The intensity of the fetal inflammatory response in intraamniotic inflammation with and without microbial invasion of the amniotic cavity

Lee, Si Eun; Romero, Roberto; Jung, Hyuk-Sang; Park, Chan-Wook; Park, Joong Shin; Yoon, Bo Hyun

doi:10.1016/j.ajog.2007.07.006

Cited by 111 publications

(81 citation statements)

References 33 publications

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“…In a significant proportion of preterm deliveries complicated by histologic chorioamnionitis, amniotic fluid is sterile (11)(12)(13), and although there is no evidence of fetal infection, elevated concentrations of cytokines in amniotic fluid (9) and fetal plasma (14) have been reported. Under these circumstances, it is likely that detrimental fetal responses occur primarily in response to exposure to elevated cytokine concentrations, rather than to direct exposure to the pathogen (14,15). Since the membranes present an effective barrier to endotoxin and most cytokines (16,17), the source of cytokines in amniotic fluid is presumed to be the fetal membranes or fetal leukocytes.…”

mentioning

confidence: 99%

“…Fetal inflammatory response syndrome, a condition associated with elevated levels of cytokines in the fetal circulation, is a risk factor for development of cerebral palsy and white matter damage (10). In a significant proportion of preterm deliveries complicated by histologic chorioamnionitis, amniotic fluid is sterile (11)(12)(13), and although there is no evidence of fetal infection, elevated concentrations of cytokines in amniotic fluid (9) and fetal plasma (14) have been reported. Under these circumstances, it is likely that detrimental fetal responses occur primarily in response to exposure to elevated cytokine concentrations, rather than to direct exposure to the pathogen (14,15).…”

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confidence: 99%

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Prevention of Inflammatory Activation of Human Gestational Membranes in an Ex Vivo Model Using a Pharmacological NF-κB Inhibitor

Keelan

Khan²,

Yosaatmadja³

et al. 2009

The Journal of Immunology

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Intrauterine inflammation plays a major role in the etiology of preterm labor and birth. We established an ex vivo model employing perfused full-thickness term gestational membranes to study membrane transport, function, and inflammatory responses. Exposure of the maternal (decidual) face of the membranes to LPS (5 μg/ml) resulted in increased accumulation of proinflammatory cytokines in the maternal compartment within 4 h, followed by a response in the fetal (amniotic) compartment. Using cytokine arrays, exposure to LPS was found to result in increased secretion of a large number of cytokines and chemokines in both compartments, most notably IL-5, IL-6, IL-7, MDC (macrophage-derived chemokine), MIG (monokine induced by IFN-γ), TARC (thymus and activation-regulated chemokine), TGF-β, and TNF-α. PGE2 accumulation also increased in response to LPS, particularly in the fetal compartment. Cotreatment with sulfasalazine, which inhibited nuclear translocation of NF-κB p65, had a rapid and marked inhibitory effect on the rate of cytokine accumulation in the maternal compartment, with lesser but significant effects observed in the fetal compartment. While membrane integrity was not discernibly impaired with LPS or sulfasalazine exposure, rates of chorionic apoptosis after 20 h were doubled in sulfasalazine-treated tissues. We conclude that the system described provides a means of accurately modeling human gestational membrane functions and inflammatory activation ex vivo. Decidual LPS exposure was shown to elicit a robust inflammatory response in both the maternal and fetal compartments. Sulfasalazine was an effective antiinflammatory agent in this model, but also exerted proapoptotic effects that raise concerns regarding its placental effects when administered in pregnancy.

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confidence: 99%

mentioning

confidence: 99%

Prevention of Inflammatory Activation of Human Gestational Membranes in an Ex Vivo Model Using a Pharmacological NF-κB Inhibitor

Keelan

Khan²,

Yosaatmadja³

et al. 2009

The Journal of Immunology

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“…Definition of FIRS with clinical and biomarker criteria has also been proposed [8]. FIRS is an independent risk factor for perinatal morbidity/mortality and is associated with long-term sequelae such as bronchopulmonary dysplasia and impaired neurological outcomes [1,2,3,4,5,6,7,8,9]. Although derangements in several biomarkers have been reported in umbilical cord blood of fetuses/neonates born to mothers with PPROM [9], prospective studies of diagnostic and prognostic markers of FIRS in neonates born to asymptomatic women with PPROM are lacking.…”

Section: Introductionmentioning

confidence: 99%

“…Intra-amniotic inflammation is found in approximately 40% of patients with preterm premature rupture of membranes (PPROM) [1,2,3,4,5]. Fetuses who are exposed to intra-amniotic inflammation can develop fetal inflammatory response syndrome (FIRS) [6] that is defined by an elevation of umbilical cord plasma interleukin-6 (IL-6) concentration [2] and/or funisitis (a histopathologic hallmark of FIRS) [7].…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide-Binding Protein as Marker of Fetal Inflammatory Response Syndrome after Preterm Premature Rupture of Membranes

Pavcnik-Arnol

Lučovnik²,

Kornhauser‐Cerar³

et al. 2013

Neonatology

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Background: Intra-amniotic inflammation with preterm premature rupture of membranes (PPROM) is a risk factor for fetal inflammatory response syndrome (FIRS) and adverse neonatal outcome. Objectives: To evaluate the diagnostic accuracy of lipopolysaccharide-binding protein (LBP) for detecting FIRS in preterm neonates born after PPROM. Methods: This was a prospective study in the level III neonatal intensive care unit (42 neonates; 23 + 6 to 31 + 6 weeks' gestation) of mothers with PPROM. Umbilical cord blood concentrations of LBP, C-reactive protein (CRP), interleukin (IL)-6 and white blood cell count with differential were measured at delivery and 24 h after birth. Neonates were classified into FIRS (n = 22) and no FIRS (n = 20) groups according to clinical criteria and IL-6 level (≥17.5 pg/ml). Histological examination of the placenta and umbilical cord was performed. Neurological examination at 12 months' corrected age was performed. Results: Umbilical cord blood concentration of LBP was significantly higher in the FIRS group than in the no FIRS group at delivery (median 21.6 mg/l vs. median 2.3 mg/l; p < 0.0001) and 24 h after birth (median 17.2 mg/l vs. median 20.0 mg/l; p < 0.001). The area under the ROC curve for FIRS at delivery was 0.98 (95% CI 0.88-1.0) for LBP, 0.92 (95% CI 0.80-0.99) for CRP and 0.82 (95% CI 0.64-0.94) for immature to total neutrophil ratio. Similar results were obtained if FIRS was defined by funisitis. Umbilical cord blood concentration of LBP at delivery was significantly higher in neonates with abnormal neurological exam at 12 months than in those with normal exam (median 19.5 mg/l vs. median 3.75 mg/l; p < 0.015). Conclusions: In preterm neonates born to asymptomatic women with PPROM, LBP in cord blood at delivery is an excellent diagnostic biomarker of FIRS/funisitis with prognostic potential.

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“…Inflamação intra-amniótica é encontrada em aproximadamente 40% dos pacientes com PPROM e é um fator de risco para parto prematuro e gestação e desfecho neonatal adversos, com a comprovação ou não da infecção microbiana do líquido amniótico através de técnicas de cultura (Lee et al, 2007;Park et al, 2009Seong et al, 2008. O ataque microbiano ao feto tem lugar em aproximadamente 10% das gestações com infecção intra-aminótica, e o feto humano é capaz de deflagrar uma resposta inflamatória (celular e humoral) no trimestre médio da gestação (Romero et al, 2007a).…”

Section: A Microbiota Vaginal E Sua Relação Com O Tipo De Parto E Comunclassified

Avaliação clínica e microbiológica em puérperas com doença periodontal e a sua relação com desfecho reprodutivo ruim.

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The intensity of the fetal inflammatory response in intraamniotic inflammation with and without microbial invasion of the amniotic cavity

Cited by 111 publications

References 33 publications

Prevention of Inflammatory Activation of Human Gestational Membranes in an Ex Vivo Model Using a Pharmacological NF-κB Inhibitor

Prevention of Inflammatory Activation of Human Gestational Membranes in an Ex Vivo Model Using a Pharmacological NF-κB Inhibitor

Lipopolysaccharide-Binding Protein as Marker of Fetal Inflammatory Response Syndrome after Preterm Premature Rupture of Membranes

Avaliação clínica e microbiológica em puérperas com doença periodontal e a sua relação com desfecho reprodutivo ruim.

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