Impact of Histological Chorioamnionitis on Tracheal Aspirate Cytokines in Premature Infants

Aghai, Zubair H.; Camacho, Jeanette; Saslow, Judy; Mody, Kartik; Eydelman, Riva; Bhat, Vishwanath; Stahl, Gary E.; Pyon, Kee H.; Bhandari, Vineet

doi:10.1055/s-0032-1311980

Cited by 19 publications

(20 citation statements)

References 14 publications

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“…[21–23] Tracheal aspirate samples collected from ventilated preterm infants showed higher concentrations of IL-1α, IL-1β, and IL-8 in a group of infants with chorioamnionitis. [24] …”

Section: Discussionmentioning

confidence: 99%

Meta-analysis of antenatal infection and risk of asthma and eczema

Zhu

Zhang

et al. 2016

Medicine

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“…[21–23] Tracheal aspirate samples collected from ventilated preterm infants showed higher concentrations of IL-1α, IL-1β, and IL-8 in a group of infants with chorioamnionitis. [24] …”

Section: Discussionmentioning

confidence: 99%

Meta-analysis of antenatal infection and risk of asthma and eczema

Zhu

Zhang

et al. 2016

Medicine

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“…Support for decreased levels of MIF being involved in the pathogenesis of BPD has also been demonstrated in tracheal aspirate fluid from extremely premature infants exposed to systemic fetal inflammation early in life [3]. Antenatal exposure to inflammation has been associated as one of the factors playing in the development of BPD [5,22,23]. …”

Section: Discussionmentioning

confidence: 99%

Small molecular modulation of macrophage migration inhibitory factor in the hyperoxia-induced mouse model of bronchopulmonary dysplasia

et al. 2013

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BackgroundThe role and mechanism of action of MIF in bronchopulmonary dysplasia (BPD) are not known. We hypothesized that increased MIF signaling would ameliorate the pulmonary phenotype of BPD in the mouse lung.MethodsWe studied newborn wild type (WT), MIF knockout (MIFKO), and lung MIF transgenic (MIFTG) mice in room air and a BPD model, and examined the effects of administering a small molecule MIF agonist and antagonist. Lung morphometry was performed and mRNA and protein expression of vascular mediators were analyzed.ResultsThe pulmonary phenotype of MIFKO and MIFTG mice lungs in room air (RA) and BPD model were comparable to the WT-BPD mice at postnatal (PN) day 14. Vascular endothelial growth factor (VEGF)-A, -R1 and Angiopoietin (Ang)1 mRNA were decreased, and Ang2 increased in the WT-BPD, MIFKO-RA, MIFKO-BPD, MIFTG-RA and MIFTG-BPD mice lungs, compared to appropriate controls. The protein expression of Ang1 in the MIFKO-RA was similar to WT-RA, but decreased in MIFTG-RA, and decreased in all the BPD groups. Ang2 was increased in MIFKO-RA, MIFTG-RA and in all 3 BPD groups. Tie2 was increased in WT-BPD compared to WT-RA, but decreased in MIFKO- and MIFTG- RA and BPD groups. VEGFR1 was uniformly decreased in MIFKO-RA, MIFTG-RA and in all 3 BPD groups. VEGF-A had a similar expression across all RA and BPD groups. There was partial recovery of the pulmonary phenotype in the WT-BPD model treated with the MIF agonist, and in the MIFTG mice treated with the MIF antagonist.ConclusionsThese data point to the careful regulatory balance exerted by MIF in the developing lung and response to hyperoxia and support the potential therapeutic value of small molecule MIF modulation in BPD.

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“…Detection of Arg1 (BD Biosciences), Ym1 (Chi3l3) (STEMCELL Technologies), iNOS, and β -actin (Santa Cruz Biotechnology Inc.) was done using appropriate antibodies by Western analysis, as described previously [18, 20, 24]. Proteins were visualized with the pico ECL Western blotting kit (Pierce), and blots were exposed to HyBlot autoradiography films (Denville Scientific Inc.).…”

Section: Methodsmentioning

confidence: 99%

Hyperoxia Exacerbates Postnatal Inflammation-Induced Lung Injury in Neonatal BRP-39 Null Mutant Mice Promoting the M1 Macrophage Phenotype

Syed

Bhandari

2013

Mediators of Inflammation

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Rationale. Hyperoxia exposure to developing lungs—critical in the pathogenesis of bronchopulmonary dysplasia—may augment lung inflammation by inhibiting anti-inflammatory mediators in alveolar macrophages. Objective. We sought to determine the O2-induced effects on the polarization of macrophages and the role of anti-inflammatory BRP-39 in macrophage phenotype and neonatal lung injury. Methods. We used RAW264.7, peritoneal, and bone marrow derived macrophages for polarization (M1/M2) studies. For in vivo studies, wild-type (WT) and BRP-39−/− mice received continuous exposure to 21% O2 (control mice) or 100% O2 from postnatal (PN) 1 to PN7 days, along with intranasal lipopolysaccharide (LPS) administered on alternate days (PN2, -4, and -6). Lung histology, bronchoalveolar lavage (BAL) cell counts, BAL protein, and cytokines measurements were performed. Measurements and Main Results. Hyperoxia differentially contributed to macrophage polarization by enhancing LPS induced M1 and inhibiting interleukin-4 induced M2 phenotype. BRP-39 absence led to further enhancement of the hyperoxia and LPS induced M1 phenotype. In addition, BRP-39−/− mice were significantly more sensitive to LPS plus hyperoxia induced lung injury and mortality compared to WT mice. Conclusions. These findings collectively indicate that BRP-39 is involved in repressing the M1 proinflammatory phenotype in hyperoxia, thereby deactivating inflammatory responses in macrophages and preventing neonatal lung injury.

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Impact of Histological Chorioamnionitis on Tracheal Aspirate Cytokines in Premature Infants

Abstract: CHORIO is associated with increased specific proinflammatory mediators in TA samples of preterm infants.

Cited by 19 publications

References 14 publications

Meta-analysis of antenatal infection and risk of asthma and eczema

Meta-analysis of antenatal infection and risk of asthma and eczema

Small molecular modulation of macrophage migration inhibitory factor in the hyperoxia-induced mouse model of bronchopulmonary dysplasia

Hyperoxia Exacerbates Postnatal Inflammation-Induced Lung Injury in Neonatal BRP-39 Null Mutant Mice Promoting the M1 Macrophage Phenotype

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