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Mus musculus

ABSTRACT: Prostaglandin E2 receptor EP4-expressing macrophages promote intestinal epithelial barrier regeneration upon inflammation

PROVIDER: PRJNA664831 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12687324_1.fastq.gz	Fastqsanger.gz
	SRR12687324_2.fastq.gz	Fastqsanger.gz
	SRR12687325_1.fastq.gz	Fastqsanger.gz
	SRR12687325_2.fastq.gz	Fastqsanger.gz

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mouse gut metagenome

Project description:Prostaglandin E2-EP4 signalling shifts intestinal microbiome during inflammation

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Epithelial EP4 plays an essential role in maintaining homeostasis in colon

Project description:The EP4 receptor is known to mediate the protective effect of prostaglandin (PG) E2 in the gastrointestinal tract; however, the exact role of epithelial EP4 in intestinal pathophysiology remains unknown. We investigated the role of epithelial EP4 in maintaining colonic homeostasis by characterizing the intestinal epithelial cell-specific EP4 knockout (EP4 cKO) mice. We found a significant enrichment of genes involved in apoptosis-related pathways in the EP4 cKO colons. Moreover, inflammation-associated pathways were highly enriched and revealed more than half of the top 20 pathways related to immune response.

2019-10-29 | GSE135859 | GEO

Post-resolution macrophage-derived lipids shapes long-term tissue immunity and integrity

Project description:Resolving inflammation is thought to return the affected tissue back to homeostasis. However, we show that within days following resolution of Streptococcus pneumonia-triggered lung inflammation there is an influx of antigen specific lymphocytes with a memory and tissue-resident phenotype as well as macrophages bearing an alveolar or interstitial phenotype. Transcriptomic analysis revealed that macrophages are enriched with genes that drive T cell chemotaxis and differentiation as well as prostaglandin biosynthesis. Therapeutic depletion of post-resolution macrophages, inhibition of PGE2 synthesis or antagonism of EP4 reduced numbers of lung CD4+/CD44+/CD62L+ and CD4+/CD44+/CD62L-/CD27+ T cells as well as their expression of the a-integrin, CD103. This intervention resulted in a failure of these cells to reappear and reactivate upon secondary challenge up to six weeks following primary infection. Concomitantly, EP4 antagonism caused accumulation of lung macrophages and marked tissue fibrosis. Hence, resolving inflammation triggers a second wave of immune activity controlled, in part, by PGE2, which through EP4, drives local tissue-resident T cell development on the one hand, whilst limiting tissue injury on the other

2024-04-17 | GSE264058 | GEO

Mus musculus

Project description:Effects of prostaglandin E2-EP4 signalling on intestinal gene expression during inflammation

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Microarray analyses of bovine CD4+ T cells treated with a EP4 agonist

Project description:To examine the effects of prostaglandin E2/EP4 signaling on bovine CD4+ T cells, CD4+ T cells were isolated from bovine peripheral blood mononuclear cells. Isolated CD4+ T cells were cultured with anti-bovine CD3 and anti-bovine CD28 monoclonal antibodies. Following 18 hours of incubation, the cultures were incubated with EP4 agonist or DMSO, a vehicle control for 4 hours. After incubation, the cells were collected and microarray analysis was performed.

2020-11-20 | E-MTAB-9576 | biostudies-arrayexpress

Prostaglandin E2 Receptor Subtype EP2- and EP4-regulated Gene Expression Profiling in Human Ciliary Smooth Muscle Cells

Project description:Changes of genome-wide mRNA transcription levels of human ciliary smooth muscle (hCSM) cells were determined by treating hCSM cells in culture with 200 nM of either an prostaglandin E2 receptor subtype EP2 or subtype EP4 selective agonist for 6 hours in comparison to untreated controls. This was followed by competitive hybridization of fluorescent Cy3 or Cy5 labeled cRNA probes derived from the treated versus untreated control total RNA samples onto an Agilent Human Whole Genome Expression oligonucleotide microarray. Log 2 (LN) of the intra-slide ratios (RATIO, PRE_VALUE) of treated versus untreated samples was reported as VALUE in the sample files. Keywords: prostaglandin E2 receptor agonists, subtype EP2, subtype EP4, hCSM

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The cyclooxygenase-expressing mesenchyme resists intestinal epithelial injury byparacrine signaling

Project description:Paracrine signals play pivotal roles in organ homeostasis. Mesenchymal stromal cells (MSCs) play a key role in regulating epithelium homeostasis in the intestine while their paracrine effects are poorly characterized. Here, we identified prostaglandin E2 (PGE2) secreted by cyclooxygenase (COX)-expressing MSCs as a vital factor to maintain the intestinal mucosal barrier. We found that MSCs-induced organoid swelling through paracrine effect in vitro, a process due to enhanced water adsorption and is mediated by the COX-PGE2-EP4 axis. To further explore the regulatory effect of this axis on the intestinal epithelial barrier in vivo, we established the conditional knockout mouse model to specifically delete COX in MSCs and found that PGE2 reduction downregulated the gene Muc2 and induced a gastric metaplasia-like phenotype. Moreover, PGE2 defects increased the susceptibility of intestinal epithelium to colitis. Our study uncovers the paracrine signaling of COX-expressing MSCs in intestinal mucosal barrier maintenance, providing a basis for understanding the role of mesenchymal cells in the psychophysiology function of the intestine.

2023-09-26 | GSE243704 | GEO

Genome-wide transcriptional profiles of intestinal macrophages from WT and Csf1r-EP4-/- mice during dextran sodium sulfate induced colitis.

Project description:To define the mechanisms that underlie regeneration driven by EP4+ macrophages, we transcriptionally compared the WT and Csf1r-EP4-/- mature macrophages isolated from colon by 39 days post DSS treatment.

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Mus musculus

Project description:Microglial response to Aβ and prostaglandin-E2 EP4 receptor activation

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Microglial response to Aβ and prostaglandin-E2 EP4 receptor activation

Project description:A persistent and non-resolving inflammatory response to accumulating Aβ peptide species is a cardinal feature in the development of Alzheimer's disease (AD). In response to accumulating Aβ peptide species, microglia, the innate immune cells of the brain, generate a toxic inflammatory response that accelerates synaptic and neuronal injury. Many pro-inflammatory signaling pathways are linked to progression of neurodegeneration. However, endogenous anti-inflammatory pathways capable of suppressing Aβ-induced inflammation represent a relatively unexplored area. Here we hypothesized that signaling through the prostaglandin-E2 (PGE2) EP4 receptor potently suppresses microglial inflammatory responses to Aβ42 peptides. In cultured microglial cells, EP4 stimulation attenuated levels of Aβ42-induced inflammatory factors and potentiated phagocytosis of Aβ42. Microarray analysis was performed and demonstrated that EP4 stimulation broadly opposed Aβ42-driven gene expression changes in microglia, with enrichment for targets of IRF1, IRF7, and NF-κB transcription factors.

2014-04-25 | GSE55627 | GEO

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