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Mechanism of activation of porcine dendritic cells by an alpha-D-glucan nanoparticle adjuvant and nanoparticle/poly(I:C) combination adjuvant.

ABSTRACT: Mechanism of activation of porcine dendritic cells by an alpha-D-glucan nanoparticle adjuvant and nanoparticle/poly(I:C) combination adjuvant.

PROVIDER: PRJNA857001 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20047268_1.fastq.gz	Fastqsanger.gz
	SRR20047268_2.fastq.gz	Fastqsanger.gz
	SRR20047269_1.fastq.gz	Fastqsanger.gz
	SRR20047269_2.fastq.gz	Fastqsanger.gz
	SRR20047270_1.fastq.gz	Fastqsanger.gz

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Mechanism of activation of porcine dendritic cells by an alpha-D-glucan nanoparticle adjuvant and nanoparticle/poly(I:C) combination adjuvant.

Project description:RNA sequencing was performed to identify immune-related genes that were differentially expressed in porcine monocyte-derived dendritic cells following stimulation with a novel phytoglycogen-based nanoparticle (Nano-11) and the TLR3 agonist poly(I:C).

2022-08-12 | GSE207745 | GEO

Mechanism of activation of porcine dendritic cells by an α-D-glucan nanoparticle adjuvant and a nanoparticle/poly(I:C) combination adjuvant.

Project description:Recent studies have shown that corn-derived cationic α-D-glucan nanoparticles, known as Nano-11, significantly increase the immune response when used as a vaccine adjuvant in mice and in pigs. Furthermore, the nanoparticles can be formulated with other immunostimulators such as poly(I:C), which further enhances the immune response. The current experiments were aimed at elucidating the mechanism of action of Nano-11 alone and in combination with poly(I:C). The effect of these adjuvants on porcine monocyte-derived dendritic cells (Mo-DCs) was determined by RNA-sequencing, supplemented with flow cytometry, cytokine analysis, and Western blots. Adsorption of poly(I:C) to Nano-11 reduced its cytotoxicity for Mo-DCs. Exposure of Mo-DCs to Nano-11 and Nano-11/poly(I:C) induced differential expression of 979 and 2016 genes, respectively. Gene Ontology enrichment and KEGG pathway analysis revealed many changes in gene expression related to inflammation, innate immunity, immune response to infections, and metabolism. Nano-11 and Nano-11/poly(I:C) induced maturation of the Mo-DCs as indicated by increased expression of costimulatory molecules and MHC II. Increased expression of genes downstream of p38 MAPK activation revealed a role for this signaling pathway in the activation of Mo-DCs by the adjuvants. This was confirmed by Western blot and inhibition of TNF-secretion upon incubation with the p38 inhibitor SB203580. These experiments provide insights into the mechanism of action of the novel adjuvants Nano-11 and Nano-11/poly(I:C).

| S-EPMC9483091 | biostudies-literature

A TLR7-nanoparticle adjuvant promotes broad immune responses against heterologous strains of Influenza and SARS-CoV-2

Project description:Effective vaccines against viruses such as Influenza and SARS-CoV-2 must elicit a diverse repertoire of antibodies against multiple variant virus strains. However, antibody responses to current vaccines often lack cross-reactivity due to immunodominance. Here, we describe the synthesis of a toll-like receptor 7 agonist (TLR7)-nanoparticle adjuvant, TLR7-NP, constructed from TLR7 agonist-initiated ring-opening polymerization of lactide and self-assembly with poly(ethylene glycol)-b-poly(lactic-co-glycolic acid). TLR7-NP can enhance lymph node targeting, leading to persistent activation of immune cells. When mixed with Alum-adsorbed antigens, this TLR7-NP adjuvant elicited cross-reactive antibodies for both dominant and subdominant epitopes, as well as antigen-specific CD8+ T cell responses, in mice. TLR7-NP adjuvanted influenza subunit vaccine successfully protected mice from heterologous viral challenge. TLR7-NP also enhanced the antibody response to a SARS-CoV-2 subunit vaccine against multiple variants and revealed the mobilization of an antiviral response. We further demonstrate enhanced antigen-specific responses in human tonsil organoids with this novel adjuvant.

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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

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Project description:Analysis of transcriptional profiles in mDC sorted from apheresed PBMC and stimulated for 6 hours with cyclic glucan or LPS. The hypothesis tested is that cyclic glucan induces maturation and T cell-activation transcripts in human mDC. Total RNA extracted from mDC sorted from apheresed PBMC and activated for 6 hours with cyclic glucan or LPS.

2012-12-31 | E-GEOD-32023 | biostudies-arrayexpress

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Project description:Adjuvant-induced human monocyte secretome profiles reveal adjuvant- and age-specific protein signatures.

2016-03-14 | PXD003534 | Pride

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Project description:Adjuvant-induced human monocyte secretome profiles reveal adjuvant- and age-specific protein signatures.

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The role of HIF-1 in beta-glucan induced response in myeloid cell

Project description:beta-glucan induced glycolysis in HIF-1 depedent manner. We reported that beta-glucan injection in mice led to upregulated glycolysis. HIF-1a plays a major role in this process. Mice receives beta-glucan via ip for 4 days. Splenocytes were isolated for RNA sequencing.

2014-09-26 | E-GEOD-57206 | biostudies-arrayexpress

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