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IL-17RA promotes pathologic epithelial inflammation in a mouse model of upper respiratory influenza infection

ABSTRACT: IL-17RA promotes pathologic epithelial inflammation in a mouse model of upper respiratory influenza infection

PROVIDER: PRJNA941228 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23705978_1.fastq.gz	Fastqsanger.gz
	SRR23705978_2.fastq.gz	Fastqsanger.gz
	SRR23705979_1.fastq.gz	Fastqsanger.gz
	SRR23705979_2.fastq.gz	Fastqsanger.gz
	SRR23705980_1.fastq.gz	Fastqsanger.gz

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IL-17RA promotes pathologic epithelial inflammation in a mouse model of upper respiratory influenza infection

Project description:The upper respiratory tract (nasopharynx or NP) is the first site of influenza replication, allowing the virus to disseminate to the lower respiratory tract or promoting community transmission. The host response in the NP regulates an intricate balance between viral control and tissue pathology. The hyper-inflammatory responses promote epithelial injury, allowing for increased viral dissemination and susceptibility to secondary bacterial infections. However, the pathologic contributors to influenza upper respiratory tissue pathology are incompletely understood. In this study, we investigated the role of IL-17RA as a modulator of influenza host response and inflammation in the upper respiratory tract. We used a combined experimental approach involving IL-17RA-/- mice and an air-liquid interface (ALI) epithelial culture model to investigate the role of IL-17 response in epithelial inflammation, barrier function, and tissue pathology. Our data show that IL-17RA-/- mice exhibited significantly reduced neutrophilia, epithelial injury, and viral load. The reduced NP inflammation and epithelial injury in IL-17RA-/- mice correlated with increased resistance against co-infection by Streptococcus pneumoniae (Spn). IL-17A treatment, while potentiating the apoptosis of IAV-infected epithelial cells, caused bystander cell death and disrupted the barrier function in ALI epithelial model, supporting the in vivo findings.

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