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Next-generation sequencing of rhesus macaques lung after treatment with a low-dose or clinical antenatal corticosteroid treatment

ABSTRACT: Next-generation sequencing of rhesus macaques lung after treatment with a low-dose or clinical antenatal corticosteroid treatment

PROVIDER: PRJNA485650 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7687140_1.fastq.gz	Fastqsanger.gz
	SRR7687140_2.fastq.gz	Fastqsanger.gz
	SRR7687150_1.fastq.gz	Fastqsanger.gz
	SRR7687150_2.fastq.gz	Fastqsanger.gz
	SRR7687141_1.fastq.gz	Fastqsanger.gz

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Next-generation sequencing of rhesus macaques lung after treatment with a low-dose or clinical antenatal corticosteroid treatment

Project description:Purpose: Evaluate fetal lung maturation and transcriptome after clinical treatment with antenatal corticosteroids compared to an alternative treatment with a slow release low-dose formulation. Methods: Lung mRNA profiles of rhesus macaques were generated by RNA sequencing. Reads that met quality thresholds were aligned to the rhesus macaque genome and number of reads per gene was counted. RNA-sequencing of the hippocampus was done. Differential expression analysis was done using read counts. Results: A relatively low dose of Beta-Ac increased lung compliance, surfactant concentration and relative airspace of the fetal lung equivalent to the clinical drug. By transcriptome analyses, the early suppression of genes associated with immune responses and the downregulation of genes associated with developmental pathways were less changed by Beta-Ac than the clinical drug. There were no significant differences between Beta-Ac and control while the clinical drug suppressed maturational pathways including genes involved in neurogenesis, neuronal differentiation and stem cell fate commitment. Conclusions: We report that low-dose betamethasone-acetate has decreased impact on lung transcriptome compared to the clinical treatment.

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Conserved DNA Methylation Signatures in the Prefrontal Cortex of Newborn and Juvenile Guinea Pigs Following Antenatal Betamethasone Exposure

Project description:We investigated the effect of antenatal corticosteroid exposure (ACS) on the DNA methylation patterns in the prefrontal cortex (PFC) of female guinea pig offspring. Guinea pig dams were treated with saline or betamethasone on gestational days 50/51. PFC was collected from newborn (post-natal day 1) and juvenile (PND 14) offspring. Methylation assessment using genomic DNA was performed with reduced representation bisulfite sequencing techniques.

2024-11-06 | GSE280726 | GEO

2-hydroxypropyl-beta-cyclodextrin treatment induces modest immune activation in healthy rhesus macaques [RNA-seq]

Project description:Experimental SIV infection of Asian macaques is an excellent model for HIV disease progression and therapeutic development. Recent coformulations of nucleoside analogs and an integrase inhibitor have been used for parenteral antiretroviral (ARV) administration in SIV-infected macaques, successfully resulting in undetectable plasma SIV RNA. In a cohort of SIVmac239-infected macaques, we recently observed that administration of co-formulated ARVs resulted in an unexpected increase in plasma levels of soluble CD14 (sCD14), associated with stimulation of myeloid cells. We hypothesized that the coformulation solubilizing agentKleptoseTM(2-hydroxypropyl-beta-cyclodextrin; HPβCD) may induce inflammation with myeloid cell activation and the release of sCD14. Herein, we stimulated peripheral blood mononuclear cells (PBMCs) from healthy macaques with HPβCD from different commercial sources and evaluated inflammatory cytokine productionin vitro.Treatment of PBMCs resulted in increased sCD14 release and myeloid cell IL-1bproduction - with stimulation varyingsignificantlyby HPβCD source - and destabilized lymphocyte CCR5 surface expression.We further treated healthy macaques withKleptosealone.In vivo, we observed modestly increased myeloid cell activation in response to Kleptose treatment without significant perturbation of the immunological transcriptome or epigenome.Our resultsdemonstrate a need for vehicle-only controls and highlight immunological perturbations that can occur when using HPβCD in pharmaceutical co-formulations.

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2-hydroxypropyl-beta-cyclodextrin treatment induces modest immune activation in healthy rhesus macaques [ATAC-seq]

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Identification of a DNA methylation signature in whole blood of newborn guinea pigs and human neonates following antenatal betamethasone exposure

Project description:We investigated the effect of antenatal corticosteroid exposure (ACS) on the DNA methylation patterns in the whole blood of female guinea pig offspring. Guinea pig dams were treated with saline or betamethasone on gestational days 50/51. Whole blood was collected from newborn offspring (post-natal day 1) and dried on blood spot cards. Methylation assessment using genomic DNA was performed with reduced representation bisulfite sequencing techniques.

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Project description:Purpose: Our goal was to evaluate the pathways through which chorioamnionitis induces fetal lung maturation and how it interacts with a low-dose treatment with antenatal corticosteroids to further enhance fetal lung maturation. Methods: We treated pregnant rhesus macaque at 132 days (80% gestation) with intre-amniotic bacterla lipopolissacharide to model chorioamnionitis or a low-dose antenatal corticosteroids treatment with betamethasone-acetate (Beta-Ac 0.125mg/kg) or both treatments. Fetuses were delivered by c-section after 5 days and RNA-sequencing of whole lung tissue was performed. Another group of fetuses exposed to LPS was delivered 16h after treatment. Preterm controls were delivered at 132 days and term controls were delivered at 155 days and received no intervention. Results: Treatment with Beta-Ac in the setting of chorioamnionitis improves lung compliance and increases surfactant production relative to either treatment alone. RNA sequencing shows that these changes are mediated by suppression of proliferation and induction of mesenchymal cellular death. The combined exposure results in a mature-like transcriptomic profile with inhibition of extracellular matrix development by suppression of collagen genes and regulators of lung development. ACS and inflammation also suppressed signature genes associated with proliferative mesenchymal progenitors similar to the term lung. Conclusion: Treatment with ACS in the setting of inflammation may result in early respiratory advantage to preterm infants, but this advantage may come at a cost of abnormal extracellular matrix development which may be associated with increased risk of chronic lung disease.

2021-02-01 | GSE148645 | GEO

Corticosteroid treatment during sepsis influences hippocampal function in survivors

Project description:Corticosteroid treatment during sepsis influences hippocampal function in survivors

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Corticosteroid treatment during sepsis influences hippocampal function in survivors

Project description:Millions of sepsis survivors annually face long-term neuropsychiatric sequelae of their illness. Corticosteroids are frequently administered in sepsis, and their use affects neuropsychiatric outcomes, but the mechanisms are unknown. We used the cecal ligation and puncture method to induce acute infection in mice and test the hypothesis that corticosteroid treatment during illness has long-term effects on hippocampal function. Functional phenotyping and hippocampal RNA-sequencing were performed in the same survivor mice to identify underlying mechanisms of behavioral and neuroendocrine outcomes. Long-term CLP survivors exhibited anxiety-like behavior, increased central hypothalamic-pituitary-adrenal (HPA) axis activity, and persistent systemic and neuro-inflammation. The relationship between gene expression and behavior suggested a protective role for inflammation and oxidative metabolism after CLP. Corticosterone treatment during illness had distinct effects on hippocampal function in survivors, including object memory impairment. The long-term behavioral effects of corticosterone treatment were associated with persistent downregulation of activity-dependent gene expression in the hippocampus. The results suggest that corticosteroid treatment for sepsis influences hippocampal function in survivors via long-lasting changes to basal hippocampal activity. Neural activity, inflammation, and oxidative metabolism should be explored as future treatment targets to modify neuropsychiatric outcomes in sepsis survivors.

2023-07-31 | GSE225868 | GEO

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