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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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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-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

Q11, a CYP2E1 inhibitor, exerts anti-hepatocellular carcinoma effect by inhibiting M2 macrophage polarization

Project description:Despite significant advancements in cancer immunotherapy, many patients continue to respond poorly. Novel therapeutic strategies and drugs are urgently needed. Here, we found that CYP2E1 is significantly upregulated in M2 macrophages. The CYP2E1 inhibitor, Q11, could inhibit M2 macrophage polarization, while CYP2E1 overexpression could promote it. Increased levels of CYP2E1 and M2 macrophages in the tumor microenvironment of HCC patients correlate with poor prognosis. Q11 could inhibit tumor cells by targeting M2 macrophages rather than directly attacking tumor cells. Both Q11 and Cyp2e1 knockout could effectively suppress tumor growth. Q11 reduces the production of CYP2E1 metabolites (±)9(10)-DiHOME and (±)12(13)-DiHOME, thus attenuating PPARγ activation and M2 macrophage polarization. In summary, our findings suggest that Q11 could suppress M2 macrophage polarization by modulating the CYP2E1/(±)9(10)-DiHOME or (±)12(13)-DiHOME/PPARγ axis, indicating that CYP2E1 inhibition may be a novel therapeutic strategy for HCC and positioning Q11 as a promising therapeutic agent.

2024-12-26 | GSE282907 | GEO

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

DNA methylation analysis during neutrophilic granulopoiesis under ELF-MF exposure

Project description:To address whether ELF-MF influences the epigenetic landscape in differentiating haematopoietic cells, we performed an in vitro haematopoietic differentiation under powerline-simulating ELF-MF exposure (50 Hz, 1 mT, 5’ on/10’ off) in comparison to sham exposure (50 Hz, 7 µT, 5’ on/10’ off) or no exposure. We differentiated CD34+ cells (allcells, CB008F, lot: CBC121009M) isolated from human cord blood into the neutrophilic lineage, and performed genome-wide methylation analysis at single CpG sites of CD34+ cells and day 5 progenitors, using the Illumina Infinium HumanMethylation 450 platform. Exposure to ELF MF did not significantly impact the programming of DNA methylation pattern during granulopoiesis. However, ELF MF exposure has an influence on the robustness of the epigenetic landscape during global chromatin programming of granulopoiesis. Our data suggests that ELF MF has a stochastic effect on the epigenetic landscape of individual cells.

2017-06-13 | GSE85392 | GEO

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