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Arhgdia regulates disease tolerance in IAV-infected epithelial cells

ABSTRACT: Arhgdia regulates disease tolerance in IAV-infected epithelial cells

PROVIDER: PRJNA795157 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17467451.fastq.gz	Fastqsanger.gz
	SRR17467452.fastq.gz	Fastqsanger.gz
	SRR17467453.fastq.gz	Fastqsanger.gz
	SRR17467454.fastq.gz	Fastqsanger.gz
	SRR17467455.fastq.gz	Fastqsanger.gz

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Arhgdia regulates disease tolerance in IAV-infected epithelial cells

Project description:When challenged with an invading pathogen, host defense mechanisms are engaged to eliminate the pathogen (resistance) and limit tissue damage that results from host-pathogen interactions (disease tolerance). We identified Arhgdia as a driver of the molecular disease-tolerance response in epithelial cells. The effect of Arhgdia on disease tolerance and resistance was evaluated at early stages of influenza A virus (IAV) infection. Our observations indicates that Arhgdia has an effect on disease tolerance during IAV infection.

2022-12-27 | GSE193160 | GEO

Transcriptome Profiling of Neutrophils from Patients Infected with IAV using RNA-seq

Project description:Purpose: To explore the roles of host lncRNAs during IAV infection Methods:profiling whole transcriptional alterations using RNA-seq in neutrophil samples from 3 patients infected with IAV in the acute stage and their matched recovery-stage samples Results:We identified a total of 404 differentially expressed genes (FC>2, p<0.05), including 234 up-regulated and 170 down-regulated genes,in each patient sample Conclusion:Our study is the first profile of the transcriptome of IAV-infected patients' neutrophils

2020-09-11 | GSE108807 | GEO

Proteomics dataset of IAV infected cells

Project description:Quantitative proteomic analysis of AGO2 interactome from IAV infected/uninfected HEK293 cells

2024-01-22 | PXD048781 |

Cyclophilin D promotes disease tolerance to influenza A virus infection by licensing NK cell development and function

Project description:An effective immune response to influenza A virus (IAV) requires two arms: host resistance, which restricts viral replication, and disease tolerance that limits tissue damage caused by the immune response to IAV. Interestingly, fatal influenza infections are more often associated with dysregulated inflammation, rather than an inability to control viral replication, highlighting the importance of mechanisms involved in disease tolerance to IAV. Here, we show that cyclophilin D (CypD), a mitochondrial protein known to regulate cell death and cytokine production, protects against IAV infection through disease tolerance. Mice deficient in CypD (CypD-/-) exhibit enhanced susceptibility to IAV infection, despite comparable myeloid immune responses and intact antiviral immunity. Instead, CypD-/- susceptibility was due to pulmonary tissue damage, caused by a lack of the cytokine IL-22 that protects the lung epithelium. We found the necessary source of IL-22 following IAV infection to be conventional natural killer (NK) cells that failed to reach the airways of infected CypD-deficient mice, as a result of dysregulated lymphopoiesis in the bone marrow. Importantly, following infection, a single administration of recombinant IL-22 in the airways abrogated pulmonary damage and rescued CypD-/- mice. Thus, the CypD/IL-22/NK cell axis is critical in immunity to IAV by promoting disease tolerance, limiting lung tissue damage and maintaining pulmonary function.

2022-06-21 | GSE163290 | GEO

Single-cell RNA sequencing of pandemic influenza A virus-infected human airway epithelial cells

Project description:To characterize the host response to pandemic IAV infection in its natural target cells, we infected primary human airway epithelial cell (hAEC) cultures wild-type pandemic IAV (WT) or a NS1 mutant virus (NS1R38A) with abrogated dsRNA binding capacity at a multiplicity of infection (MOI) of 0.03. We then profiled the transcriptomes of uninfected cells as well as cells harvested 18 hours post-infection (hpi) using single-cell RNA sequencing (scRNA-seq).

2022-09-22 | E-MTAB-12159 | biostudies-arrayexpress

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

Gene Expression Data from Influenza A Virus-Infected and Mock-infected A549 Human Aveolar Epithelial Carcinoma Cells with Exposure to Mouse Eosinophils.

Project description:Eosinophils are terminally differentiated granulocytes that participate in innate immunity against Influenza A Virus (IAV). Here, we investigate transcriptional changes that occur in IAV-infected human A549 aveolar epithelial carcinoma cells with and without direct or indirect exposure to mouse bone marrow-derived eosinophils (BMdEos). Global changes in the transcriptome of A549 cells due to Influenza A virus-infection and/or direct and indirect eosinophil exposure were assessed using ThermoFisher/Affymetrix Clariom™ S Human microarrays.

2021-03-31 | GSE163224 | GEO

Immune response of TRIM28 KO cells infected with H1N1 IAV

Project description:Immune response of TRIM28 KO cells infected with H1N1 IAV

| PRJNA849574 | ENA

microRNA-mediated GALNT3 upregulation facilitates mucin production and viral replication in influenza A virus-infected respiratory epithelial cells

Project description:Viral infections affecting the upper or lower respiratory tract induce mucin production in the epithelial surfaces of the respiratory cells. However, a little is known about how mucins are produced on the surfaces of respiratory epithelial cells and affects viral replication. In the course of the investigation of the cellular responses in the early stage of Influenza A virus (IAV) infection, we found that two miRNAs, miR-221 and miR-17-3p, which target the mRNA of GalNAc transferase 3 (GALNT3), are rapidly down-regulated as early as 1.5 h post-infection. To understand the early host cell responses to the IAV infection, we performed miRNA microarray analysis using a human alveolar adenocarcinoma cell line, A549 cells, infected with influenza A/Puerto Rico/8/34 H1N1 (PR8) virus. We isolated the cellular RNAs at 0.5, 1.5 and 4.5 h post-infection and detected significant changes in the global profile of miRNA expression after infection with IAV. mouse embryonic fibroblasts. Each sample was run in duplicate.

2015-12-08 | E-GEOD-57508 | biostudies-arrayexpress

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

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