Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA99601 | ENA |
REPOSITORIES: ENA
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Project description:Innate immune pattern recognition receptors play critical roles in pathogen detection and initiation of antimicrobial responses. We and others have previously demonstrated the importance of the beta-glucan receptor Dectin-1 in the recognition of pathogenic fungi by macrophages and dendritic cells, and have elucidated some of the mechanisms by which Dectin-1 signals to coordinate the antifungal response. While Dectin-1 signals alone are sufficient to trigger phagocytosis and Src-Syk-mediated induction of antimicrobial reactive oxygen species, collaboration with Toll-like receptor (TLR)2 signaling enhances NF-kB activation and regulates cytokine production. In this study we demonstrate that Dectin-1 signaling can also directly modulate gene expression via activation of nuclear transcription of activated T cells (NFAT) transcription factors. Dectin-1 ligation by zymosan particles or live Candida albicans yeast triggers NFAT activation in macrophages and dendritic cells. Dectin-1-triggered NFAT activation plays a role in the induction of Egr2 and Egr3 transcription factors, and cyclooxygenase 2 (Cox-2). Furthermore, we show that NFAT activation regulates IL-2, IL-10 and IL-12 p70 production by zymosan-stimulated dendritic cells. These data establish NFAT activation in myeloid cells as a novel mechanism of regulation of the innate antimicrobial response. Experiment Overall Design: Bone marrow-derived macrophages deficient in MyD88 were stimulated with zymosan, and total RNA was extracted 120 minutes after stimulation for comparison to macrophages grown under the same conditions, but not stimulated.
2008-06-14 | E-GEOD-6376 | biostudies-arrayexpress
Project description:microRNA profiling of murine wt and MyD88-/- deficient bone marrow derived macrophages upon infection with Legionella Pneumophila
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Project description:ATAC-seq profiling of Nfat5 KO and wild type macrophages derived from bone marrow (primary cells), treated or not with Lipopolysaccharide (LPS).
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Project description:Timecourse of interferon-beta stimulation of mouse bone marrow derived macrophages
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Project description:low and high dose TLR4 stimulation in bone-marrow derived mouse macrophages
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Project description:Next to their role in IgE-mediated allergic diseases and in promoting inflammation, mast cells also have antiinflammatory functions. They release pro- as well as antiinflammatory mediators, depending on the biological setting. Here we aimed to better understand the role of mast cells during the resolution phase of a local inflammation induced with the Tolllike receptor (TLR)-2 agonist zymosan. Multiple sequential immunohistology combined with a statistical neighborhood analysis showed that mast cells are located in a predominantly antiinflammatory microenvironment during resolution of inflammation and that mast cell-deficiency causes decreased efferocytosis in the resolution phase. Accordingly, FACS analysis showed decreased phagocytosis of zymosan and neutrophils by macrophages in mast cell-deficient mice. mRNA sequencing using zymosan-induced bone marrow-derived mast cells (BMMC) revealed a strong type I interferon (IFN) response, which is known to enhance phagocytosis by macrophages. Both, zymosan and lipopolysaccharides (LPS) induced IFN-b synthesis in BMMCs in similar amounts as in bone marrow derived macrophages. IFN-b was expressed by mast cells in paws from naïve mice and during zymosan-induced inflammation. As described for macrophages the release of type I IFNs from mast cells depended on TLR internalization and endosome acidification. In conclusion, mast cells are able to produce several mediators including IFN-b, which are alone or in combination with each other able to regulate the phagocytotic activity of macrophages during resolution of inflammation.
2021-01-27 | GSE165523 | GEO
Project description:MyD88 may play a direct role in STING-dependent signaling, or alternatively that STING-dependent pro-inflammatory cytokines may require downstream MyD88-dependent signaling to exert their effect. To determine this, we treated STING or MyD88-deficient murine embryonic fibroblasts (MEFs), bone marrow derived macrophages (BMDM) or dendritic cells (BMDC) with exogenous CDN’s or cytosolic dsDNA (ISD) which triggers STING-signaling and type I IFN production.
2018-02-01 | GSE107809 | GEO