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B-Glucan Reprograms Neutrophils to Induce Disease Tolerance Against Influenza A Virus

ABSTRACT: b-Glucan Reprograms Neutrophils to Induce Disease Tolerance Against Influenza A Virus

PROVIDER: PRJNA1120170 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29286300.fastq.gz	Fastqsanger.gz
	SRR29286301.fastq.gz	Fastqsanger.gz
	SRR29286302.fastq.gz	Fastqsanger.gz
	SRR29286303.fastq.gz	Fastqsanger.gz
	SRR29286304.fastq.gz	Fastqsanger.gz

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Glucan Reprograms Neutrophils to Induce Disease Tolerance Against Influenza A Virus

Project description:Disease tolerance is an evolutionarily conserved host defence strategy that preserves tissue integrity and physiology without affecting pathogen load. Unlike host resistance, the mechanisms underlying disease tolerance remain poorly understood. In the present study, we investigated whether an adjuvant (β-glucan) can reprogram innate immunity to provide protection against Influenza A virus (IAV) infection. Here we observe that β-glucan treatment reduced the morbidity and mortality against IAV infection, independent of host resistance (viral load). Increased survival of β-glucan treated mice against IAV is associated with the accumulation of neutrophils via RORgt+ T cells in the lung tissue. Using gain-and-loss-of-function approaches, we demonstrate that β-glucan reprogrammed neutrophils are essential for promoting disease tolerance, limiting pulmonary tissue damage, and enhancing survival against IAV infection. β-glucan treatment promotes granulopoiesis in a type 1 interferon-dependent manner that leads to the generation of a unique subset of neutrophils, which are less mature with higher mitochondrial mass utilizing mitochondrial oxidative (OXPHOS) metabolism. Collectively, our data indicate that β-glucan reprograms hematopoietic stem cells (HSCs) to generate neutrophils with a novel “regulatory” function, which is required for promoting disease tolerance and maintaining lung tissue integrity against viral infection.

2024-11-22 | GSE248464 | GEO

b-Glucan Reprograms Neutrophils to Induce Disease Tolerance Against Influenza A Virus

Project description:Disease tolerance is an evolutionarily conserved host defence strategy that preserves tissue integrity and physiology without affecting pathogen load. Unlike host resistance, the mechanisms underlying disease tolerance remain poorly understood. In the present study, we investigated whether an adjuvant (β-glucan) can reprogram innate immunity to provide protection against Influenza A virus (IAV) infection. Here we observe that β-glucan treatment reduced the morbidity and mortality against IAV infection, independent of host resistance (viral load). Increased survival of β-glucan treated mice against IA V is associated with the accumulation of neutrophils via RoRgt+ T cells in the lung tissue. Using gain-and-loss-of-function approaches, we demonstrate that β- glucan reprogrammed neutrophils are essential for promoting disease tolerance, limiting pulmonary tissue damage, and enhancing survival against IAV infection. β-glucan treatment promotes granulopoiesis in a type 1 interferon-dependent manner that leads to the generation of a unique subset of neutrophils, which are less mature with higher mitochondrial mass utilizing mitochondrial oxidative (OXPHOS) metabolism. Collectively, our data indicate that β-glucan reprograms hematopoietic stem cells (HSCs) to generate neutrophils with a novel “regulatory” function, which is required for promoting disease tolerance and maintaining lung tissue integrity against viral infection.

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Glucan Reprograms Neutrophils to Induce Disease Tolerance Against Influenza A Virus

Project description:Glucan Reprograms Neutrophils to Induce Disease Tolerance Against Influenza A Virus

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Project description:Induction of trained immunity by beta-glucan affects myeloid cells and their bone marrow progenitors. In particular, broad epigenetic alterations in trained myeloid cells have been demonstrated. In this study, we performed single cell ATAC sequencing in GMP and neutrophils from beta-glucan treated mice, as compared to control-treated mice, in order to investigate the impact of trained immunity on the epigenetic profile of GMP and neutrophils.

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