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Glucan Reprograms Neutrophils to Induce Disease Tolerance Against Influenza A Virus

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

PROVIDER: PRJNA1044079 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26919368_1.fastq.gz	Fastqsanger.gz
	SRR26919368_2.fastq.gz	Fastqsanger.gz
	SRR26919369_1.fastq.gz	Fastqsanger.gz
	SRR26919369_2.fastq.gz	Fastqsanger.gz
	SRR26919370_1.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.

2024-11-19 | GSE269104 | GEO

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

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

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The effect of beta-glucan - induced trained immunity on the epigenetic profile of bone marrow granulocyte-macrophage progenitors (GMP) and neutrophils

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.

2020-10-30 | GSE152353 | GEO

The effect of beta-glucan - induced trained immunity on the transcriptomic profile of tumor-associated neutrophils (TAN)

Project description:Induction of trained immunity by beta-glucan has been shown to promote transcriptomic alterations in myeloid cells. Neutrophils are involved in the immune response against tumors and can promote or inhibit tumor growth. In this study, we performed RNA sequencing in TAN from mice in order to investigate the impact of trained immunity on the transcriptomic profile of neutrophils in the tumor setting.

2020-10-30 | GSE139450 | GEO

M. tuberculosis reprograms HSCs to limit myelopoiesis and impair trained immunity via a type I IFN/iron axis [Bulk_SERIES_1]

Project description:A greater understanding of hematopoietic stem cell (HSC) regulation is required for dissecting protective versus detrimental immunity to pathogens that cause chronic infections such as Mycobacterium tuberculosis (Mtb). We have shown that systemic administration of BCG or b-glucan reprograms HSCs in the BM via a type II interferon (IFN-II) or IL1 response, respectively, that confers protective trained immunity against Mtb. Yet, whether BCG/β-Glucan is unique in its ability to induce this protection remains unknown. Herein, we demonstrate that unlike BCG or b-glucan, Mtb reprograms HSCs via IFN-I response that suppresses myelopoiesis and impairs protective trained immunity to Mtb. Mechanistically, IFN-I response dysregulates iron metabolism, depolarizes mitochondrial membrane potential, and induces cell death in myeloid progenitors. Finally, activation of IFN-I/iron axis in myeloid progenitors generates a detrimental trained immunity to Mtb infection. These results identify an unanticipated immune evasion strategy of Mtb in the bone marrow that controls the magnitude and anti-microbial capacity of innate immunity to infection

2020-08-13 | GSE156134 | GEO

M. tuberculosis reprograms HSCs to limit myelopoiesis and impair trained immunity via a type I IFN/iron axis [EG_SERIES_3]

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M. tuberculosis reprograms HSCs to limit myelopoiesis and impair trained immunity via a type I IFN/iron axis [AERO_SERIES_2]

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Siglec-F+ neutrophils in the spleen induce immunosuppression following acute infection

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