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Identification of 3 Endotypes In Pediatric ARDS Using Nasal Transcriptomics-Standard Input

ABSTRACT: Identification of 3 Endotypes In Pediatric ARDS Using Nasal Transcriptomics-Standard Input

PROVIDER: PRJNA641108 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12067631_1.fastq.gz	Fastqsanger.gz
	SRR12067631_2.fastq.gz	Fastqsanger.gz
	SRR12067632_1.fastq.gz	Fastqsanger.gz
	SRR12067632_2.fastq.gz	Fastqsanger.gz
	SRR12067633_1.fastq.gz	Fastqsanger.gz

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Identification of 3 Endotypes In Pediatric ARDS Using Nasal Transcriptomics-Standard Input

Project description:This study used nasal transcriptomic profiling of the inferior turbinate in control and pediatric ARDS subjects to identify endotypes. This data set is for non-amplified specimens. The study identfied three pediatric ARDS endotypes.

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Identification of 3 Endotypes In Pediatric ARDS Using Nasal Transcriptomics-Low Input

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Project description:The objective of this study was to identify differences in the nasal methylome of patients with Pediatric ARDS (PARDS) compared to controls and to observe how this might change over time. We found two different methylomic patterns. Subgroup 1 was comprised of entirely of PARDS subjects, and Subgroup 2 contained both control and PARDS subject. Subgroup 1was characterized by hypomethylation of genes related to cell adhesion and hypermethylation of cell metabolism-related genes. Over time, the methylation pattern of PARDS subjects changed, but the pattern of control subjects was stable. Five concurrent bronchial and nasal specimens were obtained showing very few differences in methylation between these two collection sites.

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Project description:The objective of this study was to determine if nasal transcriptomics could be used to characterize the underlying pathobiology and predict clinical course of patients with pediatric ARDS (PARDS). Subjects meeting consensus PARDS criteria or controls admitted to the Pediatric ICU without lung disease had nasal cytology brushings on days 1, 3, 7 and 14. The gene expression of these brushings was compared to identify subtypes and describe clinical course. Concurrent nasal and bronchial brushings were collected if bronchoscopy was performed. We identified four PARDS subgroups, termed A, B, C, and D. Subgroup B was marked by inflammation and ciliary cell dysfunction. Subgroup D was marked by reduced epithelial stem cell mRNAs without inflammation. Subgroup A had hypo-inflammation and upregulation of pathways important in epithelial cell repair. Subgroup C had increased ciliary cell genes. Control specimens almost entirely clustered with Subgroup C, but one that developed PARDS clustered with Subgroup B and several that developed lung injury clustereced with Subgroups B and A. Over time, Subgroups D and B transitioned to A which transitioned to C. Bronchial and nasal gene expresison were similar.

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