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Gut bacterial-derived 12,13-diHOME promotes M1-like inflammatory macrophage polarization and trained immunity targeting interferon responses [h-Mf-RNA-seq]

ABSTRACT: Gut bacterial-derived 12,13-diHOME promotes M1-like inflammatory macrophage polarization and trained immunity targeting interferon responses [h-Mf-RNA-seq]

PROVIDER: PRJNA855981 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19993615_1.fastq.gz	Fastqsanger.gz
	SRR19993615_2.fastq.gz	Fastqsanger.gz
	SRR19993616_1.fastq.gz	Fastqsanger.gz
	SRR19993616_2.fastq.gz	Fastqsanger.gz
	SRR19993617_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Gut bacterial-derived 12,13-diHOME promotes M1-like inflammatory macrophage polarization and trained immunity targeting interferon responses [h-Mf-RNA-seq]

Project description:Elevated infant fecal concentrations of bacterial-derived lipid 12,13-diHOME increases risk for atopy and asthma development in childhood, mechanistically how this lipid may contribute to disease susceptibility is unknown. Here we demonstrate macrophages exposed to 12,13-diHOME exhibit inflammatory IL-1highCD206low M1-like polarization, reduce bacterial phagocytic capacity. In co-culture assays, antigens in the presence of 12,13-diHOME further amplifies M1-like frequency, promotes CD20+CD38-IgD-CD27+ memory B cells expansion and IgE production. Epigenetic analyses indicates 12,13-diHOME exposure promotes DNA methylation, chromatin compaction, specifically diminishing access to interferon-stimulated response elements and transcription factor binding sites. In vivo, in murine airway allergic sensitization model, gut bacterial-derived 12,13-diHOME exacerbated both airway allergic inflammation and IL-1, IL-7, one-carbon metabolism and Toll-like receptor signaling. Our data suggests that 12,13-diHOME reprograms macrophage effector function, B-cell interactions and epigenetic modifications promoting phenotypes plausibly play a role in shaping early life microbiome development and innate immune dysfunction related to allergic sensitization in childhood.

2022-07-08 | GSE207528 | GEO

Gut bacterial-derived 12,13-diHOME promotes M1-like inflammatory macrophage polarization and trained immunity targeting interferon responses [h-Mf-ATAC-seq]

2022-07-08 | GSE207491 | GEO

Gut bacterial-derived 12,13-diHOME promotes M1-like inflammatory macrophage polarization and trained immunity targeting interferon responses [m-lung-RNA-seq]

Project description:Elevated infant fecal concentrations of bacterial-derived lipid 12,13-diHOME increases risk for atopy and asthma development in childhood, mechanistically how this lipid may contribute to disease susceptibility is unknown. Here we demonstrate macrophages exposed to 12,13-diHOME exhibit inflammatory IL-1bhighCD206low M1-like polarization, reduce bacterial phagocytic capacity. In co-culture assays, antigens in the presence of 12,13-diHOME further amplifies M1-like frequency, promotes CD20+CD38-IgD-CD27+ memory B cells expansion and IgE production. Epigenetic analyses indicates 12,13-diHOME exposure promotes DNA methylation, chromatin compaction, specifically diminishing access to interferon-stimulated response elements and transcription factor binding sites. In vivo, in murine airway allergic sensitization model, gut bacterial-derived 12,13-diHOME exacerbated both airway allergic inflammation and IL-1, IL-7, one-carbon metabolism and Toll-like receptor signaling. Our data suggests that 12,13-diHOME reprograms macrophage effector function, B-cell interactions and epigenetic modifications promoting phenotypes plausibly play a role in shaping early life microbiome development and innate immune dysfunction related to allergic sensitization in childhood.

2022-07-08 | GSE207492 | GEO

Gut bacterial-derived 12,13-diHOME promotes M1-like inflammatory macrophage polarization and trained immunity targeting interferon responses [h-Mf-ATAC-seq]

Project description:Gut bacterial-derived 12,13-diHOME promotes M1-like inflammatory macrophage polarization and trained immunity targeting interferon responses [h-Mf-ATAC-seq]

| PRJNA855918 | ENA

Gut bacterial-derived 12,13-diHOME promotes M1-like inflammatory macrophage polarization and trained immunity targeting interferon

Project description:Gut bacterial-derived 12,13-diHOME promotes M1-like inflammatory macrophage polarization and trained immunity targeting interferon

| PRJNA855977 | ENA

Gut bacterial-derived 12,13-diHOME promotes M1-like inflammatory macrophage polarization and trained immunity targeting interferon responses [m-lung-RNA-seq]

Project description:Gut bacterial-derived 12,13-diHOME promotes M1-like inflammatory macrophage polarization and trained immunity targeting interferon responses [m-lung-RNA-seq]

| PRJNA855917 | ENA

Gut bacterial-derived 12,13-diHOME promotes M1-like inflammatory macrophage polarization and trained immunity targeting interferon

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

2022-07-08 | GSE207529 | GEO

Myeloid cell derived inducible nitric oxide synthase suppresses M1 macrophage polarization

Project description:Analysis of gene expression between WT and iNOS defecient M1 macrophage RNA microarray was performed using RNA isolated from M1 polarized macrophages from WT and iNOS deficient mice stimulated with LPS/IFNγ for 6 hours. Total RNA was extracted using a RNeasy plus kit (QIAGEN, Valencia, CA), and the array was performed on an Illumina MouseRef-8 v2.0 expression beadchip (Illumina, USA) by the Genomics Core Facility at the Mount Sinai School of Medicine.

2015-02-02 | E-GEOD-65436 | biostudies-arrayexpress

RNA editing enzyme APOBEC3A promotes pro-inflammatory (M1) macrophage polarization

Project description:Macrophages acquire a pro-inflammatory M1 phenotype in response to microbial products or pro-inflammatory cytokines through incompletely understood molecular mechanisms. We recently described the induction of APOBEC3A-mediated cellular site-specific cytosine-to-uracil (C>U) RNA editing during M1 macrophage polarization. However, the functional significance of this RNA editing is unknown. Here, we find that cellular RNA editing by APOBEC3A can also be induced by influenza or Maraba virus infections in normal macrophages, and by interferons in tumor-associated macrophages. Gene knockdown and RNA Seq analyses show that APOBEC3A induces C>U RNA editing (range 7%-88%) of 209 exonic or UTR sites in 203 genes during M1 polarization of monocyte-derived macrophages. The highest level of deleterious protein-recoding C>U RNA editing is observed in THOC5, which encodes a key nuclear protein implicated in the export of mRNAs during M-CSF driven macrophage differentiation. Knockdown of APOBEC3A in M1 macrophages reduces pro-inflammatory IL6, IL23A, and IL12B gene expression, CD80 and CD86 surface protein expression, and TNF-α, IL-1β and IL-6 cytokine secretion, and increases glycolysis and glycolytic capacity. These results demonstrate that APOBEC3A cytidine deaminase plays an important role in transcriptomic and functional polarization of pro-inflammatory M1 macrophages.

2020-03-13 | GSE146867 | GEO

Novel transcriptome signatures and markers defining murine macrophages at the extremes of the canonical M1 and M2 polarization spectrum

Project description:Classically (M1) and alternatively activated (M2) macrophages play distinct roles in various physiological and disease processes. Understanding the gene transcription programs that contribute to macrophage polarization along the M1/M2 spectrum may lead to new tools to detect and therapeutically manipulate macrophage phenotype. Here, we define the M1 and M2 macrophage signature through mRNA microarray. The M1 macrophage signature was defined by 629 up-regulated and 732 down-regulated genes while the M2 macrophage signature was formed by 388 up-regulated and 425 down-regulated genes. While a subset of probes was common to both M1 and M2 cells, others were exclusive to each macrophage subset. The common M1/M2 pathways were characterized by changes in various transcriptional regulators and signaling partners, including increases in Kruppel-like Factor (Klf) 4, but decreases in Klf2. To identify M1 and M2 biomarkers that help discriminate these populations, we selected genes that were increased during M1 or M2 differentiation but decreased in the opposite population. Among top novel M1-distinct genes, we identified CD38, G-protein coupled receptor 18 (Gpr18) and Formyl peptide receptor 2 (Fpr2). Among top M2 genes, we found early growth response protein 2 (Egr2) and Myc. We validated these genes by Real-Time PCR and developed a CD38/Egr2-based flow cytometry assay that discriminates between M1 and M2 macrophages. Overall, this work defines the M1 and M2 signature and identifies several novel M1 and M2 genes that may be used to distinguish and manipulate M1 and M2 macrophages. Total RNA was prepared from bone marrow-derived macrophages of wild-type mice (n=2-3 independent mice) treated in M0, M1 or M2 conditions (n=2-3 replicates per condition originating from different mice)

2015-12-08 | E-GEOD-69607 | biostudies-arrayexpress

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