Funisitis

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Bo Hyun Yoon - One of the best experts on this subject based on the ideXlab platform.

  • preterm labor and preterm premature rupture of membranes have a different pattern in the involved compartments of acute histologoic chorioamnionitis and or Funisitis patho physiologic implication related to different clinical manifestations
    Pathology International, 2016
    Co-Authors: C Park, Joong Shin Park, Kyung Chul Moon, Bo Hyun Yoon
    Abstract:

    : It is unknown whether histo-topographic findings about the involved compartments (i.e., choriodecidua, amnion, chorionic-plate) of acute-histologic chorioamnionitis (acute-HCA) and/or Funisitis according to the presence or absence of intra-amniotic inflammation (IAI) and/or fetal inflammatory response syndrome (FIRS) are different between preterm labor and intact membranes (PTL) and preterm premature rupture of membranes (preterm-PROM). The involved compartments of acute-HCA and/or Funisitis were examined in 161 singleton preterm-births ( 0.1). However, IAI(+)/FIRS(+) group had a significantly higher rate of inflammation in each compartment than IAI(+)/FIRS(-) group in both PTL and preterm-PROM (each-for P < 0.05). We first demonstrated that PTL and preterm-PROM had a different pattern in the involved compartments of acute-HCA and/or Funisitis in the IAI(-)/FIRS(--) group and in the change of involved compartments from IAI(-)/FIRS(-) to IAI(+)/FIRS(-).

  • Meconium aspiration syndrome: a role for fetal systemic inflammation
    American Journal of Obstetrics and Gynecology, 2015
    Co-Authors: Roberto Romero, Piya Chaemsaithong, Steven J Korzeniewski, Bo Hyun Yoon
    Abstract:

    Background Meconium aspiration syndrome (MAS) is a leading cause of morbidity and mortality in term infants. Meconium-stained amniotic fluid (MSAF) occurs in approximately 1 of every 7 pregnancies, but only 5% of neonates exposed to MSAF develop MAS. Why some infants exposed to meconium develop MAS while others do not is a fundamental question. Patients with MSAF have a higher frequency of intraamniotic inflammation/infection than those with clear fluid. We propose that fetal systemic inflammation is a risk factor for the development of MAS in patients with MSAF. Objective We sought to investigate whether intraamniotic inflammation and Funisitis, the histopathologic landmark of a fetal inflammatory response, predispose to MAS. Study Design A prospective cohort study was conducted from 1995 through 2009. Amniotic fluid (AF) samples (n = 1281) were collected at the time of cesarean delivery from women who delivered singleton newborns at term (gestational age ≥38 weeks). Intraamniotic inflammation was diagnosed if the AF concentration of matrix metalloproteinase-8 was >23 ng/mL. Funisitis was diagnosed by histologic examination if inflammation was present in the umbilical cord. Results The prevalence of MSAF was 9.2% (118/1281), and 10.2% (12/118) of neonates exposed to MSAF developed MAS. There were no significant differences in the median gestational age or umbilical cord arterial pH at birth between neonates who developed MAS and those who did not (each P > .1). Mothers whose newborns developed MAS had a higher median of AF matrix metalloproteinase-8 (456.8 vs 157.2 ng/mL, P P  = .03], as did those exposed to Funisitis [31.3% (5/16) vs 7.3% (6/82); relative risk, 4.3; 95% confidence interval, 1.5–12.3]. Among the 89 newborns for whom both AF and placental histology were available, MAS was more common in patients with both intraamniotic inflammation and Funisitis than in those without intraamniotic inflammation and Funisitis [28.6% (4/14) vs 0% (0/28), P  = .009], while the rate of MAS did not show a significant difference between patients with intraamniotic inflammation alone (without Funisitis) and those without intraamniotic inflammation and Funisitis [10.9% (5/46) vs 0% (0/28)]. Conclusion The combination of intraamniotic inflammation with fetal systemic inflammation is an important antecedent of MAS. This concept has implications for the understanding of the mechanisms of disease responsible for MAS and for the development of prognostic models and therapeutic interventions for this disorder.

  • acute chorioamnionitis and Funisitis definition pathologic features and clinical significance
    American Journal of Obstetrics and Gynecology, 2015
    Co-Authors: Roberto Romero, Bo Hyun Yoon, Piya Chaemsaithong, Noppadol Chaiyasit
    Abstract:

    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. Intraamniotic infection generally has been considered to be the cause of acute chorioamnionitis and Funisitis; however, recent evidence indicates that “sterile” intraamniotic inflammation, which occurs in the absence of demonstrable microorganisms induced by “danger signals,” is frequently associated with these lesions. In the context of intraamniotic infection, chemokines (such as interleukin-8 and granulocyte chemotactic protein) establish a gradient that favors the migration of neutrophils from the maternal or fetal circulation into the chorioamniotic membranes or umbilical cord, respectively. Danger signals that are 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 present in 3–5% of term placentas and in 94% of pacentas delivered at 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 of the fetal inflammatory response syndrome, a condition characterized by an elevation in the fetal plasma concentration of interleukin-6, and associated with the impending onset of preterm labor, a higher rate of neonatal morbidity (after adjustment for gestational age), and multiorgan fetal involvement. This syndrome is the counterpart of the systemic inflammatory response syndrome in adults: a risk factor for short- and long-term complications (ie, sterile inflammation in fetuses, 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 disease. Illustrations of the lesions and diagrams of the mechanisms of disease are provided.

  • clinical chorioamnionitis at term vi acute chorioamnionitis and Funisitis according to the presence or absence of microorganisms and inflammation in the amniotic cavity
    Journal of Perinatal Medicine, 2015
    Co-Authors: Roberto Romero, Bo Hyun Yoon, Piya Chaemsaithong, Nikolina Docheva, Steven J Korzeniewski, Juan Pedro Kusanovic, Noppadol Chaiyasit
    Abstract:

    OBJECTIVE: Neonates born to mothers with clinical chorioamnionitis at term are at an increased risk of infection. Acute subchorionitis, chorioamnionitis, and Funisitis are considered placental histologic features consistent with acute inflammation according to the Society for Pediatric Pathology. The objectives of this study were to examine the performance of placental histologic features in the identification of: 1) microbial-associated intra-amniotic inflammation (intra-amniotic infection); and 2) fetal inflammatory response syndrome (FIRS). METHODS: This retrospective cohort study included women with the diagnosis of clinical chorioamnionitis at term (n=45), who underwent an amniocentesis to determine: 1) the presence of microorganisms using both cultivation and molecular biologic techniques [polymerase chain reaction (PCR) with broad range primers]; and 2) interleukin (IL)-6 concentrations by enzyme-linked immunosorbent assay (ELISA). The diagnostic performance (sensitivity, specificity, accuracy, and likelihood ratios) of placental histologic features consistent with acute inflammation was determined for the identification of microbial-associated intra-amniotic inflammation and FIRS. RESULTS: 1) The presence of acute histologic chorioamnionitis and Funisitis was associated with the presence of proven intra-amniotic infection assessed by amniotic fluid analysis; 2) Funisitis was also associated with the presence of FIRS; 3) the negative predictive value of acute Funisitis ≥stage 2 for the identification of neonates born to mothers with intra-amniotic infection was <50%, and therefore, suboptimal to exclude fetal exposure to bacteria in the amniotic cavity; and 4) acute Funisitis ≥stage 2 had a negative predictive value of 86.8% for the identification of FIRS in a population with a prevalence of 20%. CONCLUSION: Acute histologic chorioamnionitis and Funisitis are associated with intra-amniotic infection and the presence of FIRS. However, current pathologic methods have limitations in the identification of the fetus exposed to microorganisms present in the amniotic cavity. Further studies are thus required to determine whether molecular markers can enhance the performance of placental pathology in the identification of neonates at risk for neonatal sepsis.

  • Clinical chorioamnionitis at term VI: acute chorioamnionitis and Funisitis according to the presence or absence of microorganisms and inflammation in the amniotic cavity
    Journal of Perinatal Medicine, 2015
    Co-Authors: Roberto Romero, Bo Hyun Yoon, Piya Chaemsaithong, Nikolina Docheva, Steven J Korzeniewski, Juan Pedro Kusanovic, Noppadol Chaiyasit, Ahmed I. Ahmed, Faisal Qureshi
    Abstract:

    Neonates born to mothers with clinical chorioamnionitis at term are at an increased risk of infection. Acute subchorionitis, chorioamnionitis, and Funisitis are considered placental histologic features consistent with acute inflammation according to the Society for Pediatric Pathology. The objectives of this study were to examine the performance of placental histologic features in the identification of: 1) microbial-associated intra-amniotic inflammation (intra-amniotic infection); and 2) fetal inflammatory response syndrome (FIRS).This retrospective cohort study included women with the diagnosis of clinical chorioamnionitis at term (n=45), who underwent an amniocentesis to determine: 1) the presence of microorganisms using both cultivation and molecular biologic techniques [polymerase chain reaction (PCR) with broad range primers]; and 2) interleukin (IL)-6 concentrations by enzyme-linked immunosorbent assay (ELISA). The diagnostic performance (sensitivity, specificity, accuracy, and likelihood ratios) of placental histologic features consistent with acute inflammation was determined for the identification of microbial-associated intra-amniotic inflammation and FIRS.1) The presence of acute histologic chorioamnionitis and Funisitis was associated with the presence of proven intra-amniotic infection assessed by amniotic fluid analysis; 2) Funisitis was also associated with the presence of FIRS; 3) the negative predictive value of acute Funisitis ≥stage 2 for the identification of neonates born to mothers with intra-amniotic infection was

Roberto Romero - One of the best experts on this subject based on the ideXlab platform.

  • Meconium aspiration syndrome: a role for fetal systemic inflammation
    American Journal of Obstetrics and Gynecology, 2015
    Co-Authors: Roberto Romero, Piya Chaemsaithong, Steven J Korzeniewski, Bo Hyun Yoon
    Abstract:

    Background Meconium aspiration syndrome (MAS) is a leading cause of morbidity and mortality in term infants. Meconium-stained amniotic fluid (MSAF) occurs in approximately 1 of every 7 pregnancies, but only 5% of neonates exposed to MSAF develop MAS. Why some infants exposed to meconium develop MAS while others do not is a fundamental question. Patients with MSAF have a higher frequency of intraamniotic inflammation/infection than those with clear fluid. We propose that fetal systemic inflammation is a risk factor for the development of MAS in patients with MSAF. Objective We sought to investigate whether intraamniotic inflammation and Funisitis, the histopathologic landmark of a fetal inflammatory response, predispose to MAS. Study Design A prospective cohort study was conducted from 1995 through 2009. Amniotic fluid (AF) samples (n = 1281) were collected at the time of cesarean delivery from women who delivered singleton newborns at term (gestational age ≥38 weeks). Intraamniotic inflammation was diagnosed if the AF concentration of matrix metalloproteinase-8 was >23 ng/mL. Funisitis was diagnosed by histologic examination if inflammation was present in the umbilical cord. Results The prevalence of MSAF was 9.2% (118/1281), and 10.2% (12/118) of neonates exposed to MSAF developed MAS. There were no significant differences in the median gestational age or umbilical cord arterial pH at birth between neonates who developed MAS and those who did not (each P > .1). Mothers whose newborns developed MAS had a higher median of AF matrix metalloproteinase-8 (456.8 vs 157.2 ng/mL, P P  = .03], as did those exposed to Funisitis [31.3% (5/16) vs 7.3% (6/82); relative risk, 4.3; 95% confidence interval, 1.5–12.3]. Among the 89 newborns for whom both AF and placental histology were available, MAS was more common in patients with both intraamniotic inflammation and Funisitis than in those without intraamniotic inflammation and Funisitis [28.6% (4/14) vs 0% (0/28), P  = .009], while the rate of MAS did not show a significant difference between patients with intraamniotic inflammation alone (without Funisitis) and those without intraamniotic inflammation and Funisitis [10.9% (5/46) vs 0% (0/28)]. Conclusion The combination of intraamniotic inflammation with fetal systemic inflammation is an important antecedent of MAS. This concept has implications for the understanding of the mechanisms of disease responsible for MAS and for the development of prognostic models and therapeutic interventions for this disorder.

  • acute chorioamnionitis and Funisitis definition pathologic features and clinical significance
    American Journal of Obstetrics and Gynecology, 2015
    Co-Authors: Roberto Romero, Bo Hyun Yoon, Piya Chaemsaithong, Noppadol Chaiyasit
    Abstract:

    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. Intraamniotic infection generally has been considered to be the cause of acute chorioamnionitis and Funisitis; however, recent evidence indicates that “sterile” intraamniotic inflammation, which occurs in the absence of demonstrable microorganisms induced by “danger signals,” is frequently associated with these lesions. In the context of intraamniotic infection, chemokines (such as interleukin-8 and granulocyte chemotactic protein) establish a gradient that favors the migration of neutrophils from the maternal or fetal circulation into the chorioamniotic membranes or umbilical cord, respectively. Danger signals that are 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 present in 3–5% of term placentas and in 94% of pacentas delivered at 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 of the fetal inflammatory response syndrome, a condition characterized by an elevation in the fetal plasma concentration of interleukin-6, and associated with the impending onset of preterm labor, a higher rate of neonatal morbidity (after adjustment for gestational age), and multiorgan fetal involvement. This syndrome is the counterpart of the systemic inflammatory response syndrome in adults: a risk factor for short- and long-term complications (ie, sterile inflammation in fetuses, 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 disease. Illustrations of the lesions and diagrams of the mechanisms of disease are provided.

  • clinical chorioamnionitis at term vi acute chorioamnionitis and Funisitis according to the presence or absence of microorganisms and inflammation in the amniotic cavity
    Journal of Perinatal Medicine, 2015
    Co-Authors: Roberto Romero, Bo Hyun Yoon, Piya Chaemsaithong, Nikolina Docheva, Steven J Korzeniewski, Juan Pedro Kusanovic, Noppadol Chaiyasit
    Abstract:

    OBJECTIVE: Neonates born to mothers with clinical chorioamnionitis at term are at an increased risk of infection. Acute subchorionitis, chorioamnionitis, and Funisitis are considered placental histologic features consistent with acute inflammation according to the Society for Pediatric Pathology. The objectives of this study were to examine the performance of placental histologic features in the identification of: 1) microbial-associated intra-amniotic inflammation (intra-amniotic infection); and 2) fetal inflammatory response syndrome (FIRS). METHODS: This retrospective cohort study included women with the diagnosis of clinical chorioamnionitis at term (n=45), who underwent an amniocentesis to determine: 1) the presence of microorganisms using both cultivation and molecular biologic techniques [polymerase chain reaction (PCR) with broad range primers]; and 2) interleukin (IL)-6 concentrations by enzyme-linked immunosorbent assay (ELISA). The diagnostic performance (sensitivity, specificity, accuracy, and likelihood ratios) of placental histologic features consistent with acute inflammation was determined for the identification of microbial-associated intra-amniotic inflammation and FIRS. RESULTS: 1) The presence of acute histologic chorioamnionitis and Funisitis was associated with the presence of proven intra-amniotic infection assessed by amniotic fluid analysis; 2) Funisitis was also associated with the presence of FIRS; 3) the negative predictive value of acute Funisitis ≥stage 2 for the identification of neonates born to mothers with intra-amniotic infection was <50%, and therefore, suboptimal to exclude fetal exposure to bacteria in the amniotic cavity; and 4) acute Funisitis ≥stage 2 had a negative predictive value of 86.8% for the identification of FIRS in a population with a prevalence of 20%. CONCLUSION: Acute histologic chorioamnionitis and Funisitis are associated with intra-amniotic infection and the presence of FIRS. However, current pathologic methods have limitations in the identification of the fetus exposed to microorganisms present in the amniotic cavity. Further studies are thus required to determine whether molecular markers can enhance the performance of placental pathology in the identification of neonates at risk for neonatal sepsis.

  • Clinical chorioamnionitis at term VI: acute chorioamnionitis and Funisitis according to the presence or absence of microorganisms and inflammation in the amniotic cavity
    Journal of Perinatal Medicine, 2015
    Co-Authors: Roberto Romero, Bo Hyun Yoon, Piya Chaemsaithong, Nikolina Docheva, Steven J Korzeniewski, Juan Pedro Kusanovic, Noppadol Chaiyasit, Ahmed I. Ahmed, Faisal Qureshi
    Abstract:

    Neonates born to mothers with clinical chorioamnionitis at term are at an increased risk of infection. Acute subchorionitis, chorioamnionitis, and Funisitis are considered placental histologic features consistent with acute inflammation according to the Society for Pediatric Pathology. The objectives of this study were to examine the performance of placental histologic features in the identification of: 1) microbial-associated intra-amniotic inflammation (intra-amniotic infection); and 2) fetal inflammatory response syndrome (FIRS).This retrospective cohort study included women with the diagnosis of clinical chorioamnionitis at term (n=45), who underwent an amniocentesis to determine: 1) the presence of microorganisms using both cultivation and molecular biologic techniques [polymerase chain reaction (PCR) with broad range primers]; and 2) interleukin (IL)-6 concentrations by enzyme-linked immunosorbent assay (ELISA). The diagnostic performance (sensitivity, specificity, accuracy, and likelihood ratios) of placental histologic features consistent with acute inflammation was determined for the identification of microbial-associated intra-amniotic inflammation and FIRS.1) The presence of acute histologic chorioamnionitis and Funisitis was associated with the presence of proven intra-amniotic infection assessed by amniotic fluid analysis; 2) Funisitis was also associated with the presence of FIRS; 3) the negative predictive value of acute Funisitis ≥stage 2 for the identification of neonates born to mothers with intra-amniotic infection was

  • Soluble ST2 in the fetal inflammatory response syndrome: in vivo evidence of activation of the anti-inflammatory limb of the immune response
    Journal of Maternal-fetal & Neonatal Medicine, 2013
    Co-Authors: Tamara Stampalija, Roberto Romero, Piya Chaemsaithong, Steven J Korzeniewski, Jezid Miranda, Zhong Dong, Sonia S. Hassan, Tinnakorn Chaiworapongsa
    Abstract:

    AbstractObjective: Inflammation is a mechanism of host response to infection, which can be harmful when inappropriately modulated. Soluble ST2 (sST2) is a decoy receptor of interleukin (IL)-33, and this complex modulates the balance in the Th1/Th2 immune response. Moreover, sST2 inhibits the production of pro-inflammatory cytokines in cooperation with an anti-inflammatory cytokine, IL-10. The objectives of this study were to: (1) determine whether umbilical cord plasma sST2 concentration differs between preterm neonates with and without Funisitis and between those with and without the fetal inflammatory response syndrome (FIRS); and (2) evaluate the relationship between sST2 and IL-10 among neonates with Funisitis and/or FIRS.Methods: Umbilical cord plasma was collected from neonates delivered prematurely due to preterm labor or preterm prelabor rupture of membranes with (n = 36), and without Funisitis (n = 30). FIRS (umbilical cord IL-6 concentration ≥17.5 pg/mL) was identified in 29 neonates. Plasma sST...

Christian P Speer - One of the best experts on this subject based on the ideXlab platform.

  • Funisitis is associated with increased interleukin 10 gene expression in cord blood mononuclear cells in preterm infants 32 weeks of gestation
    European Journal of Obstetrics & Gynecology and Reproductive Biology, 2011
    Co-Authors: Johannes Wirbelauer, Silvia Seidenspinner, Wolfgang Thomas, Steffen Kunzmann, Christian P Speer
    Abstract:

    Abstract Objectives A systemic inflammatory response after intrauterine Funisitis is assumed to be an important priming factor for acute and chronic pulmonary morbidity and neurological impairment in premature infants. Fetal lymphocytes and monocytes modulate the primary immune response. Genetic regulation of the cytokine-mediated process is partially known. The objective of our study was to examine the pro-inflammatory and anti-inflammatory responses in umbilical cord blood mononuclear cells (CBMC) of preterm infants on the transcriptional level. Study design Fifteen preterm infants with a gestational age ≤32 weeks were enrolled in this prospective study. Funisitis was diagnosed in five of the 15 by histological examination. Gene expression of pro-inflammatory cytokines (TNF-α, IL-8, IL-1β and IL-17) and anti-inflammatory cytokines (IL-10 and TGF-β1) was examined in CBMC by real time reverse transcription polymerase chain reaction. Results Gene expression of IL-10 was significantly higher in the Funisitis group compared to unexposed controls ( p Conclusions Funisitis is associated with increased IL-10 gene expression in CBMC of preterm infants with a gestational age ≤32 weeks. This might contribute to modulation of postnatal immunoreactions and immunoregulation in these individuals.

  • Funisitis is associated with increased interleukin-10 gene expression in cord blood mononuclear cells in preterm infants ≤32 weeks of gestation
    European Journal of Obstetrics & Gynecology and Reproductive Biology, 2010
    Co-Authors: Johannes Wirbelauer, Silvia Seidenspinner, Wolfgang Thomas, Steffen Kunzmann, Christian P Speer
    Abstract:

    Abstract Objectives A systemic inflammatory response after intrauterine Funisitis is assumed to be an important priming factor for acute and chronic pulmonary morbidity and neurological impairment in premature infants. Fetal lymphocytes and monocytes modulate the primary immune response. Genetic regulation of the cytokine-mediated process is partially known. The objective of our study was to examine the pro-inflammatory and anti-inflammatory responses in umbilical cord blood mononuclear cells (CBMC) of preterm infants on the transcriptional level. Study design Fifteen preterm infants with a gestational age ≤32 weeks were enrolled in this prospective study. Funisitis was diagnosed in five of the 15 by histological examination. Gene expression of pro-inflammatory cytokines (TNF-α, IL-8, IL-1β and IL-17) and anti-inflammatory cytokines (IL-10 and TGF-β1) was examined in CBMC by real time reverse transcription polymerase chain reaction. Results Gene expression of IL-10 was significantly higher in the Funisitis group compared to unexposed controls ( p Conclusions Funisitis is associated with increased IL-10 gene expression in CBMC of preterm infants with a gestational age ≤32 weeks. This might contribute to modulation of postnatal immunoreactions and immunoregulation in these individuals.

  • soluble receptor for advanced glycation end products srage in tracheobronchial aspirate fluid and cord blood of very low birth weight infants with chorioamnionitis and Funisitis
    Early Human Development, 2010
    Co-Authors: Wolfgang Thomas, Silvia Seidenspinner, Natalia Kawczynskaleda, Johannes Wirbelauer, Marta Szymankiewicz, Christian P Speer
    Abstract:

    Abstract Background A systemic fetal inflammatory response, reflected by histological Funisitis is associated with pulmonary morbidity and increased mortality after premature birth. The receptor for advanced glycation end products (RAGE) is a membrane-bound multiligand receptor with a key role in inflammation. Soluble RAGE (sRAGE) is created by alternative mRNA splicing or shedding of the receptor's extracellular domain and can inhibit RAGE-activation. Aims To assess the association of Funisitis with airway and systemic concentrations of sRAGE in very premature infants. Methods Forty-two ventilated infants (gestational age: 27.4±1.8weeks, birth weight: 1017±229g [mean±SD]) were studied. sRAGE concentrations were measured in tracheobronchial aspirate fluid (TAF) on days of life 1, 3, 5, 7 and 10 and in umbilical cord serum of 28 infants by ELISA. The secretory component for IgA (SC) served as reference protein in TAF. Placental tissue, membranes and umbilical cords were examined microscopically to distinguish three groups: chorioamnionitis ( n =9), Funisitis ( n =17) and controls ( n =16). Results The Funisitis group had lower sRAGE concentrations than both other groups in cord blood serum (median: 0.52ng/ml [25th–75th centile: 0.32–0.91]; control, 1.72 [1.02–2.69]; chorioamnionitis, 1.44 [0.92–1.63], p p p Conclusions Decreased sRAGE in airways and circulation after Funisitis may contribute to an imbalance between pro- and anti-inflammatory factors priming very premature infants for pulmonary injury and increasing the risk of adverse outcome.

  • airway concentrations of angiopoietin 1 and endostatin in ventilated extremely premature infants are decreased after Funisitis and unbalanced with bronchopulmonary dysplasia death
    Pediatric Research, 2009
    Co-Authors: Wolfgang Thomas, Boris W Kramer, S Seidenspinner, Alexander Marx, Natalia Kawczynskaleda, Johannes Wirbelauer, Marta Szymankiewicz, Maria Chmielnickakopaczyk, Christian P Speer
    Abstract:

    A systemic inflammatory response of the fetus, reflected by histologic Funisitis, is a risk factor for bronchopulmonary dysplasia (BPD). Impaired pulmonary angiogenesis accompanied by simplification and rarification of alveoli is a histologic hallmark of BPD. Angiopoietin-1 mediates vascular development, maturation, and stabilization. Endostatin mainly acts as an angiostatic factor. We hypothesized that Funisitis was associated with changes of endostatin and angiopoietin-1 concentrations in the airways and that an imbalance between the factors might be associated with BPD or death. We measured concentrations of angiopoietin-1 and endostatin by enzyme-linked immunosorbent assay in tracheobronchial aspirate fluid samples of 42 ventilated preterm infants during postnatal days 1 through 15. The secretory component for IgA served as reference protein. A standardized histologic examination was used to distinguish three groups: chorioamnionitis, Funisitis, and controls without inflammation. Concentrations of the mediators steadily decreased. Funisitis was associated with lower concentrations of both proteins, which might impair their physiologic activities in pulmonary angiogenesis. An increase of the ratio angiopoietin-1/endostatin until day 7 of life indicated a shift of the mediators potentially favoring angiogenesis. However, infants, who developed BPD or died, had a decreased ratio on days 1, 3, and 15, suggesting an imbalance toward inhibition of pulmonary angiogenesis.

  • Decreased Expression of Angiogenic Factors in Placentas with Chorioamnionitis after Preterm Birth
    Pediatric Research, 2005
    Co-Authors: Boris W Kramer, Alexander Marx, D Berg, Peter Groneck, Ulrike Kaemmerer, Michaela Kapp, Daniele Herbst, Christian P Speer
    Abstract:

    Chorioamnionitis and Funisitis are associated with neonatal morbidity and mortality. We hypothesized that chorioamnionitis may stress fetal endothelium, activate proinflammatory gene transcription. and affect angiogenic homeostasis in fetal capillaries. Placentas from preterm infants were stained for heat-shock protein 70, nuclear factor-κB, hypoxia-inducible factor-1α, and vascular endothelial growth factor (VEGF). VEGF receptors (VEGF-R) 1 and 2 as well as the receptor tyrosine kinase with immunoglobulin and epidermal growth factor homology domains (TIE-2), which is involved in vascular remodeling, were quantified. Immunohistochemistry was analyzed by counting positive capillaries in placental terminal villi. Staining intensity was quantified by a three-step semiquantitative scale. The samples were divided into three matched groups according to histology: chorioamnionitis with Funisitis (“Funisitis”), chorioamnionitis without Funisitis (“chorioamnionitis”), and control group with no inflammation. In tissues from the Funisitis or chorioamnionitis group, heat-shock protein 70 expression was increased over the control group. More nuclear factor-κB–positive nuclei of endothelial cells in capillaries were counted in the Funisitis and chorioamnionitis groups. Expression of VEGF and VEGF-R1 and -R2 were reduced in cases of Funisitis or chorioamnionitis in comparison with controls. Hypoxia-inducible factor-1α expression tended to be slightly lower in the Funisitis and chorioamnionitis groups but did not reach statistical significance. We speculate that cellular stress and changes in angiogenic homeostasis induced by proinflammatory activation of fetal endothelium in chorioamnionitis may not be limited to the placenta but may also involve other fetal organs.

T Terao - One of the best experts on this subject based on the ideXlab platform.

Joong Shin Park - One of the best experts on this subject based on the ideXlab platform.

  • preterm labor and preterm premature rupture of membranes have a different pattern in the involved compartments of acute histologoic chorioamnionitis and or Funisitis patho physiologic implication related to different clinical manifestations
    Pathology International, 2016
    Co-Authors: C Park, Joong Shin Park, Kyung Chul Moon, Bo Hyun Yoon
    Abstract:

    : It is unknown whether histo-topographic findings about the involved compartments (i.e., choriodecidua, amnion, chorionic-plate) of acute-histologic chorioamnionitis (acute-HCA) and/or Funisitis according to the presence or absence of intra-amniotic inflammation (IAI) and/or fetal inflammatory response syndrome (FIRS) are different between preterm labor and intact membranes (PTL) and preterm premature rupture of membranes (preterm-PROM). The involved compartments of acute-HCA and/or Funisitis were examined in 161 singleton preterm-births ( 0.1). However, IAI(+)/FIRS(+) group had a significantly higher rate of inflammation in each compartment than IAI(+)/FIRS(-) group in both PTL and preterm-PROM (each-for P < 0.05). We first demonstrated that PTL and preterm-PROM had a different pattern in the involved compartments of acute-HCA and/or Funisitis in the IAI(-)/FIRS(--) group and in the change of involved compartments from IAI(-)/FIRS(-) to IAI(+)/FIRS(-).

  • the presence of Funisitis is associated with a decreased risk for the development of neonatal respiratory distress syndrome
    Placenta, 2011
    Co-Authors: Kyungjoon Oh, C Park, Joong Shin Park, B H Yoon
    Abstract:

    Abstract Objectives Fetal lung maturation and respiratory outcomes are influenced by the exposure to intrauterine inflammation. Funisitis is considered as the histologic hallmark of fetal inflammatory response. This study was performed to determine if there is a difference in the rate of neonatal respiratory distress syndrome (RDS) according to the presence or absence of Funisitis in preterm gestations. Study design The relationship between the presence of Funisitis and the development of neonatal RDS was examined in 301 consecutive singleton preterm births (24–32 weeks’ gestation). Cases without placental histological examination and those with major congenital anomalies were excluded. Funisitis was diagnosed in the presence of neutrophil infiltration into the umbilical vessel walls or Wharton’s jelly on the placental histological examination. Results Funisitis was diagnosed in 25% and RDS was diagnosed in 46% of cases. The rate of RDS in babies with Funisitis was lower than in those without Funisitis (28.4% vs. 51.1%, p = 0.001). Logistic regression analysis demonstrated that the presence of Funisitis was associated with a decreased risk for RDS after adjusting for confounding variables (Odds ratio = 0.44, 95% CI 0.22–0.90). The downward trend of the frequency of RDS was related to the presence of histologic chorioamnionitis and Funisitis (p  Conclusions The presence of Funisitis is associated with a decreased risk for the development of neonatal RDS in preterm gestations. Furthermore, this observation suggests that the fetal involvement of placental inflammation may be beneficial to the maturation of the fetal lung.

  • 186 the presence of Funisitis is associated with a decreased risk for the development of neonatal respiratory distress syndrome
    American Journal of Obstetrics and Gynecology, 2011
    Co-Authors: Kyungjoon Oh, C Park, Joong Shin Park, Bo Hyun Yoon
    Abstract:

    Objectives: Fetal lung maturation and respiratory outcomes are influenced by the exposure to intrauterine inflammation. Funisitis is considered as the histologic hallmark of fetal inflammatory response. This study was performed to determine if there is a difference in the rate of neonatal respiratory distress syndrome (RDS) according to the presence or absence of Funisitis in preterm gestations. Study design: The relationship between the presence of Funisitis and the development of neonatal RDS was examined in 301 consecutive singleton preterm births (24e32 weeks’ gestation). Cases without placental histological examination and those with major congenital anomalies were excluded. Funisitis was diagnosed in the presence of neutrophil infiltration into the umbilical vessel walls or Wharton’s jelly on the placental histological examination. Results: Funisitis was diagnosed in 25% and RDS was diagnosed in 46% of cases. The rate of RDS in babies with Funisitis was lower than in those without Funisitis (28.4% vs. 51.1%, p ¼ 0.001). Logistic regression analysis demonstrated that the presence of Funisitis was associated with a decreased risk for RDS after adjusting for confounding variables (Odds ratio ¼ 0.44, 95% CI 0.22e0.90). The downward trend of the frequency of RDS was related to the presence of histologic chorioamnionitis and Funisitis (p < 0.001). Conclusions: The presence of Funisitis is associated with a decreased risk for the development of neonatal RDS in preterm gestations. Furthermore, this observation suggests that the fetal involvement of placental inflammation may be beneficial to the maturation of the fetal lung.

  • the antenatal identification of Funisitis with a rapid mmp 8 bedside test
    Journal of Perinatal Medicine, 2008
    Co-Authors: C Park, Joong Shin Park, Roberto Romero, Bo Hyun Yoon
    Abstract:

    Aims: The purpose of this study was to determine if a bedside test, the MMP-8 PTD Check™, can be of value in the antenatal identification of Funisitis. This test can be performed in 15 min without any laboratory equipment. Methods: The relationship between the presence or absence of Funisitis and the results of an MMP-8 PTD Check™ was examined in 139 patients who delivered preterm singleton neonates (gestational age <35 weeks) within 72 h of amniocentesis. Amniotic fluid (AF) was cultured for aerobic and anaerobic bacteria and for genital mycoplasmas. AF was analyzed for white blood cell (WBC) count, interleukin-6 (IL-6) and an MMP-8 PTD Check™. The IL-6 concentration was also determined in umbilical cord plasma collected at birth. Funisitis was diagnosed in the presence of neutrophil infiltration into the umbilical vessel walls or Wharton's jelly. Results: 1) Funisitis was present in 27% (38/139) of cases; 2) A positive MMP-8 PTD Check™ had a sensitivity of 97% (37/38), a specificity of 63% (64/101), a positive predictive value of 50% (37/74) and a negative predictive value of 99% (64/65) in the identification of Funisitis; 3) Among cases without Funisitis, patients with a positive MMP-8 PTD Check™ had a significantly higher median AF IL-6 concentration, AF WBC count, and umbilical cord plasma IL-6 concentration at birth than those with a negative MMP-8 PTD Check™ (P<0.05 for each). Conclusions: The MMP-8 PTD Check™ is a rapid, simple and sensitive bedside test which allows assessment of the risk of Funisitis.

  • The antenatal identification of Funisitis with a rapid MMP-8 bedside test
    Journal of Perinatal Medicine, 2008
    Co-Authors: C Park, Joong Shin Park, Roberto Romero, Bo Hyun Yoon
    Abstract:

    Aims: The purpose of this study was to determine if a bedside test, the MMP-8 PTD Check™, can be of value in the antenatal identification of Funisitis. This test can be performed in 15 min without any laboratory equipment. Methods: The relationship between the presence or absence of Funisitis and the results of an MMP-8 PTD Check™ was examined in 139 patients who delivered preterm singleton neonates (gestational age

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