of antibody-dependent cellular cytotoxicity (ADCC). Compared with M⌽ from healthy adults [peripheral blood monocyte-derived macrophages (PBM⌽)], cord blood M⌽ (CBM⌽) were found less capable of generating Mh-M⌽. Here we tested the hypothesis that their generation of Mc-M⌽ via IL-10 is also impaired. M⌽ surface markers were phenotyped. IL-10 protein and mRNA production were detected after stimulation [␣CD3 monoclonal antibody (mAb)]. CBM⌽ or PBM⌽ were co-cultured with M⌽-depleted mononuclear cells of adults and CD4-targeting antibodies as models for ADCC were added. In cord blood, we found diminished ␣CD3-induced IL-10 protein and mRNA production (p Ͻ 0.05 versus adults). Basal CD16 and HLA-DR expressions on CBM⌽ of preterm and full-term neonates were lower (p Ͻ 0.05 versus PBM⌽). IL-10 had reduced effects on CD16 up-and HLA-DR down-modulation on CBM⌽ (p Ͻ 0.05 versus PBM⌽). CD4-directed receptor modulation and deletion were reduced in the presence of CBM⌽ (p Ͻ 0.05 versus PBM⌽). IL-10 failed to enhance their ADCC capacity, which was in contrast to PBM⌽ (p Ͻ 0.05). These data suggest that CBM⌽ have an impaired cytotoxic capacity via lower sensitivity toward IL-10. (Pediatr Res 60: 152-157, 2006)

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supporting

confidence: 76%

Diminished Response to Interleukin-10 and Reduced Antibody-Dependent Cellular Cytotoxicity of Cord Blood Monocyte-Derived Macrophages

et al. 2006

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“…The prevalence of microorganisms-positive cultures of amniotic fluid cultures was 21.6% (29/134). The FIRS was associated with a significant increase in the fetal plasma concentrations of TNF-R1 and TNF-R2 [32]. The authors suggested that microbial products and cytokines released during the fetal inflammatory response syndrome may be responsible for the increased availability of soluble TNF receptors, because endotoxin and TNF-α administration induces the shedding of soluble TNF-α receptors.…”

Section: Inflammationmentioning

confidence: 90%

“…(a) Microbial involvement Romero et al found that FIRS (defined as a fetal plasma IL-6 concentration of >11 pg/mL) was present in 20% (19/95) of patients with preterm labor and intact membranes and in 38.4% (15/39) of patients with PPROM [32]. The prevalence of microorganisms-positive cultures of amniotic fluid cultures was 21.6% (29/134).…”

Section: Inflammationmentioning

confidence: 99%

“…The mean fetal plasma concentrations of soluble tumor necrosis factor receptors TNF-R1 and TNF-R2 were significantly higher in fetuses with fetal inflammatory response syndrome (FIRS) than in those without the syndrome after adjustment for gestational age and fetal membrane status. Fetuses of patients who delivered within 72 h of cordocentesis had significantly higher concentrations of TNF-R1 and TNF-R2 receptors than those with longer latency periods [32]. Figure 2: PPROM classification in second trimester.…”

Section: Pathologic Anatomical Remodelingmentioning

confidence: 99%

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Mid-trimester preterm premature rupture of membranes (PPROM): etiology, diagnosis, classification, international recommendations of treatment options and outcome

Tchirikov

Schlabritz‐Loutsevitch

Mäher

et al. 2017

Journal of Perinatal Medicine

176

153

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Mid-trimester preterm premature rupture of membranes (PPROM), defined as rupture of fetal membranes prior to 28 weeks of gestation, complicates approximately 0.4%-0.7% of all pregnancies. This condition is associated with a very high neonatal mortality rate as well as an increased risk of long-and short-term severe neonatal morbidity. The causes of the mid-trimester PPROM are multifactorial. Altered membrane morphology including marked swelling and disruption of the collagen network which is seen with PPROM can be triggered by bacterial products or/and pro-inflammatory cytokines. Activation of matrix metalloproteinases (MMP) have been implicated in the mechanism of PPROM. The propagation of bacteria is an important contributing factor not only in PPROM, but also in adverse neonatal and maternal outcomes after PPROM. Inflammatory mediators likely play a causative role in both disruption of fetal membrane integrity and activation of uterine contraction. The "classic PPROM" with oligo/anhydramnion is associated with a short latency period and worse neonatal outcome compared to similar gestational aged neonates delivered without antecedent PPROM. The "high PPROM" syndrome is defined as a defect of the chorio-amniotic membranes, which is not located over the internal cervical os. It may be associated with either a normal or reduced amount of amniotic fluid. It may explain why sensitive biochemical tests such as the Amniosure (PAMG-1) or IGFBP-1/alpha fetoprotein test can have a positive result without other signs of overt ROM such as fluid leakage with Valsalva. The membrane defect following fetoscopy also fulfils the criteria for "high PPROM" syndrome. In some cases, the rupture of only one membrane -either the chorionic or amniotic membrane, resulting in "pre-PPROM" could precede "classic PPROM" or "high PPROM". The diagnosis of PPROM is classically established by identification of nitrazine positive, fern positive watery leakage from the cervical canal observed during in specula investigation. Other more recent diagnostic tests include the vaginal swab assay for placental alpha macroglobulin-1 test or AFP and IGFBP1. In some rare cases amniocentesis and infusion of indigo carmine has been used to confirm the diagnosis of PPROM. The management of the PPROM requires balancing the potential neonatal benefits from prolongation of the pregnancy with the risk of intraamniotic infection and its consequences for the mother and infant. Close monitoring for signs of chorioamnionitis (e.g. body temperature, CTG, CRP, leucocytes, IL-6, procalcitonine, amniotic fluid examinations) is necessary to minimize the risk of neonatal and maternal complications. In addition to delayed delivery, broad spectrum antibiotics of penicillin or cephalosporin group and/or macrolide and corticosteroids have been show to improve neonatal outcome [reducing risk of chorioamnionitis (average risk ratio (RR) = 0.66), neonatal infections (RR = 0.67) and abnormal ultrasound scan of neonatal brain (RR = 0.67)]. The positive effect of continuo...

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“…Microbial invasion of the amniotic cavity and intrauterine inflammation have been associated with microbial invasion of the human fetus [415] and the development of the Fetal Inflammatory Response Syndrome (FIRS) [249,407,[416][417][418]. This condition has been operationally defined as an elevation in fetal plasma IL-6 concentration, and is a risk factor for spontaneous preterm labour, neonatal morbidity and mortality, as well as multisystemic involvement (cardiac dysfunction [419,420], adrenal stress response [421], neurologic injury [422][423][424][425][426][427][428][429][430][431][432][433][434][435][436][437][438], as well as lung disease [128,[439][440][441][442][443][444][445]) (Figure 3).…”

Section: Inflammation As a Mechanism For Term And Preterm Parturitionmentioning

confidence: 99%

The preterm parturition syndrome and its implications for understanding the biology, risk assessment, diagnosis, treatment and prevention of preterm birth

Gotsch

Romero²,

Erez

et al. 2009

The Journal of Maternal-Fetal & Neonatal Medicine

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117

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Further observations on the fetal inflammatory response syndrome: A potential homeostatic role for the soluble receptors of tumor necrosis factor α

Cited by 67 publications

References 24 publications

Diminished Response to Interleukin-10 and Reduced Antibody-Dependent Cellular Cytotoxicity of Cord Blood Monocyte-Derived Macrophages

Diminished Response to Interleukin-10 and Reduced Antibody-Dependent Cellular Cytotoxicity of Cord Blood Monocyte-Derived Macrophages

Mid-trimester preterm premature rupture of membranes (PPROM): etiology, diagnosis, classification, international recommendations of treatment options and outcome

The preterm parturition syndrome and its implications for understanding the biology, risk assessment, diagnosis, treatment and prevention of preterm birth

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