Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA669056 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12820551.fastq.gz	Fastqsanger.gz
	SRR12820552.fastq.gz	Fastqsanger.gz
	SRR12820553.fastq.gz	Fastqsanger.gz
	SRR12820554.fastq.gz	Fastqsanger.gz
	SRR12820555.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 9

Similar Datasets

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 <i>Lactiplantibacillus plantarum</i> 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 are poorly understood. Here, we show that innate immune memory promotes anti-inflammatory homeostasis, using as 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.

| S-EPMC8259724 | biostudies-literature

cecum mononuclear phagocytes

Project description:scRNAseq of cecum mononuclear phagocytes of PBS/LPS-treated mice

| PRJEB46461 | ENA

ImmGen ULI: OpenSource Mononuclear Phagocytes Project

Project description:ImmGen ULI: OpenSource Mononuclear Phagocytes Project

| PRJNA503607 | ENA

Mononuclear phagocytes in neonatal Peyer's patches

Project description:Mononuclear phagocytes in neonatal Peyer's patches

| PRJNA779989 | ENA

ImmGen ULI: OpenSource Mononuclear Phagocytes Project

Project description:Primary RNASeq data for progenitor, resident, and stimulated (C.alb, LPS, injury, APAP+ starved overnight and pIC) mononuclear phagocytes from fourteen organs.

2018-11-03 | GSE122108 | GEO

Identification of Fcmr-dependent heterogeneity in tumor associated mononuclear phagocytes

Project description:The mononuclear phagocytic system (MPS) is characterized by functional diversity and plasticity, including within the tumor microenvironment (TME). Tumor-associated mononuclear phagocytes (TMPs) within the TME come from various ontological origins. To determine how Fcmr deficiency might impact the functional heterogeneity of mature mononuclear phagocytes (MPs) within the TME, we performed single-cell RNA sequencing (scRNAseq) on MPs isolated from B16 tumors resected from Fcmr-/- and Fcmr+/+ mice. To evaluate a homogenous population of MPs within the TME we chose to examine cells harboring expression of markers found in more mature, differentiated MPs. Therefore, we then sorted MerTk+ CD64+ TMPs by FACS and subjected these cells to single-cell transcriptomic analyses using the Chromium 10X Genomics platform. We obtained RNAseq profiles from 6352 Fcmr+/+ and 7999 Fcmr-/- TMPs.

2019-06-18 | GSE130287 | GEO

Mononuclear phagocytes in muscle after notexin injury in C57Bl/6, Cx3cr1-/-, Ccl2-/-,Cx3cr1-/-Ccl2-/- mice

Project description:Muscle injury triggers inflammation in which infiltrating mononuclear phagocytes are crucial for tissue regeneration. The interaction of the CCL2/CCR2 and CX3CL1/CX3CR1 chemokine axis that guides phagocyte infiltration is incompletely understood. Here, we show that CX3CR1 deficiency promotes muscle repair and rescues Ccl2-/- mice from impaired muscle regeneration as a result of altered macrophage function, not infiltration. Transcriptomic analysis of muscle mononuclear phagocytes reveals that Apolipoprotein E (ApoE) is up-regulated in mice with efficient regeneration. ApoE treatment enhances phagocytosis by mononuclear phagocytes in vitro, and restores phagocytic activity and muscle regeneration in Ccl2-/- mice. Because CX3CR1 deficiency may compensate for defective CCL2-dependant monocyte recruitment by modulating ApoE-dependent macrophage phagocytic activity, targeting CX3CR1 expressed by macrophages might be a powerful therapeutic approach to improve muscle regeneration.

2015-09-29 | GSE73473 | GEO

RNA-seq of of bone marrow derived mononuclear phagocytes

Project description:RNA-seq of of bone marrow derived mononuclear phagocytes

| PRJEB26391 | ENA

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data