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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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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

Gut microbial metabolite butyrate improves anticancer therapy by regulating intracellular calcium homeostasis

Project description:Gut microbiota are recognized to be important for anticancer therapy, yet the underlying mechanism is not clear. Herein, we demonstrate that gut microbial metabolite butyrate improves anticancer therapy efficacy by regulating intracellular calcium homeostasis. Butyrate metabolism is activated in hepatocellular carcinoma (HCC) patients. Butyrate supplementation or depletion of short-chain Acyl-CoA dehydrogenase (ACADS), a key enzyme for butyrate metabolism, significantly inhibit HCC proliferation and metastasis. Profiling analysis of genes upregulated by butyrate supplementation or ACADS knockdown reveal that calcium signaling pathway is activated, leading to dysregulation of intracellular calcium homeostasis and production of reactive oxygen species (ROS). Butyrate supplementation improves the therapy efficacy of a tyrosine kinase inhibitor sorafenib. Butyrate and sorafenib co-encapsulated monomethoxy (polyethylene glycol)-poly (D, L-lactide-co-glycolide)-poly(L-lysine)-glypican 3 (PEAL-GPC3) nanoparticles significantly reduce HCC progression. Our findings provide new insight into the mechanisms that the gut microbial metabolites inhibit HCC progression and suggest a translatable therapeutics approach to enhance the clinical targeted therapeutic efficacy.

2025-07-20 | GSE210156 | GEO

Clostridium butyricum and its metabolite butyrate promote ferroptosis susceptibility in pancreatic ductal adenocarcinoma.

Project description:Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive disease with limited therapeutic options. The diversity and composition of intra-tumoral microbiota are associated with PDAC outcomes, and modulating the tumor microbiota has the potential to influence tumor growth and host-immune response. Here, we explore whether intervention with butyrate-producing probiotic can limit PDAC progression. By analyzing TCGA (PAAD) dataset, we found that tumoral butyrate-producing microbiota links to better prognosis and less aggressive features of PDAC. Intervention with Clostridium butyricum or its metabolite butyrate triggered superoxidative stress and intracellular lipid accumulation, which enhanced ferroptosis susceptibility of PDAC. Our study reveals a novel antitumor mechanism of butyrate, and suggests the therapeutic potential of butyrate-producing probiotics in PDAC.

2025-03-15 | GSE227418 | GEO

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

Gut microbial metabolite butyrate improves anticancer therapy by regulating intracellular calcium homeostasis

Project description:Gut microbial metabolite butyrate improves anticancer therapy by regulating intracellular calcium homeostasis

| PRJNA864053 | ENA