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

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

PROVIDER: PRJNA855977 | 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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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: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 | GSE207491 | GEO

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]

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 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 responses [h-Mf-RNA-seq]

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

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Proteomic Identification of Interferon-induced Proteins with Tetratricopeptide Repeats (IFITs) as Markers of M1 Macrophage Polarization

Project description:Proteomic studies of macrophage polarization to pro-inflammatory (M1) or tissue reparative (M2) phenotypes has identified interferon-induced proteins with tetratricopeptide repeats (IFIT1, IFIT2 and IFIT3) as potential biomarkers of inflammatory diseases such as atherosclerosis.

2018-03-15 | PXD008204 | Pride

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

Differential lipid partitioning between adipocytes and tissue macrophages modulates macrophage lipotoxicity and M2/M1 polarization in obese mice.

Project description:Obesity-associated insulin resistance is characterized by a state of chronic, low-grade inflammation that is associated with the accumulation of M1 proinflammatory macrophages in adipose tissue. Although different evidence explains the mechanisms linking the expansion of adipose tissue and adipose tissue macrophage (ATM) polarization, in the current study we investigated the concept of lipid-induced toxicity as the pathogenic link that could explain the trigger of this response. We addressed this question using isolated ATMs and adipocytes from genetic and diet-induced murine models of obesity. Through transcriptomic and lipidomic analysis, we created a model integrating transcript and lipid species networks simultaneously occurring in adipocytes and ATMs and their reversibility by thiazolidinedione treatment. We show that polarization of ATMs is associated with lipid accumulation and the consequent formation of foam cell–like cells in adipose tissue. Our study reveals that early stages of adipose tissue expansion are characterized by M2-polarized ATMs and that progressive lipid accumulation within ATMs heralds the M1 polarization, a macrophage phenotype associated with severe obesity and insulin resistance. Furthermore, rosiglitazone treatment, which promotes redistribution of lipids toward adipocytes and extends the M2 ATM polarization state, prevents the lipid alterations associated with M1 ATM polarization. Our data indicate that the M1 ATM polarization in obesity might be a macrophage-specific manifestation of a more general lipotoxic pathogenic mechanism. This indicates that strategies to optimize fat deposition and repartitioning toward adipocytes might improve insulin sensitivity by preventing ATM lipotoxicity and M1 polarization. 15 samples; 2 genotypes and 2 time points

2012-03-22 | E-GEOD-36669 | 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

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