Differential Patterns of 27 Cord Blood Immune Biomarkers Across Gestational Age

Matoba, Nana; Yu, Yunxian; Mestan, Karen K.; Pearson, Colleen; Ortiz, Katherin; Porta, Nicolas F M; Thorsen, Poul; Skogstrand, Kristin; Hougaard, David M.; Zuckerman, Barry; Wang, Xiaobin

doi:10.1542/peds.2008-1222

Cited by 127 publications

(118 citation statements)

References 31 publications

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“…In this study, the higher levels of IL6 and IL8 in premature versus full-term infants are consistent with similar results in dried infant blood samples (38). Higher IL6, IL8, and MCP1 were found in cord blood from lower GA infants compared with full-term neonates (39). IL6 and IL8 were higher in the amniotic fluid of patients with premature labor or preterm premature rupture of membrane (40).…”

Section: Discussionsupporting

confidence: 85%

Biomarkers of Epidermal Innate Immunity in Premature and Full-Term Infants

et al. 2010

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ABSTRACT:Epidermal innate immunity is a complex process involving a balance of pro-and anti-inflammatory cytokines, structural proteins, and specific antigen presenting cells occurring against a background of neuroendocrine modulators such as cortisol. In this study, a multiplex array system was used to simultaneously determine multiple molecular factors critical for development of epidermal innate immune function from the skin surface of premature and term infants, healthy adults, and vernix caseosa. Samples were analyzed for Keratin 1,10,11, Keratin 6, involucrin, albumin, fibronectin and cortisol, and cytokines IL-1, TNF␣, IL-6, IL-8, MCP1, IP10, IFN␥, and IL-1 receptor antagonist. Keratin 1,10,11 was decreased and involucrin was increased in infants versus adults. All infants had elevated IL1␣ and reduced TNF␣ versus adults. IL-6, IL-8, and MCP1 were significantly increased in premature versus term infants and adults. Skin surface cortisol and albumin were significantly elevated in premature infants. The biomarker profile in premature infants was unique with differences in structural proteins, albumin, and cytokines IL-6, IL-1␤, IL-8, and MCP1. The higher infant IL1␣ may be associated with skin barrier maturation. The significant elevations in skin surface cortisol for preterm infants may reflect a neuroendocrine response to the stress of premature birth. (Pediatr Res 67: 382-386, 2010)

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Section: Discussionsupporting

confidence: 85%

Biomarkers of Epidermal Innate Immunity in Premature and Full-Term Infants

et al. 2010

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“…This finding was also described by Matoba et al who quantified twenty-seven types of cytokines in cord blood at different gestational ages and found that MCP-1 was the one that was most strongly associated with PTB [40]. Significantly higher levels of MCP-1 have also been measured in cervicovaginal fluid [41] …”

Section: Page 6 Ofsupporting

confidence: 77%

Microbiologic and Inflammatory Markers of Periodontitis are Different to those of Preterm Birth

M¹,

Gayet-Ageron²,

Roux‐Lombard³

et al. 2017

Gynecol Obstet

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Citation: Lumbreras Areta M, Gayet-Ageron A, Roux-Lombard P, Schrenzel J, AbstractBackground: Comparing microbiologic and inflammatory markers of periodontitis with those of preterm birth (PTB).Methods: Secondary analysis of a prior prospective case-control study done at the Geneva University Hospitals. Cases were women delivering at 22-34 6/7 weeks (early PTB, n=30) and controls were women delivering at ≥ 37 weeks (term delivery, n=87). We collected dental plaque during labour to quantify RNA levels from Aggregatibacter actinomycetemcomitans (Aa), Tannerella forsythia (Tf), Porphyromonas gingivalis (Pg) and Treponema denticola (Td). We also collected cord blood for cultures and cytokine quantification (IL-1Ra, IL-6, IL-8, IL-10, IL-17, TNF-α, MCP-1 and RANTES). Periodontal status was evaluated at the immediate postpartum using the American Consensus definition. Data was analysed by univariate and multivariate logistic regression.Results: Levels of Pg and Td were significantly higher in dental plaque of women with severe and moderate periodontitis. Microbiologic composition of dental plaque was not different between preterm and term delivery groups. There were no differences in cord blood cultures between groups. Cord TNF-α ≥ 8 pg/ml and IL-10 ≥ 1.3 pg/ml were associated with a higher risk of periodontitis (OR 2.78, 95% CI: 1.09-7.13, P=0.033; OR 2.78, 95% CI: 1.09-7.08, P=0.032 respectively), but differences were not significant at multivariate analysis. Cord MCP-1 ≥ 350 pg/ml was associated with a higher risk of PTB at both univariate (OR 40.25, P<0.001) and multivariate analysis (OR 53.71, P<0.001). Conclusion:In labour, microbiologic markers and inflammatory responses associated with periodontitis and PTB are different. The mechanisms linking periodontitis and PTB therefore still need to be elucidated. Page 2 of 9Citation: Lumbreras Areta M, Gayet-Ageron A, Roux-Lombard P, Schrenzel J, 2.38, 95% CI: 1.36-4.14, P=0.002) [20]. In this secondary analysis, we aim to compare the type of bacteria (in dental plaque and cord blood) and cytokines/chemokines (in cord blood) in women with severe periodontitis with those in women with early PTB. The objective is to determine if the microbiological and/or inflammatory pathways in periodontitis are the same as those involved in early PTB. A shared molecular pathway would explain the aetiology of the association between periodontitis and increased risk of PTB that was observed in our previous study. Methods Study designThis is a planned secondary analysis of women included in a prior prospective case-control (1:4) study performed between 09 November, 2007 and 18 March, 2010 at the maternity unit of the Geneva University Hospitals, Switzerland [20]. Briefly, the study evaluated the association of periodontitis in cases (women delivering spontaneously between 22 and 34, 6/7 weeks of gestation) compared to controls (women delivering as term [≥ 37 weeks]). The study was approved by the Ethics Committee of Geneva (study number 07-008, approved 28 March 2007). All partic...

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“…MIF has been found in cord blood (32,33). However, to the best of our knowledge, no data are available in blood of term and preterm neonates.…”

Section: Discussionmentioning

confidence: 94%

A Polymorphism in the Macrophage Migration Inhibitory Factor Promoter Is Associated With Bronchopulmonary Dysplasia

et al. 2011

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Bronchopulmonary dysplasia (BPD) is a common adverse outcome of prematurity, causing severe morbidity and mortality. The cytokine macrophage migration inhibitory factor (MIF) has been recently shown to favor murine fetal lung development. In this prospective study, we evaluate the expression of MIF in the lung and in the serum of preterm infants (n ϭ 50) and investigate whether the Ϫ173 G/C MIF promoter polymorphism is associated with the risk of BPD (n ϭ 103). MIF was highly expressed in lung tissue from preterm infants. Serum MIF levels were measured by ELISA at d 1 after birth. MIF levels were increased [median (interquartile range), 71.01 (44.9 -162.3) ng/mL], particularly in those infants with 2) ng/mL] compared with healthy adults [2.4 (1.2-5.0) ng/mL], (p Ͻ 0.001). The MIF Ϫ173*C allele, which predisposes to higher MIF production, was associated with a lower incidence of BPD (OR, 0.2; 95% CI, 0.04 -0.93), independently from mechanical ventilation and oxygen exposure (p ϭ 0.03). In conclusion, these data show that MIF expression is increased in lung and serum of preterm infants and suggest that the high producing MIF Ϫ173*C allele may be a protective factor for BPD. (Pediatr Res 69: 142-147, 2011) R DS and bronchopulmonary dysplasia (BPD) are major causes of morbidity and mortality in preterm neonates. RDS is an acute condition that appears in the first hours of life and is caused by the lack of pulmonary surfactant, with progressive atelectasis and respiratory insufficiency. BPD is a chronic condition, which appears later in life and is characterized by an initial inflammatory component, followed by alveolar edema and fibrosis, resulting in impaired development of the immature lung (1,2). Prematurity, RDS, mechanical ventilation, lung disruption, and oxygen (O 2 ) toxicity play a major role in BPD pathogenesis (3). The contribution of inflammation remains controversial (4). Chorioamnionitis and cytokine exposure in utero seem to protect from RDS, suggesting that inflammatory mediators and cytokines may promote lung maturation (5,6). Conversely, there is evidence that a postnatal exaggerated and/or prolonged inflammatory response may amplify lung damage, resulting in tissue autoinjury, structural changes, and ultimately BPD (7). In addition to environmental factors, heritability studies demonstrated that genetic factors also contribute to the susceptibility to BPD (8), and potential candidate genes have been identified (9 -15).Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine, which plays a critical role in immune and inflammatory responses. MIF induces macrophage production of cytokines and promotes T lymphocytes proliferation (16). It has been implicated in the pathogenesis of immune and inflammatory diseases, including sepsis, asthma, allergic neuritis, and rheumatoid arthritis (17,18). MIF has also been reported to be involved in angiogenesis (19,20). In lungs, MIF is expressed in alveolar macrophages, bronchial epithelial cells, and alveolar endothelium (21,22).Anima...

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Differential Patterns of 27 Cord Blood Immune Biomarkers Across Gestational Age

Cited by 127 publications

References 31 publications

Biomarkers of Epidermal Innate Immunity in Premature and Full-Term Infants

Biomarkers of Epidermal Innate Immunity in Premature and Full-Term Infants

Microbiologic and Inflammatory Markers of Periodontitis are Different to those of Preterm Birth

A Polymorphism in the Macrophage Migration Inhibitory Factor Promoter Is Associated With Bronchopulmonary Dysplasia

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