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Comparison of gene expression by sheep and human blood stimulated with the TLR4 agonists lipopolysaccharide and monophosphoryl lipid A

ABSTRACT: Comparison of gene expression by sheep and human blood stimulated with the TLR4 agonists lipopolysaccharide and monophosphoryl lipid A

PROVIDER: PRJNA294324 | ENA |

REPOSITORIES: ENA

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Comparison of gene expression by sheep and human blood stimulated with the TLR4 agonists lipopolysaccharide and monophosphoryl lipid A [sheep]

2015-12-16 | GSE72558 | GEO

Comparison of gene expression by sheep and human blood stimulated with the TLR4 agonists lipopolysaccharide and monophosphoryl lipid A [sheep]

Project description:11,431 and 4,992 genes were determined in whole blood of healthy human volunteers and normal sheep, respectively following MPLA and LPS exposure Following the exposure 1,029 human and 175 sheep genes were differentially expressed. Of those 175 sheep genes, 54 had a known human ortolog. The major inflammatory mediators, such as IL-1-6-8, TNFa, NFkB, ETS2, PTGS2, PTX3, CXCL18, KYNU, and CLEC4E were similarly (>2-fold) upregulated in both human and sheep blood. Six healthy human volunteers and six normal sheep blood was incubated with LPS or MPLA for 90 minutes, then the blood was transferred to the Paxgene blood RNA tubes and the gene expression microarrays were scanned with G2556 Microaaray Scanner

2015-12-16 | E-GEOD-72558 | biostudies-arrayexpress

Comparison of gene expression by sheep and human blood stimulated with the TLR4 agonists lipopolysaccharide and monophosphoryl lipid A

Project description:This SuperSeries is composed of the SubSeries listed below.

2015-12-16 | GSE72559 | GEO

Comparison of gene expression by sheep and human blood stimulated with the TLR4 agonists lipopolysaccharide and monophosphoryl lipid A

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-12-16 | E-GEOD-72559 | biostudies-arrayexpress

Comparison of gene expression by sheep and human blood stimulated with the TLR4 agonists lipopolysaccharide and monophosphoryl lipid A [human]

2015-12-16 | GSE72557 | GEO

Comparison of gene expression by sheep and human blood stimulated with the TLR4 agonists lipopolysaccharide and monophosphoryl lipid A [human]

2015-12-16 | E-GEOD-72557 | biostudies-arrayexpress

Single-Cell Epitope-Transcriptomics Reveal Lung Stromal and Immune Cell Response Kinetics to Nanoparticle-delivered RIG-I and TLR4 Agonists

Project description:Lung-resident and circulatory lymphoid, myeloid, and stromal cells, expressing various pattern recognition receptors (PRRs), detect pathogen and danger-associated molecular patterns (PAMPs/DAMPs), and defend against respiratory pathogens and injuries. Here, we report the early responses of murine lungs to nanoparticle-delivered PAMPs, specifically the RIG-I agonist poly-U/UC (PUUC), with or without the TLR4 agonist monophosphoryl lipid A (MPLA). Using cellular indexing of transcriptomes and epitopes by sequencing (CITE-seq), we characterized the responses at 4 and 24 hours after intranasal administration. Within 4 hours, ribosome-associated transcripts decreased in both stromal and immune cells, followed by widespread interferon-stimulated gene (ISG) expression. Using RNA velocity, we show that lung-neutrophils dynamically regulate the synthesis of cytokines like CXCL-10, IL-1α, and IL-1β. Co-delivery of MPLA and PUUC increased chemokine synthesis and upregulated antimicrobial binding proteins targeting iron, manganese, and zinc in many cell types, including fibroblasts, endothelial cells, and epithelial cells. Overall, our results elucidate the early PAMP-induced cellular responses in the lung and demonstrate that stimulation of the RIG-I pathway, with or without TLR4 agonists, induces a ubiquitous microbial defense state in lung stromal and immune cells. Nanoparticle-delivered combination PAMPs may have applications in intranasal antiviral and antimicrobial therapies and prophylaxis.

2022-12-12 | GSE220436 | GEO

TLR4 deficiency reduces inflammatory signaling by reprogramming macrophage lipid metabolism

Project description:Chronic inflammation is a hallmark of obesity and is linked to the development of numerous diseases. The activation of toll-like receptor 4 (TLR4) by long-chain saturated fatty acids (lcSFAs) is an important process in understanding how obesity initiates inflammation. While experimental evidence supports an important role for TLR4 in obesity-induced inflammation in vivo, via a mechanism thought to involve direct binding to and activation of TLR4 by lcSFAs, several lines of evidence argue against lcSFAs being direct TLR4 agonists. Using multiple orthogonal approaches, we herein provide evidence that while loss-of-function models confirm that TLR4 does, indeed, regulate lcSFA-induced inflammation, TLR4 is not a receptor for lcSFAs. Rather, we show that TLR4-dependent priming alters gene expression, lipid metabolic pathways, and membrane lipid composition, which are necessary for lcSFA-induced inflammation. These results reconcile previous discordant observations and challenge the prevailing view of TLR4's role in initiating obesity-induced inflammation.

2018-04-22 | GSE100526 | GEO

BCR repertoire analysis by Next-generation sequencing of lymphocytes harvested from mice vaccinated with liposomal TLR4 and TLR7 agonists

Project description:BALB/c mice were vaccinated with inactivated influenza A virus adjuvanted with liposomal TLR4 (2B182C) and TLR7 agonists (2B182C) on days 0 and 21. To examine whether the liposomal combined adjuvant increase BCR diversity, lymphocytes in the draining lymph nodes harvested on day 28 were analyzed using next-generation RNA sequencing technology.

2021-03-01 | E-MTAB-8870 | biostudies-arrayexpress

Lipopolysaccharide (LPS) response in macrophages from TLR4-deficient mice

Project description:Lipid A (a hexaacylated 1,4 bis-phosphate) is a potent immune stimulant for TLR4/MD-2. Upon lipid A ligation, the TLR4/MD-2 complex dimerizes and initiates signal transduction. Historically, studies also suggested the existence of TLR4/MD-2-independent LPS signaling. Here we define the role of TLR4 and MD-2 in LPS signaling by using genome wide expression profiling in TLR4- and MD-2-deficient macrophages after stimulations with peptidoglycan-free LPS and synthetic E.coli lipid A. Of the 1,396 genes found significantly induced or repressed by any one of the treatments in the wildtype macrophages, none was present in the TLR4- or MD-2-deficient macrophages, confirming that the TLR4/MD-2 complex is the only receptor for endotoxin, and are both absolutely required for responses to LPS. Using a molecular genetics approach, we investigated the mechanism of TLR4/MD-2 activation by combining the known crystal structure of TLR4/MD-2 with computer modeling. We used lipid IVa, a defined lipid A mimetic to model the activation of mouse TLR4/MD2. The two phosphates on lipid A were predicted to interact extensively with the two positively charged patches mouse TLR4 according to our dimeric murine TLR4/MD-2/lipid IVa model. These two patches are composed of K263, R337, and K360 (Positive Patch 1), and K367 and R434 (Positive Patch 2). When either Positive Patch was abolished by mutagenesis into Ala, the responses to LPS and lipid A were almost abrogated. Thus, ionic interactions between the two phosphates on lipid A and the two positively charged patches on murine TLR4 appear to be essential for LPS receptor activation.

2011-07-31 | GSE31066 | GEO

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