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- W4313356427 startingPage "202.20" @default.
- W4313356427 abstract "Abstract Glucocorticoids promote the survival of neutrophils, the mechanism of which is not clear. We found that glucocorticoids and proinflammatory cytokines synergistically induced G-CSF in primary human neutrophils and macrophages and multiple cell lines. The induction is at the transcriptional level and mediated by NF-κB and the glucocorticoid receptor as demonstrated by site-directed mutagenesis and ChIP assays. In both an LPS-induced airway inflammation model and a chronic OVA-induced airway inflammation model, BAL G-CSF, but not KC or IL-6, was resistant to glucocorticoid suppression. Glucocorticoids together with NF-κB inhibitors, but not either agent alone, decreased BAL G-CSF and neutrophils. Neutrophils from G-CSFR null mice, in contrast to those from wild type animals, were no longer protected by glucocorticoids. Furthermore, knockdown of G-CSF abolished the ability of BEAS 2B bronchial epithelial cells to protect neutrophils from spontaneous apoptosis. These data identify G-CSF as a potential target to increase glucocorticoid sensitivity in neutrophil-driven inflammatory conditions such as chronic obstructive pulmonary disease and neutrophil-dominant endotypes of asthma." @default.
- W4313356427 created "2023-01-06" @default.
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- W4313356427 date "2016-05-01" @default.
- W4313356427 modified "2023-09-25" @default.
- W4313356427 title "Glucocorticoids enhance neutrophil survival via G-CSF" @default.
- W4313356427 doi "https://doi.org/10.4049/jimmunol.196.supp.202.20" @default.
- W4313356427 hasPublicationYear "2016" @default.
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