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Platelet activating factor (PAF) promotes immunosuppressive neutrophil differentiation within tumors

ABSTRACT: Platelet activating factor (PAF) promotes immunosuppressive neutrophil differentiation within tumors

PROVIDER: PRJNA1144399 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30143022.fastq.gz	Fastqsanger.gz
	SRR30143023.fastq.gz	Fastqsanger.gz
	SRR30143024.fastq.gz	Fastqsanger.gz
	SRR30143025.fastq.gz	Fastqsanger.gz
	SRR30143026.fastq.gz	Fastqsanger.gz

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Platelet activating factor (PAF) promotes immunosuppressive neutrophil differentiation within tumors

Project description:Chronic inflammatory milieu in the tumor microenvironment (TME) leads to the recruitment and differentiation of myeloid-derived suppressor cells (MDSCs). Polymorphonuclear (PMN)-MDSCs, which are phenotypically and morphologically defined as a subset of neutrophils, cause major immune suppression in the TME, posing a significant challenge in the development of effective immunotherapies. Despite recent advances in our understanding of PMN-MDSC functions, the mechanism that gives rise to immunosuppressive neutrophils within the TME remains elusive. Both in vivo and in vitro, newly recruited neutrophils into the tumor sites remained activated and highly motile for several days and developed immunosuppressive phenotypes, as indicated by increased arginase 1 (Arg1) and dcTrail-R1 expression and suppressed anti-cancer CD8 T cell cytotoxicity. The strong suppressive function was successfully recapitulated by incubating naïve neutrophils with cancer cell culture supernatant in vitro. Cancer metabolite secretome analyses of the culture supernatant revealed that both murine and human cancers released lipid mediators to induce the differentiation of immunosuppressive neutrophils. Liquid chromatography–mass spectrometry (LC-MS) lipidomic analysis identified platelet activation factor (PAF; 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) as a common tumor-derived lipid mediator that induces neutrophil differentiation. Lysophosphatidylcholine acyltransferase 2 (LPCAT2), the PAF biosynthetic enzyme, is upregulated in human pancreatic ductal adenocarcinoma (PDAC) and shows an unfavorable correlation with patient survival across multiple cancer types. Our study identifies PAF as a novel lipid-driven mechanism of MDSC differentiation in the TME, providing a potential target for cancer immunotherapy.

2024-09-13 | GSE273979 | GEO

Transcription profiling of human keratinocytes treated with arachidonic acid and platelet activiating factor 16

Project description:Functional role of platelet-activating factor (PAF) induced arachidonic acid release

2009-10-31 | E-TABM-472 | biostudies-arrayexpress

HSD17B13 liquid-liquid phase separation activates autocrine platelet-activating factor signaling in NASH

Project description:Loss-of-function variants in 17-beta hydroxysteroid dehydrogenase 13 (HSD17B13) are associated with decreased inflammation in human chronic liver disease. The underlying mechanism by which HSD17B13 promotes liver inflammation remains largely elusive. Here we find that HSD17B13 undergoes liquid-liquid phase separation (LLPS) around lipid droplets (LDs) in the liver of NASH patients. Dimerization of HSD17B13 drives LLPS formation and regulates its enzyme activity. HSD17B13 LLPS promotes leukocyte adhesion and fibrinogen expression in hepatocytes via activating autocrine platelet activating factor (PAF) signaling. Importantly, adeno-associated viral (AAV)-mediated xeno-expression of human HSD17B13 promotes liver inflammation in Hsd17b13-/- mice induced by high fat diet/carbon tetrachloride treatment. In conclusion, HSD17B13 LLPS triggers liver inflammation via promoting PAF-mediated leukocyte adhesion. Targeting HSD17B13 phase transition would be a promising approach to treat liver inflammation in chronic liver disease.

2024-12-19 | GSE238060 | GEO

Effects of the circulating environment of COVID-19 on platelet and neutrophil behavior

Project description:Thromboinflammatory complications are well described sequalae of Coronavirus Disease 2019 (COVID-19), and there is evidence of both hyperreactive platelet and inflammatory neutrophil biology that contributes to the thromoinflammatory milieu. It has been demonstrated in other thromboinflammatory diseases that the circulating environment may affect cellular behavior, but what role this environment exerts on platelets and neutrophils in COVID-19 remains unknown. We tested the hypotheses that 1) plasma from COVID-19 patients can induce a prothrombotic platelet functional phenotype, and 2) contents released from platelets (platelet releasate) from COVID-19 patients can induce a proinflammatory neutrophil phenotype. We treated platelets with COVID-19 patient and disease control plasma and found that COVID-19 patient plasma promoted auto-aggregation, thereby reducing response to further stimulation ex-vivo. Neither disease condition increased the number of platelets adhered to a collagen and thromboplastin coated parallel plate flow chamber, but both markedly reduced platelet size. We treated healthy neutrophils with COVID-19 patient and disease control platelet releasate and found that COVID-19 patient platelet releasate increased myeloperoxidase-deoxyribonucleic acid complexes and induced changes to neutrophil gene expression. Together these results suggest aspects of the soluble environment of COVID-19 stimulate circulating platelets, and that the contents released from those platelets can elicit inflammatory neutrophil behavior independent of direct cellular contact.

2023-03-08 | GSE225217 | GEO

Impact of Ino-C2-PAF on the gene expression profile of HaCaT cells after stimulation with pro-inflammatory cytokines

2013-01-01 | GSE37361 | GEO

Impact of Ino-C2-PAF on the gene expression profile of HaCaT cells after stimulation with pro-inflammatory cytokines

Project description:New alkyl-phospholipids (APLs) that are structurally derived from the platelet-activating factor are promising candidates for anticancer treatment. After the incorporation into cell membranes, APLs are able to interfere with a wide variety of key enzymes implicated in cell growth, motility, invasion and apoptosis. Recently, using Agilent cDNA microarray technology, we could demonstrate that the glycosidated APL Ino-C2-PAF inhibited the expression of several genes associated with immune response and inflammation in immortalized keratinocytes HaCaT. Here, we analyzed the impact of Ino-C2-PAF on the gene expression profile of HaCaT cells treated with several pro-inflammatory cytokines (IL-1M-NM-1, IL-17, IL-22, TNF-M-NM-1 and oncostatin-M). The influence of Ino-C2-PAF on the transcriptional profile of immortalized keratinocytes (HaCaT) was analyzed treating HaCaT cells with 5 M-BM-5M Ino-C2-PAF in the presence of a mixture of pro-inflammatory cytokines (IL-1M-NM-1, IL-17, IL-22, TNF-M-NM-1 and oncostatin-M) for 24 h. Control cells were left untreated. Three independent experiments were performed for each condition, except for control cells where only two experiments were performed. Control cells were mainly necessary to demonstrate the efficiency of this in vitro inflammation model for keratinocytes.

2013-01-01 | E-GEOD-37361 | biostudies-arrayexpress

Spleen vs Platelet activating factor Treated B cell

Project description:total RNA from mouse (male c57BL/6) spleen labeled with Cy3 vs total RNA from mouse (male c57BL/6) B cells treated with Platelet activating factor labeled with Cy5- time course with repeats Keywords: ordered

2003-04-14 | GSE394 | GEO

Effect of Hyperoxia Exposure on the Neonatal Lungs of WT C57BL6 and PTAFR KO C57BL6 mice

Project description:To assess the role of signaling via platelet-activating factor (PAF) in a murine model of BPD, we used WT and PTAFR KO mice on a C57BL6 background

2024-03-23 | GSE228125 | GEO

The PAF complex regulates alternative splicing.

Project description:The conserved Eukaryotic PAF complex binds to transcribing RNA polymerase II to control deposition of histone marks during transcription. Recently its role in alternative polyadenylation (selection of mRNA 3’end cleavage sites by CPSF) was described. In this work we show that the PAF complex also regulates alternative splicing.

2024-11-05 | GSE250246 | GEO

mRNA profiles in PAF KO intestinal adenoma

Project description:mRNA profiles in PAF KO intestinal adenoma

2018-02-15 | GSE109209 | GEO