The fetal inflammatory response syndrome

Gomez, Ricardo; Romero, Roberto; Ghezzi, Fabio; Yoon, Bo Hyun; Mazor, Moshe; Berry, Stanley M.

doi:10.1016/s0002-9378(98)70272-8

Cited by 1,005 publications

(842 citation statements)

References 22 publications

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“…Although infection in amniotic fluid is common, systemic sepsis soon after birth is detected in only 2% of these preterm infants (2). However, ϳ50% of infants exposed to chorioamnionitis have a systemic inflammatory response, referred to as fetal inflammatory response syndrome (FIRS) 3 (3)(4)(5). Unlike the cytokine storm associated with the adult systemic inflammatory response, FIRS is often a more subtle inflammatory response (4,6).…”

Section: Pulmonary and Systemic Endotoxin Tolerance In Pretermmentioning

confidence: 99%

“…However, ϳ50% of infants exposed to chorioamnionitis have a systemic inflammatory response, referred to as fetal inflammatory response syndrome (FIRS) 3 (3)(4)(5). Unlike the cytokine storm associated with the adult systemic inflammatory response, FIRS is often a more subtle inflammatory response (4,6). At birth, most preterm infants with chorioamnionitis and FIRS cannot be distinguished clinically from those not exposed to chorioamnionitis, suggesting an adaptive response.…”

Section: Pulmonary and Systemic Endotoxin Tolerance In Pretermmentioning

confidence: 99%

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Pulmonary and Systemic Endotoxin Tolerance in Preterm Fetal Sheep Exposed to Chorioamnionitis

Kallapur

Jobe

Ball

et al. 2007

The Journal of Immunology

110

139

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In a model of human chorioamnionitis, fetal sheep exposed to a single injection, but not repeated injections, of intra-amniotic endotoxin develop lung injury responses. We hypothesized that repeated exposure to intra-amniotic endotoxin induces endotoxin tolerance. Fetal sheep were given intra-amniotic injections of saline (control) or Escherichia coli LPS O55:B5 (10 mg) either 2 days (2-day group, single exposure), 7 days (7-day group, single exposure), or 2 plus 7 days (2- and 7-day repeat exposure) before preterm delivery at 124 days gestation (term = 150 days). Endotoxin responses were assessed in vivo in the lung and liver, and in vitro in monocytes from the blood and the lung. Compared with the single 2-day LPS exposure group, the (2 plus 7 days) repeat LPS-exposed lambs had: 1) decreased lung neutrophil and monocyte inducible NO synthase (NOSII) expression, and 2) decreased lung cytokine and liver serum amyloid A3 mRNA expression. In the lung, serum amyloid A3 mRNA expression decreased in the airway epithelial cells but not in the lung inflammatory cells. Unlike the single 7-day LPS exposure group, peripheral blood and lung monocytes from the repeat-LPS group did not increase IL-6 secretion or hydrogen peroxide production in response to in vitro LPS. Compared with controls, TLR4 expression did not change but IL-1R-associated kinase M expression increased in the monocytes from repeat LPS-exposed lambs. These results are consistent with the novel finding of endotoxin tolerance in preterm fetal lungs exposed to intra-amniotic LPS. The findings have implications for preterm infants exposed to chorioamnionitis for both responses to lung injury and postnatal nosocomial infections.

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Section: Pulmonary and Systemic Endotoxin Tolerance In Pretermmentioning

confidence: 99%

Section: Pulmonary and Systemic Endotoxin Tolerance In Pretermmentioning

confidence: 99%

Pulmonary and Systemic Endotoxin Tolerance in Preterm Fetal Sheep Exposed to Chorioamnionitis

Kallapur

Jobe

Ball

et al. 2007

The Journal of Immunology

110

139

View full text Add to dashboard Cite

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“…32,49 Epidemiological data suggest a strong association between chorioamnionitis and the development of BPD, and increased concentrations of proinflammatory cytokines in human amniotic fluid and fetal cord blood -indicating a systemic inflammatory response during chorioamnionitis -were shown to be an independent risk factor for the development of BPD. 50,51 Furthermore, chorioamnionitis, mechanical ventilation, and postnatal sepsis have clearly been identified as modulators of BPD. The two postnatal factors interact with antenatal infection to further increase the risk of BPD.…”

Section: Inflammatory Cells Endothelial Interactions and Chemotaxismentioning

confidence: 99%

Pulmonary inflammation and bronchopulmonary dysplasia

Speer

2006

J Perinatol

131

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Various pre-and postnatal risk factors, which act additively or synergistically induce an injurious inflammatory response in the airways and the pulmonary interstitium of preterm infants with bronchopulmonary dysplasia. This inflammatory response is characterized by an accumulation of neutrophils and macrophages as well as an arsenal of proinflammatory mediators that affect the endothelium and alveolar-capillary integrity. Besides proinflammatory cytokines and toxic oxygen radicals, lipid mediators as well as potent proteases may be responsible for acute lung injury. There is increasing evidence that an imbalance between pro-and anti-inflammatory factors, which should protect the alveoli and lung tissue, are key features in the pathogenesis of bronchopulmonary dysplasia. In addition, a subnormal generation of growth factors may affect alveolarization and vascular development in preterm infants with bronchopulmonary dysplasia. In this condensed review article, the current concepts on the possible role of inflammation in the evolution of bronchopulmonary dysplasia will be summarized.

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“…10 This is relevant, considering that a fetal inflammatory response syndrome, with a complex series of events, which include an inflammatory cascade, increased surfactant production and alterations to lung structure 11,12 are present in nearly one-half of fetuses with PPROM or preterm labour and intact membranes. 13,14 Furthermore, several studies suggested that PPROM confers protection against RDS. [15][16][17][18] However, a large review did not confirm this protective effect.…”

Section: Introductionmentioning

confidence: 99%

Preterm premature rupture of membranes, chorioamnion inflammatory scores and neonatal respiratory outcome

Zanardo¹,

Vedovato²,

Cosmi

et al. 2009

BJOG

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Objective To evaluate whether histological chorioamnionitis (HCA), in the setting of preterm premature rupture of membranes (PPROM), affects infant respiratory outcome.Design A prospective histological study on 287 consecutive placentas was performed in preterm infants (£32 +6 weeks gestation), categorised into four groups: according to the presence or absence of HCA, in the setting or in absence of PPROM. Results Among the 287 NICU admitted preterm infants, 68/287 (23.6%) presented with HCA, 16/68 (23.5%) with a coexisting fetal inflammatory response, and 74/287 (25.7%) with PPROM. HCA was associated with a greater frequency of vaginal delivery (P < 0.0001), lower gestational age (P < 0.0001) and lower birth weight (P < 0.01). HCA had no effect on fetal lung maturation, however, it was a significant risk factor for CLD (RR; 95% CI 2.08; 1.30-3.33). HCA and the fetal inflammatory response were also significant risk factors for PPROM (RR; 95% CI 2.07; 1.42-3.03 and 2.64; 1.71-4.09 respectively). Conversely, HCA in the setting of PPROM failed to reveal any RDS protection or subtype CLD risk. Multivariate analysis demonstrated significant independent effects of presence of maternal HCA (P = 0.04), gestational age (P < 0.0001) and interaction HCA-gestational age (P = 0.04) on CLD development, regardless of the presence of fetal HCA or fetal HCA-gestational age interaction, PPROM or PPROM-gestational age interaction.Conclusions Histological chorioamnionitis is a significant PPROM and CLD risk factor, but it fails to provide any protection from RDS. HCA in the setting of PPROM also failed to reveal any RDS protection or subtype CLD risk.Keywords Chronic lung disease, fetal inflammatory response syndrome, histological chorioamnionitis, preterm premature rupture of membranes, respiratory distress syndrome.Please cite this paper as: Zanardo V, Vedovato S, Cosmi E, Litta P, Cavallin F, Trevisanuto D, Chiarelli S. Preterm premature rupture of membranes, chorioamnion inflammatory scores and neonatal respiratory outcome. BJOG 2010;117:94-98.

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The fetal inflammatory response syndrome

Cited by 1,005 publications

References 22 publications

Pulmonary and Systemic Endotoxin Tolerance in Preterm Fetal Sheep Exposed to Chorioamnionitis

Pulmonary and Systemic Endotoxin Tolerance in Preterm Fetal Sheep Exposed to Chorioamnionitis

Pulmonary inflammation and bronchopulmonary dysplasia

Preterm premature rupture of membranes, chorioamnion inflammatory scores and neonatal respiratory outcome

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