Peritoneal cavity macrophage response to IFNg and IFNa
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE112876
PROVIDER: PRJNA433974 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We seeked to determine in vivo effects of IFNg and IFNa response in peritoneal cavity macrophages. These cells were part of ImmGen Interferon cytokine study and immunocytes were sorted according to Immgen's standard lineage panel. Profiles from peritoneal cavity macrophages were used to analyze cell specific responses to IFNg.
2018-02-14 | GSE110549 | GEO
Project description:In order to fully characterize emodin's effects on macrophage activation, peritoneal macrophages were stimulated with LPS+IFNg with or without emodin and gene expression was analyzed using a whole genome microarray. Emodin significantly attenuated the IFNg/LPS induced changes in a large percentage of responsive genes (31%) through inhibiting multiple signaling pathways. RT-qPCR was used to confirm the results in several genes associated with M1 macrophage activation including: TNF, IL6, IL1b, iNOS, MMP2, and MMP9. Three-condition, one-color experiment: Vehicle control, LPS-IFNg or LPS-IFNg-Emodin treated periferal WBC PMN samples: 4 biological replicates each.
2016-07-04 | E-GEOD-73310 | biostudies-arrayexpress
Project description:In order to fully characterize emodin's effects on macrophage activation, peritoneal macrophages were stimulated with LPS+IFNg with or without emodin and gene expression was analyzed using a whole genome microarray. Emodin significantly attenuated the IFNg/LPS induced changes in a large percentage of responsive genes (31%) through inhibiting multiple signaling pathways. RT-qPCR was used to confirm the results in several genes associated with M1 macrophage activation including: TNF, IL6, IL1b, iNOS, MMP2, and MMP9.
2016-01-02 | GSE73310 | GEO
Project description:The goal of this study is to compare the transcriptome profile (RNA-seq) of peritoneal cavity macrophages of RXRa-deficient and WT mice to identify genes which are controlled by the expression of the TF RXRa
2019-09-01 | GSE129095 | GEO
Project description:Bone marrow derived macrophage vs peritoneal macrophage
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Project description:In this study, we profiled the precision N-glycoproteome of the murine peritoneal macrophage under different stimulation.
2021-06-12 | PXD026629 | Pride
Project description:Enteric helminth infections shape host immunity to other pathogens. However, it remains uncertain whether helminth infections following deworming treatment could induce long-term alterations in the host immune system. Here, we demonstrate that infection with Hpb, even after anthelmintic-mediated clearance, induces trained immunity to confer long-lasting cross-protection against lethal S. aureus challenge. This protective effect is associated with the prolonged expansion and functional reprogramming of peritoneal macrophages. Mechanistically, we identify the IL-4/IL-4Rα signaling axis, driven by Hpb-induced Th2 skewing, is essential for both peritoneal macrophage accumulation and Cybb-dependent reactive oxygen species (ROS) enrichment. Notably, Th2 cells, rather than eosinophils or basophils, serve as the predominant source of IL-4 and persist in the peritoneal cavity for at least three weeks post Hpb clearance. Collectively, these findings uncover a novel helminth-mediated trained immunity that promotes host resistance to systemic bacterial infection through Th2-dependent reprogramming of peripheral peritoneal macrophage.
2026-01-01 | GSE301338 | GEO
Project description:To investigate the function of CD1d in the regulation of macrophage homeostasis we performed transcriptomic analyses of cells isolated from the peritoneal cavity of WT and CD1d-deicient mice
2022-10-19 | GSE215837 | GEO
Project description:Enteric helminth infections shape host immunity to other pathogens. However, it remains uncertain whether helminth infections following deworming treatment could induce long-term alterations in the host immune system. Here, we demonstrate that infection with Hpb, even after anthelmintic-mediated clearance, induces trained immunity to confer long-lasting cross-protection against lethal S. aureus challenge. This protective effect is associated with the prolonged expansion and functional reprogramming of peritoneal macrophages. Mechanistically, we identify the IL-4/IL-4Rα signaling axis, driven by Hpb-induced Th2 skewing, is essential for both peritoneal macrophage accumulation and Cybb-dependent reactive oxygen species (ROS) enrichment. Notably, Th2 cells, rather than eosinophils or basophils, serve as the predominant source of IL-4 and persist in the peritoneal cavity for at least three weeks post Hpb clearance. Collectively, these findings uncover a novel helminth-mediated trained immunity that promotes host resistance to systemic bacterial infection through Th2-dependent reprogramming of peripheral peritoneal macrophage.
2026-01-01 | GSE301337 | GEO
Project description:Immunometabolism is a rapidly growing field, which has led to greater understanding of innate immune cell functions. Macrophages are at the core of this research: polarized subsets of in vitro-derived cells reportedly utilize select metabolic pathways to maintain their phenotype. However, relevance of these in vitro studies to the in vivo setting is not known, and metabolic requirements are likely dependent on unique physiological and cellular metabolic environments. Here we define the metabolic requirements of peritoneal tissue-resident macrophages, the accessibility of these metabolites to cells in the peritoneum, and we dissect the role of this unique environment in maintaining a crucial macrophage function. We find that the peritoneal cavity is enriched in amino acids, most notably glutamate. Peritoneal tissue-resident macrophages have an extraordinarily large mitochondrial capacity compared with other phagocytes; this is primarily fueled by glutaminolysis, which is additionally required to maintain an extensive respiratory burst. Glutaminolysis fuels the electron transport chain, which is enhanced during tissue-resident macrophage respiratory burst via a switch to dependence of mitochondrial complex-II. This is not dependent on the level of NADPH, but requires p47 maintained NADPH-oxidase activity. Therefore, we propose that tissue-resident macrophages exploit their unique metabolic niche by implementing their glutamine-fueled mitochondrial-rich phenotype to sustain respiratory burst to assault pathogens, showing that cell-specific metabolic underpinning is important for function. Importantly, we also find that glutamine is required for the respiratory burst in human monocytes, which highlights that metabolites are not species-specific and can be the link between cellular mechanism in mouse and man.
2017-10-13 | GSE104920 | GEO