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Autonomous neutrophil ageing in the lung governed by the pulmonary microbiome

ABSTRACT: Autonomous neutrophil ageing in the lung governed by the pulmonary microbiome

PROVIDER: PRJNA646201 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12216286.fastq.gz	Fastqsanger.gz
	SRR12216287.fastq.gz	Fastqsanger.gz
	SRR12216288.fastq.gz	Fastqsanger.gz
	SRR12216289.fastq.gz	Fastqsanger.gz
	SRR12216290.fastq.gz	Fastqsanger.gz

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Autonomous neutrophil ageing in the lung governed by the pulmonary microbiome

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Project description:Epidemics of influenza virus are of great challenges to the public concern. The lung inflammation and injury caused by excessive inflammatory cell infiltration into the lungs and overproduction of inflammatory mediators are major consequences during influenza virus infection. Neutrophils are vital for anti-microbial defense. However, the roles of neutrophils during viral infections are less clear. Furthermore, the molecular regulation of neutrophil fate and function at the viral infected sites is largely elusive. We found that BCL6 deficiency in neutrophils, but not in monocytes nor lung macrophages, attenuated host inflammation and morbidity following influenza infection. Mechanistically, BCL6 bound to the neutrophil gene loci involved in cellular apoptosis specifically at the site of infection. As such, BCL6 disruption resulted in increased expression of apoptotic genes in neutrophils in the respiratory tract, but not in the circulation nor bone marrow. Consequently, BCL6 deficiency promoted tissue neutrophil apoptosis. Our results have revealed a previously unappreciated role of BCL6 in modulating neutrophil apoptosis at the site of infection for the regulation of host disease development following viral infection.

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