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The commensal-derived metabolite butyrate imprints an antimicrobial program in macrophages

ABSTRACT: The commensal-derived metabolite butyrate imprints an antimicrobial program in macrophages

PROVIDER: PRJNA435719 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6766962.fastq.gz	Fastqsanger.gz
	SRR6766963.fastq.gz	Fastqsanger.gz
	SRR6766964.fastq.gz	Fastqsanger.gz
	SRR6766965.fastq.gz	Fastqsanger.gz

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Similar Datasets

The commensal-derived metabolite butyrate imprints an antimicrobial program in macrophages

Project description:The balance between tolerogenic and inflammatory responses determines immune homeostasis in the gut. Dysbiosis and a defective host defense against invading intestinal bacteria can shift this balance via bacterial-derived metabolites and trigger chronic inflammation. We show that the short chain fatty acid butyrate modulates monocyte to macrophage differentiation by promoting antimicrobial effector functions. The presence of butyrate modulates antimicrobial activity via a shift in macrophage metabolism and reduction in mTOR activity. This mechanism is furthermore dependent on the inhibitory function of butyrate on histone deacetylase 3 (HDAC3) driving transcription of a set of antimicrobial peptides including calprotectin. The increased antimicrobial activity against several bacterial species is not associated with increased production of conventional cytokines. Butyrate imprints antimicrobial activity of intestinal macrophages in vivo. Our data suggest that commensal bacteria derived butyrate stabilize gut homeostasis by promoting antimicrobial host defense pathways in monocytes that differentiate into intestinal macrophages.

2019-01-30 | GSE111049 | GEO

Expression data from CD4+ naïve T cells under Treg-inducing condition in the presence or absence of butyrate

Project description:Commensal bacteria shape the gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms are not yet known. To reveal the mechanism, we isolated naïve CD4+ T cells from the spleen of C57BL/6 mice and cultured the cells under Treg-inducing condition culture in the presence or absence of butyrate, a metabolite produced by commensal bacteria. Naïve T cells were isolated from spleen and were cultured in the presence of IL-2, TGF-beta and in the presence or absene of Butyrate. RNA was extracted at Day 2.

2015-06-12 | E-GEOD-48045 | biostudies-arrayexpress

Expression data from CD4+ NaM-CM-/ve T cells under Treg-inducing condition in the presence or absence of butyrate

Project description:Commensal bacteria shapes gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms has not yet been unknown. To reveal the mechanism, we isolated NaM-CM-/ve CD4+ T cells from spleen of C57BL/6 mice and cultured the cells under Treg-inducing condition culture in the presence or absence of butyrate, a metabolite produced by commensal bacteria. NaM-CM-/ve T cells were isolated from spleen and were cultured in the presence of IL-2, TGF-beta and in the presence or absene of Butyrate. RNA was extracted at Day 2

2013-11-20 | E-GEOD-49619 | biostudies-arrayexpress

Expression data from CD4+ naïve T cells under Treg-inducing condition in the presence or absence of butyrate

2015-06-12 | GSE48045 | GEO

Expression data from CD4+ Naïve T cells under Treg-inducing condition in the presence or absence of butyrate

Project description:Commensal bacteria shapes gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms has not yet been unknown. To reveal the mechanism, we isolated Naïve CD4+ T cells from spleen of C57BL/6 mice and cultured the cells under Treg-inducing condition culture in the presence or absence of butyrate, a metabolite produced by commensal bacteria.

2013-11-20 | GSE49619 | GEO

The commensal bacterium Lactiplantibacillus plantarum imprints innate memory-like responses in mononuclear phagocytes

Project description:Gut microbiota is a constant source of antigens and stimuli to which the resident immune system has developed tolerance. However, the mechanisms by which mononuclear phagocytes, specifically monocytes/macrophages, cope with these usually pro-inflammatory signals is poorly understood. Here, we show that innate immune memory promotes anti-inflammatory homeostasis using as a model strains of the commensal bacterium, Lactiplantibacillus plantarum. Priming of monocytes/macrophages with bacteria, especially in its live form, enhances bacterial intracellular survival and decreases the release of pro-inflammatory signals to the environment, with lower production of TNF and higher levels of IL-10. Analysis of the transcriptomic landscape of these cells shows downregulation of pathways associated with the production of reactive oxygen species (ROS) and the release of cytokines, chemokines and antimicrobial peptides. Indeed, the induction of ROS prevents memory-induced bacterial survival. In addition, there is a dysregulation in gene expression of several metabolic pathways leading to decreased glycolytic and respiratory rates in memory cells. These data support commensal microbe-specific metabolic changes in innate immune memory cells that might contribute to homeostasis in the gut.

2021-07-06 | GSE159496 | GEO

The commensal bacterium Lactiplantibacillus plantarum imprints innate memory-like responses in mononuclear phagocytes

Project description:The commensal bacterium Lactiplantibacillus plantarum imprints innate memory-like responses in mononuclear phagocytes

| PRJNA669056 | ENA

Clostridium acetobutylicum ATCC 824 butyrate stress (29 mM)

Project description:Metabolite accumulation has pleiotropic, including toxic, effects on cellular physiology, but such effects are not well understood at the genomic level. Using DNA microarrays, the Clostridium acetobutylicum transcriptional stress response to butyrate was analyzed. Keywords: stress response

2007-12-29 | GSE4992 | GEO

The Short Chain Fatty Acid Butyrate Imprints an Antimicrobial Program in Macrophages.

Project description:Host microbial cross-talk is essential to maintain intestinal homeostasis. However, maladaptation of this response through microbial dysbiosis or defective host defense toward invasive intestinal bacteria can result in chronic inflammation. We have shown that macrophages differentiated in the presence of the bacterial metabolite butyrate display enhanced antimicrobial activity. Butyrate-induced antimicrobial activity was associated with a shift in macrophage metabolism, a reduction in mTOR kinase activity, increased LC3-associated host defense and anti-microbial peptide production in the absence of an increased inflammatory cytokine response. Butyrate drove this monocyte to macrophage differentiation program through histone deacetylase 3 (HDAC3) inhibition. Administration of butyrate induced antimicrobial activity in intestinal macrophages in vivo and increased resistance to enteropathogens. Our data suggest that (1) increased intestinal butyrate might represent a strategy to bolster host defense without tissue damaging inflammation and (2) that pharmacological HDAC3 inhibition might drive selective macrophage functions toward antimicrobial host defense.

| S-EPMC6382411 | biostudies-literature

Butyrate alters gene expression profiles in gBT-I cells

Project description:Purpose: The aim of this study is to dissect if the microbiota-derived metabolite butyrate alters the transcriptome of antigen-activated CD8+ T cells. Methods: mRNA profiles from Ctrl and Butyrate-treated gBT-I were generated by deep sequencing, in triplicates, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Results: The analysis of RNAseq data of Ctrl and Butyrate-treated gBT-I lead to ~2,000 differentially expressed genes (FDR < 0.05; fold change>2). GSEA enrichment analysis revealed enrichment of memory T cells signatures in gBT-I following butyrate-treatment (Sarkar et al., 2008). Conclusions: Our data shows that butyrate alters the transcriptome of effector CD8+ T cells, in particular their memory signature.

2019-06-07 | GSE132285 | GEO

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