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

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

PROVIDER: PRJNA855918 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19979955_1.fastq.gz	Fastqsanger.gz
	SRR19979955_2.fastq.gz	Fastqsanger.gz
	SRR19979956_1.fastq.gz	Fastqsanger.gz
	SRR19979956_2.fastq.gz	Fastqsanger.gz
	SRR19979957_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 [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]

2022-07-08 | GSE207528 | 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-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]

| PRJNA855981 | 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

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

Determination of Pseudomonas aeruginosa transcriptome induced by oleic acid or its derived oxylipins 10-HOME and 7,10-DiHOME.

Project description:Oxygenated unsaturated fatty acids, known as oxylipins, are signaling molecules commonly used for cell-to-cell communication in eukaryotes. However, a role for oxylipins in mediating communication in prokaryotes has not previously been described. Bacteria mainly communicate via quorum sensing (QS) , which involves the production and detection of diverse small molecules termed autoinducers. We showed that oleic acid-derived oxylipins 10-HOME and 7,10-DiHOME produced by Pseudomonas aeruginosa function as autoinducers of a novel quorum sensing system termed Oxylipin-Dependent QS Sytem (ODS). This experiment was designed to determine the genes whose expression is altered by these P. aeruginosa oxylipins. We found that the ODS system controls the cell density-dependent expression of a P. aeruginosa gene subset through the mediation of 10-HOME and 7,10-DiHOME oxylipins.

2018-12-05 | GSE123356 | GEO

TRIM21 aggravates cardiac injury after myocardial infarction via promoting M1 macrophage polarization

Project description:Macrophage polarization followed by acute myocardial infarction (MI) is essential for the regulation of inflammation and scar formation. Tripartite motif-containing protein 21 (TRIM21), a member of E3 ubiquitin ligases, is a crucial mediator in the process of inflammation and heart failure. However, the potential roles of TRIM21 in modulating post-MI inflammation and macrophage polarization remain elusive. We detected that the levels of TRIM21 were significantly reduced in macrophages of WT mice after MI. In contrast, MI was ameliorated in TRIM21 knockout (TRIM21-/-) mice with improved cardiac remodeling, characterized by a marked decrease in mortality, increased wall thickness, and improved cardiac function in comparison with wild-type (WT) MI mice. Importantly, TRIM21 deficiency decreased the post-MI apoptosis and DNA damage in the hearts of mice, and the accumulation of M1 phenotype macrophages in infarcted hearts significantly decreased in TRIM21-/- mice compared with WT controls. Mechanistically, depletion of TRIM21 orchestrated the process of M1 macrophage polarization via a PI3K/Akt signaling pathway. Overall, these data reveal that TRIM21 drives the inflammatory response and cardiac remodeling after MI via stimulating M1 macrophage polarization through a PI3K/Akt signaling pathway.

2022-12-31 | GSE214696 | GEO

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