Ontology highlight
ABSTRACT:
PROVIDER: PRJNA131203 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR063314.fastq.gz | Fastqsanger.gz | |||
| SRR063315.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 2 of 2 |
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Project description:Polarization of macrophages to M1 or M2 cells is important for mounting responses against bacterial and helminth infection respectively. Jumonji domain containing 3 (JMJD3), a histone 3 K27 demethylase, has been implicated in the activation of macrophages. Here we show that JMJD3 is essential for M2 macrophage polarization to helminth infection and chitin, though JMJD3 is dispensable for M1 responses. Furthermore, Jmjd3 is critical for proper bone marrow macrophage differentiation in a demethylase activity-dependent manner. Jmjd3 deficiency affected trimethylation of H3K27 in only a limited numbers of genes. Among them, we identified Irf4 as the target transcription factor critical for controlling M2 macrophage polarization. Collectively, these results show that JMJD3-mediated H3K27 demethylation is critical for regulating M2 macrophage development leading to anti-helminth host responses. This SuperSeries is composed of the SubSeries listed below.
2010-08-22 | GSE23306 | GEO
Project description:Jmjd3 is trimethyl H3K27 specific demethylase required for M2 macrophage polarization. Genomic fragments obtained from wild-type and Jmjd3-/- mouse macrophages were immunoprecipitated with anti H3K27me3 Ab, and deep sequencing was performed. wild-type and Jmjd3-/- macrophages
2010-08-22 | E-GEOD-23297 | biostudies-arrayexpress
Project description:Jmjd3 is trimethyl H3K27 specific demethylase required for M2 macrophage polarization. Genomic fragments obtained from wild-type and Jmjd3-/- mouse macrophages were immunoprecipitated with anti H3K27me3 Ab, and deep sequencing was performed.
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Project description:BRD4 inhibition suppressed M2 macrophage polarization. Particularly, we deeply investigated the underlying molecular mechanism of how BRD4 epigenetically regulate M2 genes expression. And finished the cut&tag experiment using BRD4, H3K27ac, IRF4 as antibody to find out the binding sites change in M2 macrophage treated with ARV825.
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Project description:MYC activates different metabolic programs in a cell-type and cell-status dependent manner. However, the role of MYC in inflammatory macrophages has not yet been determined. Metabolic and molecular analyses reveal that MYC, but not HIF1, is involved in enhancing early glycolytic flux during inflammatory macrophage polarization. Ablation of MYC decreases lactate production by regulating lactate dehydrogenase (LDH) activity and causes increased inflammatory cytokines by regulating interferon regulatory factor 4 (IRF4) in response to lipopolysaccharide (LPS). Moreover, myeloid-specific deletion of MYC and pharmacological inhibition of MYC/LDH axis enhance inflammation and the bacterial clearance in vivo. These results elucidate the potential role of the MYC/LDH/IRF4 axis in inflammatory macrophages by connecting early glycolysis and inflammatory responses and suggest that modulating early glycolytic flux mediated by the MYC/LDH axis can be utilized to open new avenues for the therapeutic modulation of macrophage polarization to fight against bacterial infection.
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Project description:Macrophage recruitment into tumors is correlated with poor outcomes in cancer, which correlate with STAT6-dependent M2 macrophage polarization and wound healing-type responses. Using penetrant, genetic models of neuroblastoma, we found macrophage recruitment was protective against tumor formation while disabling STAT6-mediated M2 polarization had no effect on tumorigenesis, progression or expression of key immunosuppressive pathways. Thus while macrophages are drivers of cancer in this model, non-classical M2 STAT6-independent pathways are plausible targets for cancer therapy.
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Project description:Macrophages form a primary immune cells population in tumor tissues and malignant ascites microenvironment (MAM). They can be activated and polarized into tumor-associated macrophages (TAM) by the embedded environment and promote tumor progression and metastasis However, the molecular mechanisms of MAM in macrophage polarization and the effects on epithelial ovarian cancer (EOC) metastatic progression remain elusive. Here, we found that that MAM modulates RhoA-GTPase-F-actin-Hippo signaling cascade in facilitating M2-like macrophage polarization that, in turn, promotes tumor dissemination. PUFA enriched magligant ascites microenvironment promote macrophage lipid oxidative phosphorylation and supression RhoA-GTPase-Yap1 axis. Genetic ablation Yap1 in macrophage exhibited M2-like polarization and enhanced ovrian tumor dissemination. Pharmacology inhibit Mst1/2 could rescue M2-like TAM polarization in MAM and alter the lipid oxidation of macrophages in MAM, more importantly, inhibit ovarian metastatic properties. Through comparasion primary TAM (P-TAM) and metastasis TAM (M-TAM), we proved that Hippo-Yap1 siganl results M-TAM with high M2/M1 ratio. These findings implicate critical functions of PUFA modulate RhoA-Hippo axis in facility TAM polarization and also suggest manipulation of PUFA metabolism or RhoA-Hippo siganl as a therapeutic strategy aganist EOC metastasis.
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Project description:Enteric helminth infections shape host immunity to other pathogens. However, it remains uncertain whether helminth infections following deworming treatment could induce long-term alterations in the host immune system. Here, we demonstrate that infection with Hpb, even after anthelmintic-mediated clearance, induces trained immunity to confer long-lasting cross-protection against lethal S. aureus challenge. This protective effect is associated with the prolonged expansion and functional reprogramming of peritoneal macrophages. Mechanistically, we identify the IL-4/IL-4Rα signaling axis, driven by Hpb-induced Th2 skewing, is essential for both peritoneal macrophage accumulation and Cybb-dependent reactive oxygen species (ROS) enrichment. Notably, Th2 cells, rather than eosinophils or basophils, serve as the predominant source of IL-4 and persist in the peritoneal cavity for at least three weeks post Hpb clearance. Collectively, these findings uncover a novel helminth-mediated trained immunity that promotes host resistance to systemic bacterial infection through Th2-dependent reprogramming of peripheral peritoneal macrophage.
2026-01-01 | GSE301338 | GEO
Project description:Enteric helminth infections shape host immunity to other pathogens. However, it remains uncertain whether helminth infections following deworming treatment could induce long-term alterations in the host immune system. Here, we demonstrate that infection with Hpb, even after anthelmintic-mediated clearance, induces trained immunity to confer long-lasting cross-protection against lethal S. aureus challenge. This protective effect is associated with the prolonged expansion and functional reprogramming of peritoneal macrophages. Mechanistically, we identify the IL-4/IL-4Rα signaling axis, driven by Hpb-induced Th2 skewing, is essential for both peritoneal macrophage accumulation and Cybb-dependent reactive oxygen species (ROS) enrichment. Notably, Th2 cells, rather than eosinophils or basophils, serve as the predominant source of IL-4 and persist in the peritoneal cavity for at least three weeks post Hpb clearance. Collectively, these findings uncover a novel helminth-mediated trained immunity that promotes host resistance to systemic bacterial infection through Th2-dependent reprogramming of peripheral peritoneal macrophage.
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