ArticlePloS one2012
GM-CSF priming drives bone marrow-derived macrophages to a pro-inflammatory pattern and downmodulates PGE2 in response to TLR2 ligands.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Type 3 secretion system induced leukotriene B4 synthesis by leukocytes is actively inhibited by Yersinia pestis to evade early immune recognition.PLoS pathogens · 2024Article
- Manganese-Implanted Titanium Modulates the Crosstalk between Bone Marrow Mesenchymal Stem Cells and Macrophages to Improve Osteogenesis.Journal of functional biomaterials · 2023Article
- GM-CSF elicits antibodies to tumor-associated proteins when used as a prostate cancer vaccine adjuvant.Cancer immunology, immunotherapy : CII · 2022Article
- T cell transgressions: Tales of T cell form and function in diverse disease states.International reviews of immunology · 2022Review
- Article
- Isolation and culture of murine bone marrow-derived macrophages for nitric oxide and redox biology.Nitric oxide : biology and chemistry · 2020Article
- GM-CSF: A Promising Target in Inflammation and Autoimmunity.ImmunoTargets and therapy · 2020Review
- The Pleiotropic Effects of the GM-CSF Rheostat on Myeloid Cell Differentiation and Function: More Than a Numbers Game.Frontiers in immunology · 2019Review
- Stromal C-type lectin receptor COLEC12 integrates H. pylori, PGE2-EP2/4 axis and innate immunity in gastric diseases.Scientific reports · 2018Article
- IL-17AFrontiers in immunology · 2018Article
- Dormant 5-lipoxygenase in inflammatory macrophages is triggered by exogenous arachidonic acid.Scientific reports · 2017Article
- A neuropeptide, Substance-P, directly induces tissue-repairing M2 like macrophages by activating the PI3K/Akt/mTOR pathway even in the presence of IFNγ.Scientific reports · 2017Article
- Interactions between Type 1 Interferons and the Th17 Response in Tuberculosis: Lessons Learned from Autoimmune Diseases.Frontiers in immunology · 2017Review
- Molecular Analysis of a Short-term Model of β-Glucans-Trained Immunity Highlights the Accessory Contribution of GM-CSF in Priming Mouse Macrophages Response.Frontiers in immunology · 2017Article
- Effects of bile acids on human airway epithelial cells: implications for aerodigestive diseases.ERJ open research · 2017Article
- Effect of cytokines on Siglec-1 and HIV-1 entry in monocyte-derived macrophages: the importance of HIV-1 envelope V1V2 region.Journal of leukocyte biology · 2016Article
- AMP-activated protein kinase suppresses urate crystal-induced inflammation and transduces colchicine effects in macrophages.Annals of the rheumatic diseases · 2016Article
- The Inflammatory Cytokine IL-21 is Expressed by Splenic Neutrophils in Response to Transplantation of Allogeneic Cells.SOJ immunology · 2016Article
- GM-CSF and uPA are required for Porphyromonas gingivalis-induced alveolar bone loss in a mouse periodontitis model.Immunology and cell biology · 2015Article
- Combination therapies prevent the neuropathic, proinflammatory characteristics of bone marrow in streptozotocin-induced diabetic rats.Diabetes · 2015Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In response to pathogen recognition by Toll-like receptors (TLRs) on their cell surface, macrophages release lipid mediators and cytokines that are widely distributed throughout the body and play essential roles in host responses. Granulocyte macrophage colony-stimulating factor (GM-CSF) is important for the immune response during infections to improve the clearance of microorganisms. In this study, we examined the release of mediators in response to TLR2 ligands by bone marrow-derived macrophages (BMDMs) primed with GM-CSF. We demonstrated that when stimulated with TLR2 ligands, non-primed BMDMs preferentially produced PGE(2) in greater amounts than LTB(4). However, GM-CSF priming shifted the release of lipid mediators by BMDMs, resulting in a significant decrease of PGE(2) production in response to the same stimuli. The decrease of PGE(2) production from primed BMDMs was accompanied by a decrease in PGE-synthase mRNA expression and an increase in TNF-α and nitric oxide (NO) production. Moreover, some GM-CSF effects were potentiated by the addition of IFN-γ. Using a variety of TLR2 ligands, we established that PGE(2) release by GM-CSF-primed BMDMs was dependent on TLR2 co-receptors (TLR1, TLR6), CD14, MyD88 and the nuclear translocation of NFκB but was not dependent on peroxisome proliferator-activated receptor-γ (PPAR-γ) activation. Indeed, GM-CSF priming enhanced TLR2, TLR4 and MyD88 mRNA expression and phospho-IκBα formation. These findings demonstrate that GM-CSF drives BMDMs to present a profile relevant to the host during infections.
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