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Surfactant plus budesonide decreases lung and systemic responses to injurious ventilation in preterm sheep

ABSTRACT: Surfactant plus budesonide decreases lung and systemic responses to injurious ventilation in preterm sheep

PROVIDER: PRJNA542880 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9054250_1.fastq.gz	Fastqsanger.gz
	SRR9054250_2.fastq.gz	Fastqsanger.gz
	SRR9054260_1.fastq.gz	Fastqsanger.gz
	SRR9054260_2.fastq.gz	Fastqsanger.gz
	SRR9054270_1.fastq.gz	Fastqsanger.gz

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Surfactant plus budesonide decreases lung and systemic responses to injurious ventilation in preterm sheep

Project description:Background: Intratracheal budesonide mixed with surfactant has been investigated as an alternative to decrease lung injury and prevent bronchopulmonary dysplasia in preterm infants. However, possible systemic effects are not known. Our goal was identify systemic effects of intra-tracheal instilled budesonide by transcriptome analysis of the brain and lung in a preterm lamb model of mechanical ventilation. Methods: We performed RNA-sequencing of the fetal periventricular white matter and liver from preterm sheep after treatment with intratracheal budesonide mixed with surfactant or surfactant alone followed by mechanical ventilation. Unventilated animals were used as controls. mRNA profiles were generated from polyA selected RNA using Illumina platform. Read sequences were aligned to the sheep genome (Oar 4.0) using Bowtie2 followed read counts using featureCounts. We performed differential expression analysis using EdgeR. Results: We identified large and significant gene expression genes both in the liver and in the priventricular white matter in animals treated with budesonide+surfactant compared to surfactant alone and unventilated animals. There were complexes synergies and antagonism of effect of ventilation and budesonide on gene expression. Ventilation induced inflammatory signaling in the periventricular white matter and liver which was partially antagonized by budesonide. Budesonide also suppressed developmental pathways in the periventricular white matter. Conclusions: Intratracheal budesonide had systemic effects including suppression of developmental pathways in the brain. These effects could have clinical implication in affecting the neurodevelopmental outcomes of preterm newborns.

2019-11-26 | GSE131195 | GEO

MAP Kinase Phosphatase-1 Modulates Regional Effects of Injurious Mechanical Ventilation in Rodent Lungs

Project description:Scientific knowledge on the subjects: Injurious mechanical ventilation amplifies acute lung injury in a heterogeneous and regional fashion but the molecular mechanisms underlying regional lung injury and the protective effects of prone positioning are unclear. Regionally injurious ventilation is associated with discrete differential lung transcriptomic changes. Ventilating in the prone, compared with the supine position abrogates regional injury by depressing MKP-1.

2011-08-27 | GSE31678 | GEO

Surfactant plus budesonide decreases lung and systemic responses to injurious ventilation in preterm sheep.

Project description: Not available

| S-EPMC6985873 | biostudies-literature

MAP Kinase Phosphatase-1 Modulates Regional Effects of Injurious Mechanical Ventilation in Rodent Lungs

2011-08-26 | E-GEOD-31678 | biostudies-arrayexpress

Impact of aging on pulmonary cellular responses during mechanical ventilation

Project description:Acute respiratory distress syndrome (ARDS) results in significant morbidity and mortality, especially in the elderly. Mechanical ventilation, a common supportive treatment for ARDS, is necessary for maintaining gas exchange, but can also propagate injury. We hypothesized that aging would exacerbate the pathophysiological responses to mechanical ventilation. Young and aged male mice were mechanically ventilated and changes in surfactant function, inflammation, and vascular permeability were assessed. Additionally, single-cell RNA sequencing was used to delineate cell-specific transcriptional changes. The results showed that surfactant dysfunction was augmented in aged mice, while inflammation was less pronounced in aged animals. Futhermore, vascular permeability was significantly increased with aging. Differential gene expression and pathway analyses revealed that aged endothelial cells exhibited altered cell-cell junction formation and that alveolar macrophages in aged mice showed a blunted inflammatory response. These results highlight the complex interplay between aging and mechanical ventilation, including an age-related predisposition to endothelial barrier dysfunction due to altered cell-cell junction formation and decreased inflammation, potentially due to immune exhaustion. It is concluded that age-related vascular changes may underlie the increased susceptibility to injury during mechanical ventilation in elderly patients.

2025-03-02 | GSE274828 | GEO

Anti-Inflammatory Effects of Budesonide in Human Fetal Lung

Project description:Rationale. Lung inflammation in premature infants contributes to development of bronchopulmonary dysplasia (BPD), a chronic lung disease with long-term sequelae. Pilot studies administering budesonide suspended in surfactant have found reduced BPD without apparent adverse effects as occur with systemic dexamethasone therapy. Objectives. To determine effects of budesonide on differential genes expression in human fetal lung Methods. We prepared RNA from 3 samples of human fetal lung at 23 weeks gestation before (preculture, PC) and after 4 days culture as explants with (Bud) or without (Way) budesonide (30 nM) and performed RNAseq on the 9 samples.

2016-06-30 | E-GEOD-83888 | biostudies-arrayexpress

Lung ventilation

Project description:This project focuses both on the separate and combined effects of large tidal volume ventilation and hyperoxia on gene expression in the lungs of anesthetized rats. Rats were either mechanically or spontaneously ventilated at either 21 or 100% oxygen and expression levels were evaluated on RG_U34 GeneChips. Keywords: other

2003-07-16 | GSE489 | GEO

Alveolar epithelial glycocalyx degradation mediates surfactant dysfunction and contributes to acute respiratory distress syndrome

Project description:Acute Respiratory Distress Syndrome (ARDS) is a common cause of respiratory failure yet has few pharmacologic therapies, reflecting the mechanistic heterogeneity of lung injury. We hypothesized that damage to the alveolar epithelial glycocalyx, a layer of glycosaminoglycans interposed between the epithelium and surfactant, contributes to lung injury in ARDS patients. Using mass spectrometry of airspace fluid noninvasively collected from mechanically-ventilated patients, we found that airspace glycosaminoglycan shedding (an index of glycocalyx degradation) occurred predominantly in patients with direct lung injury and was associated with duration of mechanical ventilation. Male patients had increased shedding which correlated with airspace concentrations of matrix metalloproteinases. Selective epithelial glycocalyx degradation in mice was sufficient to induce surfactant dysfunction, a key characteristic of ARDS, leading to microatelectasis and decreased lung compliance. Rapid colorimetric quantification of airspace glycosaminoglycans was feasible and could provide point-of-care prognostic information to clinicians and/or be used for predictive enrichment in clinical trials.

2021-12-07 | GSE186705 | GEO

Anti-Inflammatory Effects of Budesonide in Human Fetal Lung

2016-06-30 | GSE83888 | GEO

Mechanisms of variable ventilation in experimental lung injury

Project description:In the present study we seek to identify changes in lung gene expression under mechanical ventilation in uninjured as well as acutely and chronically injured lungs. A standard volume-controlled lung-protective ventilatory protocol is compared to a concept of mechanical ventilation using variable tidal volumes.

2017-02-17 | GSE78008 | GEO

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