Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB18183 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR570908.fastq.gz | Fastqsanger.gz | |||
| DRR570909.fastq.gz | Fastqsanger.gz | |||
| DRR570910.fastq.gz | Fastqsanger.gz | |||
| DRR570911.fastq.gz | Fastqsanger.gz | |||
| DRR570912.fastq.gz | Fastqsanger.gz |
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Project description:Background: Dupilumab, a fully human monoclonal antibody that binds IL-4Ra and inhibits signaling of both IL-4 and IL-13, has shown efficacy across multiple diseases with underlying type 2 signatures and is approved for treatment of asthma, atopic dermatitis and chronic sinusitis with nasal polyposis. We sought to provide a comprehensive analysis of the redundant and distinct roles of IL-4 and IL-13 in type 2 inflammation and report dupilumab mechanisms of action. Methods: Using primary cell assays and a mouse model of house dust mite induced asthma, we compared IL-4 versus IL-13 versus IL-4Ra blockers. Results: Intranasal administration of either IL-4 or IL-13 confers an asthma-like phenotype in mice by inducing immune cell lung infiltration, including eosinophils, increasing cytokine/chemokine expression and mucus production, thus demonstrating redundant functions of these cytokines. We further teased out their respective contributions using human in vitro culture systems. Then, in a mouse asthma model by comparing in head to head studies, either IL-4 or IL-13 inhibition to dual IL-4/IL-13 inhibition, we demonstrate that blockade of both IL-4 and IL-13 is required to broadly block type 2 inflammation, which translates to protection from allergen-induced lung function impairment. Notably, only dual IL-4/IL-13 blockade prevented eosinophil infiltration into lung tissue without affecting circulating eosinophils, demonstrating that tissue, but not circulating eosinophils contribute to disease pathology. Conclusions: Overall, these data support IL-4 and IL-13 as key drivers of type 2 inflammation, and help provide insight into the therapeutic mechanism of dupilumab, a dual IL-4/IL-13 blocker, in multiple type 2 diseases.
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Project description:Purpose: We aimed to characterize the role of apoptotic cells in regulating eosinophils' response to diverse stimuli. Methods:Eosinophils were purified from the peritoneal cavity of Il5Tg mice and stimulated with IL-4 (i.e. type 2 activated eosinophils), IFN-γ, and a combination of lipopolysaccharide (LPS, i.e. type 1 activated eosinophils) and IFN-γ in the presence of apoptotic cells. Thereafter, RNA was obtained and the transcriptome signature following each stimulation was determined using RNA sequencing. Raw sequencing reads were trimmed and filtered using fastp, then aligned to mouse genome assembly (GRCm38) using STAR 2.7.2a. Normalization and differential expression analysis were performed in R 4.0.3 using the package DESeq2. Finally, gene ontology annotations were obtained from Ensembl and pathway graphs were obtained from KEGG. Results:RNAseq analysis revealed that apoptotic cells induce transcriptional changes in eosinophils and resulted in enrichment in pathways related to wounding and cell migration. Conclusion:RNAseq analysis of transcripts that were downregulated by apoptotic cells revealed that apoptotic cells inhibit pathways as defense responses and inflammatory responses and that apoptotic cells augmented eosinophils' response to IL-4.
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