Amniotic fluid cytokines (interleukin-6, tumor necrosis factor-α, interleukin-1β, and interleukin-8) and the risk for the development of bronchopulmonary dysplasia

Yoon, Bo Hyun; Romero, Roberto; Jun, Jong Kwan; Park, Kyo Hoon; Park, June Dong; Ghezzi, Fabio; Kim, Beyong Il

doi:10.1016/s0002-9378(97)70276-x

Cited by 457 publications

(294 citation statements)

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“…24,26,27 Inactivation of surfactant components, activation of elastase activity and impairment of alveolarization and vascularization are part of the initiated pathologic Association between MBL and pulmonary morbidity in preterms A Hilgendorff et al processes. [33][34][35][36][37] In line with our findings, Gibson et al 38 have shown previously an association between genetic polymorphisms in the MBL gene at codon 54 and the presence of long-term neurological outcome, that is, cerebral palsy in infants. Furthermore, the potential role of MBL in apoptotic processes has to be discussed in context with our findings.…”

Section: Discussionsupporting

confidence: 91%

Association of polymorphisms in the mannose-binding lectin gene and pulmonary morbidity in preterm infants

et al. 2007

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Deficiency in the collectin mannose-binding lectin (MBL) increases the risk for pulmonary and systemic infections and its complications in children and adults. The aim of this prospective cohort study was to determine the genetic association of sequence variations within the MBL gene with systemic infections and pulmonary short-and long-term complications in preterm infants below 32 weeks gestational age (GA). Three single-nucleotide polymorphisms (SNPs) in the coding region and one SNP in the promotor region of MBL2 were genotyped by direct sequencing and with sequence-specific probes in 284 newborn infants o32 weeks GA. Clinical variables were comprehensively monitored. An association was found between two SNPs and the development of bronchopulmonary dysplasia (BPD), defined as persistent oxygen requirement at 36 weeks postmenstrual age, adjusting for covariates GA, grade of respiratory distress syndrome and days on mechanical ventilation (rs1800450 (exon 1 at codon 54, B variant): odds ratio dominant model (OR) ¼ 3.59, 95% confidence interval (CI) ¼ 1.62-7.98; rs7096206 (À221, X variant): OR ¼ 2.40, 95% CI ¼ 1. 16-4.96). Haplotype analyses confirmed the association to BPD, and a single haplotype (frequency 56%) including all SNPs in their wild-type form showed a negative association with the development of BPD. We detected no association between the MBL gene variations and the development of early-onset infections or further pulmonary complications. Frequent variants of the MBL gene, leading to low MBL concentrations, are associated with the diagnosis of BPD in preterm infants. This provides a basis for potential therapeutic options and further genetic and proteomic analysis of the function of MBL in the resistance against pulmonary long-term complications in preterm infants.

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Section: Discussionsupporting

confidence: 91%

Association of polymorphisms in the mannose-binding lectin gene and pulmonary morbidity in preterm infants

et al. 2007

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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

130

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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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“…[4][5][6] In this study, we focused on urinary excretion of B2M obtained from premature infants at birth as an alternative inflammatory marker, because a routine measurement of these cytokines in such clinical specimens is not yet feasible.…”

Section: Discussionmentioning

confidence: 99%

“…Elevated inflammatory mediators such as interleukin-6, interleukin-8 and tumor necrosis factor-in the umbilical cord plasma or amniotic fluid have already been reported to be sensitive indicators of CAM and independent risk factors for the development of BPD. 4,6 However, a direct assay of proinflammatory cytokines, which is both expensive and time consuming, is not suitable for routine laboratory testing in neonatal intensive care practice.…”

Section: Introductionmentioning

confidence: 99%

Urinary β-2-microglobulin as an alternative marker for fetal inflammatory response and development of bronchopulmonary dysplasia in premature infants

et al. 2010

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Objective: To evaluate the clinical utility of urinary b-2-microglobulin (B2M) at birth, an alternative to proinflammatory cytokines, as an indicative marker of fetal inflammatory response and subsequent higher risk of bronchopulmonary dysplasia (BPD) in premature infants.Study Design: The relationship between urinary B2M at birth and the occurrence of BPD was examined in 96 premature infants with a description of perinatal backgrounds. Constructing a receiver-operating characteristic curve to determine the cutoff value of urinary B2M at birth for the development of BPD, a multivariate logistic regression analysis was performed to evaluate whether elevated urinary B2M at birth can be used as a predictor of BPD.Results: BPD was diagnosed in 34% (33/96) of the infants. Neonates with BPD had a significantly higher occurrence rate of chorioamnionitis and greater levels of median urinary B2M at birth than did those without BPD. The selected cutoff value of urinary B2M at birth correlated with the development of BPD, even after adjusting for gestational age and other confounding factors.Conclusions: Elevated urinary B2M levels at birth can be used as an alternative marker of fetal inflammatory response and subsequent higher risk of BPD in premature infants.

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Amniotic fluid cytokines (interleukin-6, tumor necrosis factor-α, interleukin-1β, and interleukin-8) and the risk for the development of bronchopulmonary dysplasia

Cited by 457 publications

References 22 publications

Association of polymorphisms in the mannose-binding lectin gene and pulmonary morbidity in preterm infants

Association of polymorphisms in the mannose-binding lectin gene and pulmonary morbidity in preterm infants

Pulmonary inflammation and bronchopulmonary dysplasia

Urinary β-2-microglobulin as an alternative marker for fetal inflammatory response and development of bronchopulmonary dysplasia in premature infants

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