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Interferon Regulatory Factor 5 represses mitochondrial matrix protein GHITM to limit macrophage oxidative capacity in early response to obesity [bmdm]

ABSTRACT: To investigate the involvement of IRF5 in macrophages during obesity-related inflammation, we analyzed bone marrow-derived macrophages stimulated for 2 or 24 hours with Lipopolysaccharide (LPS), Palmitate or carrier (bovine serum albumin), from mice with a myeloid-specific deletion of IRF5 or their wild-type littermates.

ORGANISM(S): Mus musculus

PROVIDER: GSE208667 | GEO | 2022/07/25

REPOSITORIES: GEO

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Interferon Regulatory Factor 5 represses mitochondrial matrix protein GHITM to limit macrophage oxidative capacity in early response to obesity [atm]

Project description:To investigate the involvement of IRF5 in macrophages during obesity-related inflammation, we analyzed adipose-tissue macrophages (ATM) from mice with a myeloid-specific deletion of IRF5 or their wild-type littermates, fed with high fat diet.

2022-07-25 | GSE208648 | GEO

GEF-H1-IRF5 mediated gene expression changes in BMDM by MDP recognition

Project description:The transcription factor IRF5 is essential for immune defense against pathogens. Here, the authors show that the microtubule-associated factor GEF-H1 plays a critical role in host defense against Listeria monocytogenes in macrophages via activation of the IRF5 kinase IKKe

2019-04-02 | GSE126749 | GEO

Palmitate-induced gene expression in human gingival fibroblasts (HGF)

Project description:DNA microarray analysis was performed to investigate the expression of genes in HGF stimulated with palmitate Type 2 diabetes (T2D) is characterized by decreased insulin sensitivity and higher concentrations of free fatty acids (FFAs) in plasma. Among FFAs, saturated fatty acids (SFAs), such as palmitate, have been proposed to promote inflammatory responses. Although many epidemiological studies have shown a link between periodontitis and T2D, little is known about the clinical significance of SFAs in periodontitis. The goal of this study is to demonstrate a potential link between the pathogenesis of periodontitis and SFAs in plasma. HGF were treated with either with 0 (1% Bovine serum albumin) or 100 ÂµM Palmitate for 36 hours (n=2 each).

2015-12-31 | E-GEOD-62761 | biostudies-arrayexpress

IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype [small_bulk_rnaseq]

Project description:Mononuclear phagocytes (MNPs) play a key role in maintaining intestinal homeostasis but also in triggering immunopathology in response to acute microbial stimulation, which induces the recruitment of masses of Ly6Chi monocytes to the gut. The regulators that control monocyte tissue adaptation in the gut remain poorly understood. Interferon Regulatory Factor 5 (IRF5) is a transcription factor previously shown to play a key role in maintaining the inflammatory phenotype of macrophages Here we investigate the impact of IRF5 on the MNP system and physiology of the gut at homeostasis and during inflammation. We demonstrate that IRF5 deficiency has a limited impact on colon physiology at steady state, but ameliorates immunopathology during Helicobacter hepaticus induced colitis. Inhibition of IRF5 activity in MNPs phenocopies global IRF5 deficiency. Using a combination of bone marrow chimera and single cell RNA-sequencing approaches we compare the differentiation trajectories of wild type and IRF5 deficient monocytes in a shared inflammatory environment and demonstrate that IRF5 stipulates a choice in monocyte differentiation towards macrophages. Specifically, IRF5 promotes the generation of pathogenic CD11c+ macrophages and controls the production of inflammatory mediators by these cells. Thus, we identify IRF5 as a key transcriptional controller of pathogenic monocyte differentiation in the gut.

2020-04-01 | GSE129257 | GEO

IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype [single_cell_rnaseq]

2020-04-01 | GSE129256 | GEO

IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype [scrnaseq_steady_state]

2020-06-11 | GSE152198 | GEO

Metabolomics Workbench ST000684 - GNPS - Effect of fatty acids on macrophage (wild type versus knockout) lipid levels

Project description:Macrophages from wild type or knockout mice with various treatments [none, BSA (control), palmitate + oleate, conditioned media from adipocytes treated with either BSA or palmitate + oleate). N=4/group.

2018-08-02 | MSV000082722 | GNPS

RNA-seq analysis of the effect of BSA and NaOH added to standard culturing medium on THP-1 macrophages

Project description:The data is supplementary to the RNA-seq analysis of LPS and palmitate stimulation of THP-1 macrophages (E-MTAB-6064), where palmitate for the cell treatment was dissolved in sodium hydroxide and coupled with BSA at a molar ratio 7.5:1. Here we stimulated THP-1 macrophages with the corresponding concentration of BSA (4%) and NaOH (0.4 mM) in the presence of 10 nM phorbol 12-myristate 13-acetate (PMA) for 24 hours added to the standard RPMI 1640 medium with 10% fetal bovine serum (FBS) to estimate the effects and compared them with unstimulated THP-1 macrophages cultured in RPMI 1640 medium with 10% FBS and 10nM PMA.

2019-05-17 | E-MTAB-6439 | biostudies-arrayexpress

WT BMDM M2 vs RON TK- BMDM M2

Project description:Introduction: HGFL-Ron signaling is augmented in human breast cancer and is associated with poor overall prognosis. Here, we investigate the role of HGFL-Ron signaling in RON-modulated murine macrophages through RNA-sequencing of bone marrow-derived macrophages from FVB WT or FVB RON tyrosine kinase -/- mice. BMDM of each genotype M2-polarized via 72 hour treatment with IL-4 were submitted for transcriptomic characterization on the Illumina HiSeq 2500. High quality reads were aligned to the mm10 genome and quantified to generate RPKM

2021-08-10 | GSE166575 | GEO

Protein-tyrosine kinase 2-beta activates Interferon Regulatory Factor 5 to control inflammation

Project description:Interferon regulatory factor 5 (IRF5) plays a distinct role in the regulation of immune responses in health and disease and is a genetic risk factor several autoimmune conditions, including systemic lupus erythematosus, diabetes, arthritis and inflammatory bowel disease. IRF5 function as a transcription factor requires post-translational modifications of the protein such as phosphorylation. Though several upstream signalling regulators of IRF5 have been identified, there is as yet little understanding of how they control IRF5 activity or whether other unknown kinases are involved. In this study, we systematically searched for IRF5 kinases using a reporter-based method for screening a library of 365 inhibitors of protein kinases. Based on the pool of the identified IRF5-inhibiting compounds we have compiled a list of putative IRF5 kinases, which we tested in subsequent in vitro assays. Protein-tyrosine kinase 2-beta (Ptk2b or PYK2) was one of the top hits, capable of binding to and phosphorylating mouse IRF5 at tyrosine (Y) 171. We have shown that IRF5 recruitment to target genes and IRF5-dependent transcription was impaired in cells treated with highly selective PYK2 inhibitors or in PYK2-deficient cells. Moreover, expression of pro-inflammatory cytokines was blocked in the supernatants of human biopsies from inflamed colon of patients with ulcerative colitis and treated ex vivo with a PYK2 inhibitor. Thus, we have identified a major role for PYK2 in regulating the inflammatory response and mapped its activity to the IRF5 innate sensing pathways.

2021-10-14 | PXD014033 | Pride

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