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Inhibition of γ-glutamyl transpeptidase suppresses LPS induced asthma exacerbation in a mouse model

ABSTRACT: Inhibition of γ-glutamyl transpeptidase suppresses LPS induced asthma exacerbation in a mouse model

PROVIDER: PRJNA900797 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22266605_1.fastq.gz	Fastqsanger.gz
	SRR22266605_2.fastq.gz	Fastqsanger.gz
	SRR22266606_1.fastq.gz	Fastqsanger.gz
	SRR22266606_2.fastq.gz	Fastqsanger.gz
	SRR22266607_1.fastq.gz	Fastqsanger.gz

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Inhibition of γ-glutamyl transpeptidase suppresses LPS induced asthma exacerbation in a mouse model

Project description:To investigate the role of γ-glutamyltranspeptidase in severe asthma, we established an OVA/ LPS-induced asthma model. Inflammation analysis and second-generation sequencing revealed the mechanism by which inhibition of γ-glutamyltranspeptidase inhibited LPS-induced asthma exacerbation in mice.

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Project description:Our study aimed to better understand the immune responses during an acute asthma exacerbation in children. Gene expression profiles were examined by RNA-sequencing in blood samples. Samples were collected on average 2.5 day after systemic corticosteroid treatment. Our findings show that pro-inflammatory genes and pathways related to innate responses and signaling remained increased in children hospitalized for acute asthma exacerbation. Genes and pathways involved in adaptive immune respones, particularly T lymphocyte activation, were decreased in children hospitalized for acute asthma exacerbation. These studies suggest that innate immune responses may remain activated following hospitalization for asthma exacerbation.

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Project description:Background: Clinical transcriptomics of peripheral blood mononuclear cells (PBMC) are coming into focus as a surrogate approach for prognosis, diagnosis, biomarker discovery and examination disease mechanisms. However, bioassays paired with transcriptomic analytic tools are yet to be developed and made available at point of care. Harnessing personal dynamic genomic responses to tailor patient asthma treatment or prevent disease exacerbations remain unmet medical needs. Method: We developed a rhinovirus-stimulated peripheral blood based-assay (virogram assay) coupled with single-subject analytics (N-of-1-patwhays) to capture dynamic genome-wide expression and dysregulated pathways to retrospectively predict childhood asthma exacerbation. We hypothesized that some genomic factors might predispose any given individual, healthy or asthmatic, to a set of similar transcriptional responses to rhinovirus stimulation. We first generated a classifier from paired sample microarrays, control and stimulated PBMC from healthy subjects and applied this classifier on the transcriptomic analysis of control and HRV-stimulated PBMC samples (virogram assay) from children with asthma. Results: The analysis of the different genomic responses of single-subject paired PBMC samples (HRV-stimulated and control) derived from healthy individuals (external dataset) enabled the discovery of dysregulated pathways related to acquired immunity, epigenetics and morphogenesis. The classifier built on these results and applied on the transcriptional analysis derived from the virogram assay predicted that the risk of asthma exacerbation among asthmatic subjects with an accuracy of 70%. Conclusion: We provide evidence that clinical prognosis can be predicted with a PBMC based-bioassay aligned with adequate single-subject analytics to assess dynamic transcriptomic response to specific disease-associated stimuli.

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Project description:A model of human asthma exacerbation identifies mechanisms that drive allergic asthma

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A model of human asthma exacerbation identifies mechanisms that drive allergic asthma

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