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Identifying modulators of inflammation in an in vitro airway epithelial inflammation model using an arrayed CRISPRi screen

ABSTRACT: Identifying modulators of inflammation in an in vitro airway epithelial inflammation model using an arrayed CRISPRi screen

PROVIDER: PRJNA1130987 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29683600.fastq.gz	Fastqsanger.gz
	SRR29683700.fastq.gz	Fastqsanger.gz
	SRR29683601.fastq.gz	Fastqsanger.gz
	SRR29683701.fastq.gz	Fastqsanger.gz
	SRR29683602.fastq.gz	Fastqsanger.gz

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Identifying modulators of inflammation in an in vitro airway epithelial inflammation model using an arrayed CRISPRi screen

Project description:To study modulators of inflammatory airway disease, we developed an in vitro bronchial epithelial cell model system based on the BEAS-2B cell line exposed to lipopolysaccharide (LPS) and diesel exhaust particles (DEP). Combined LPS and DEP exposure triggered a molecular inflammatory phenotype, including elevated TSLP and IL-8 mRNA expression, similar to that observed in airway epithelial cells from asthma patients. In this model, we performed high-throughput perturbation of 24 mRNA and long non-coding (lncRNA) target genes through an arrayed CRISPR-interference screen, followed by shallow RNA-sequencing to identify modulators of inflammation. Perturbation of individual targets had a significant impact on the BEAS-2B DEP/LPS transcriptome. Some mRNA targets reversed the DEP/LPS gene expression signature upon knockdown and could serve as candidate therapeutic targets. Perturbation of other target genes however further amplified the pro-inflammatory signature and thus may have an anti-inflammatory role in these cells. In conclusion, we present a novel in vitro model system for airway inflammation that exhibited an inflammatory profile relevant for asthmatic patients, and demonstrate the feasibility to perform high-throughput target perturbation and molecular phenotyping by integrating CRISPR-interference and shallow RNA-sequencing.

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