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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.

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

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

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

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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).

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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.

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

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

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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.

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