Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Intestinal stroma guides monocyte differentiation to macrophages through GM-CSF

ABSTRACT: Stroma provides tissues with structural integrity and organization, but its capacity to shape myeloid cells is poorly understood. Here we quantify stromal response to inflammation in pediatric inflammatory bowel disease (IBD) and reveal subset-specific inflammatory responses across colon segments and intestinal layers. Using data from a murine dynamic gut injury model and human ex vivo transcriptomic/protein/spatial analysis, we found that PDGFRA+CD142-/low fibroblasts and monocytes/macrophages co-localize in the intestine. Primary human fibroblast-monocyte co-cultures showed that intestinal PDGFRA+CD142-/low fibroblasts foster monocyte transition to CCR2+CD206+ macrophages through granulocyte-macrophage colony-stimulating factor (GM-CSF). Monocyte-derived CCR2+CD206+ cells from co-cultures had a phenotype similar to intestinal CCR2+CD206+ macrophages from newly diagnosed pediatric IBD patients, with higher levels of PD-L1 and lower levels of GM-CSF receptor. The study depicts subset-specific changes in stromal response to inflammation and demonstrates the stromal potential to guide intestinal macrophage differentiation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE171582 | GEO | 2024/01/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression of the mannose receptor (CD206) defines distinct populations of human colonic macrophages in health and inflammatory bowel disease

Project description:BACKGROUND & AIMS: Intestinal mononuclear phagocytes (MNP) are phenotypically similar, but have different functions. Macrophages contribute to the pathogenesis of inflammatory bowel disease (IBD). To understand this contribution it is necessary to distinguish macrophages from other MNPs, and identify functionally-different macrophage populations. We aimed to accurately identify intestinal macrophage populations, and to ascertain their functions in patients with inflammatory bowel disease (IBD). METHODS: We developed 12-parameter flow cytometry protocols to identify and characterise human intestinal MNPs. We then used RNA sequencing, qPCR, and flow cytometry to analyse colonic biopsies from patients with CD, UC, or non-inflamed controls, in a cross-sectional study. RESULTS: We unambiguously differentiate macrophage populations (CD45+CD64+ HLA-DR+) from dendritic cells (CD45+CD64- HLA-DR+ CD11c;). We identify two distinct subsets within the macrophage population, differentiated by their expression of the mannose receptor, CD206. Further examination of these macrophage sub-populations showed that CD206+ macrophages expressed markers consistent with a mature macrophage phenotype: high levels of CD68 and CD163, higher transcription of IL-10 and lower expression of Trem1. On the contrary, CD64+ HLA-DR- CD206- cells appear to be semi-mature intermediaries in the development of mature intestinal macrophages from their monocyte precursors. CONCLUSIONS: We identified and purified MNP and macrophage populations from human intestinal lamina propria. Thorough characterisation reveals that human colonic macrophages appear to be derived from a monocytic precursor with high CCR2 and low CD206 expression. As these cells mature they lose their proliferative properties and acquire expression of IL-10, CD206, CD63, and CD168. Targeting the newly recruited monocyte-derived cells may represent a fruitful avenue to ameliorate chronic inflammation in IBD.

2018-12-26 | GSE124350 | GEO

Intestinal stroma guides monocyte differentiation to macrophages through GM-CSF

Project description:Intestinal stroma guides monocyte differentiation to macrophages through GM-CSF

| PRJNA720131 | ENA

The immunomodulatory effects of periostin on monocyte-derived macrophages

Project description:To explore the effects of periostin on tumor-associated macrophagess, we first sorted CD14+ monocytes from peripheral blood mononuclear cells of healthy donors using magnetic-activated cell sorting and then induced their differentiation into macrophages by culture with M-CSF for 5 days. In the absence of IL-4 stimulation, these macrophages expressed CD163 and Arg1 (a marker of M2 macrophage activation) but not CD206, suggesting that they were similar to macrophages in the early stage of mycosis fungoides (low frequency of CD206+ cells and low IL-4 expression). We then stimulated these macrophages with or without 100 ng/ml of periostin for 6 hours and examined gene expression using a cDNA microarray. Periostin stimulated gene expression on monocyte-derived macrophages was measured at 6 hours after exposure to doses of 100 ng/ml periostin.

2015-07-14 | E-GEOD-70821 | biostudies-arrayexpress

IL10RA signaling deficiency change the anti-inflammatory signature of Ccr2-independent resident macrophages

Project description:In adult mice the majority of intestinal macrophages exhibit a mature phenotype and are derived from blood monocytes. In the steady state replenishment of these cells is reduced in the absence of the chemokine receptor Ccr2. Within the intestine of mice with colitis there is marked increase in the accumulation of immature macrophages that demonstrate an inflammatory phenotype. However, whether Ccr2 is necessary for the accumulation of these immature macrophages and further for the development of colitis in susceptible mouse models is incompletely defined. Here, we ask whether Ccr2 is necessary for the development of colitis in mice lacking the receptor for IL10. We compared the development of intestinal inflammation in mice lacking IL10RA or both IL10RA and Ccr2. The absence of Ccr2 interfered with the accumulation of immature macrophages in IL10R-deficien mice, including a novel population of rounded submucosal Iba1+ cells and reduced the severity of colitis in these mice. In contrast, the absence of Ccr2 did not reduce augmented inflammatory gene expression observed in mature intestinal macrophages isolated from mice lacking IL10RA. These data suggest that both newly recruited Ccr2-dependent immature macrophages and Ccr2-independent residual mature macrophages contribute to the development of intestinal inflammation observed in IL10R-deficient mice.

2022-01-19 | GSE183960 | GEO

Two distinct subsets are identified from the peritoneal myeloid mononuclear cells expressing both CD11c and CD115

Project description:The peritoneal cavity is home to various immune cells. Previous studies have investigated the heterogenous nature of peritoneal myeloid mononuclear cells. However, up to this date, there are no clear criteria to distinguish peritoneal macrophages and dendritic cells (DCs). In the present study, we delineate the subsets of myeloid mononuclear cells in the mouse peritoneal cavity. Considering phenotypical, functional, and ontogenic features, peritoneal myeloid mononuclear cells are divided into 5 subsets: large peritoneal macrophages (LPMs), small peritoneal macrophages (SPMs), DCs, and 2 MHCII+CD11c+CD115+ subpopulations (i.e., MHCII+CD11c+CD115+CD14-CD206- and MHCII+CD11c+CD115+CD14+CD206+). Among them, 2 subsets of competent antigen presenting cells are demonstrated with distinct functional characteristics, one being DCs and the other being MHCII+CD11c+CD115+CD14-CD206- cells. DCs are able to promote fully activated T cells and superior in expanding cytokine producing inflammatory T cells, whereas MHCII+CD11c+CD115+CD14-CD206- cells generate partially activated T cells and possess a greater ability to induce regulatory T cells under TGF-β and retinoic acid conditions. While the development of DCs and MHCII+CD11c+CD115+CD14-CD206- cells are responsive to the treatment of FLT3L and GM-CSF, the numbers of LPMs, SPMs, and MHCII+CD11c+CD115+CD14+CD206+ cells are only influenced by the injection of GM-CSF. In addition, the analysis of transcriptomes reveals that the gene expression profile of MHCII+CD11c+CD115+CD14+CD206+ cells share high similarity with that of SPMs. Collectively, our study identifies 2 distinct subpopulations of MHCII+CD11c+CD115+ cells, (i) MHCII+CD11c+CD115+CD14-CD206- cells closely related to DCs and (ii) MHCII+CD11c+CD115+CD14+CD206+ cells to SPMs.

2019-07-01 | GSE130424 | GEO

Gene profile of human monocyte-derived macrophages treated with MTX

Project description:Comparison of the transcriptome macrophages derived from CD14+ human monocyte-derived macrophages generated in the presence of M-CSF (M-Mphage) or GM-CSF (GM-Mphage) and MTX.

2023-06-14 | GSE228475 | GEO

Macrophages heterogeneity in human atherosclerotic plaques

Project description:This study aims to characterize the transcriptional profile of Granulocyte-macrophage colony-stimulating factor induced macrophages (GM-MÃ) and M-CSF macrophages (M-MÃ) and to investigate in situ a subset of genes and their products specific to each phenotype in human atherosclerosis plaques 18 RNG/MRC two-colour oligonucleotide microarrays (Le Brigand et al. 2006) were used to generate global mRNA expression profiles for GM-CSF-induced, M-CSF-induced, and peritoneal macrophages. The microarray experiments were conducted either as a common reference (peritoneal-like macrophages) design or using a direct design by hybridizing Granulocyte-macrophage colony-stimulating factor (GM-CSF)-induced human monocyte-derived macrophage (GM-MÃ) and CSF-induced human monocyte-derived macrophages(M-MÃ) on the same arrays

2010-05-16 | E-GEOD-18275 | biostudies-arrayexpress

WT and Ccr2-/- small intestinal macrophages

Project description:WT and Ccr2-/- small intestinal macrophages

| PRJNA979195 | ENA

RNA sequence analysis between ECM1- sufficient and -deficient peritoneal macrophage

Project description:We report the differential gene expression between ECM1- sufficient and -deficient peritoneal macrophage. Inflammatory bowel disease (IBD) comprises chronic relapsing disorders of the gastrointestinal tract characterized pathologically by intestinal inflammation and epithelial injury. Here, we uncover a new function of extracellular matrix protein 1 (ECM1) in promoting the pathogenesis of human and mouse IBD. ECM1 was highly expressed in macrophages, particularly tissue-infiltrated macrophages under inflammatory conditions, and ECM1 expression was significantly induced during IBD progression. The macrophage-specific knockout of ECM1 resulted in increased arginase 1 (ARG1) expression and impaired polarization into the M1 macrophage phenotype following LPS treatment.RNA-sequencing data indicated an alternative metabolic process and a higher arginine metabolic level in ECM1-deficient macrophages compared with ECM1-sufficient macrophages. A mechanistic study showed that ECM1 can negatively regulate M1 macrophage polarization through the GM-CSF/STAT5 signalling pathway. Pathological changes in mice with dextran sodium sulphate-induced IBD were alleviated by the specific knockout of the ECM1 gene in macrophages. Taken together, our findings show that ECM1 has an important function in promoting M1 macrophage polarization, which is critical for controlling inflammation and tissue repair in the intestine.

2019-11-22 | GSE140766 | GEO

High throughput quantitative whole transcriptome analysis of individual macrophages 7 days post-pneumonectomy in a B6 CSF1R-GFP mouse

Project description:Using fluorescence activated cell sorting, we isolated CD45+, CSF1R-GFP+, F4/80+, Ly6G- mouse lung monocytes and macrophages at 7 days after pneumonectomy procedure. We then used microfluidic single cell RNA-sequencing to transcriptional profile unique myeloid subsets. Using the pneumonectomy dataset, we identified 6 cell groups and 4 gene groups that marked several regenerative macrophage subsets including CCR2+, Ly6C+ monocytes and CD206+, Chil3+ M2-like macrophages.

2017-06-19 | GSE96104 | 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