{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang J"],"funding":["BLRD VA","NCI NIH HHS","U.S. Department of Veterans Affairs"],"pagination":["1166-1178"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6557664"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["593(11)"],"pubmed_abstract":["A causal relationship exists between macrophage cholesterol levels and inflammation, for example, Interleukin-1β (IL-1β) secretion. A decrease in intracellular K<sup>+</sup> is essential for inflammasome activation/IL-1β secretion and, herein, we examined the hypothesis that cellular cholesterol affects K<sup>+</sup> -channel activity and K<sup>+</sup> -efflux using mouse peritoneal macrophages (MPMs) and human/THP1 macrophages. An increase in cellular cholesterol led to a significant increase in K<sup>+</sup> currents (> 350% in both MPM and THP1). Enhancing cholesterol efflux returned K<sup>+</sup> currents back to basal levels with corresponding increase in intracellular K<sup>+</sup> (11.2-14.5%) and reduced IL-1β secretion (32-62%). These data demonstrate a novel mechanism by which ce"],"journal":["FEBS letters"],"pubmed_title":["Regulation of interleukin-1 beta secretion from macrophages via modulation of potassium ion (K<sup>+</sup> ) channel activity."],"pmcid":["PMC6557664"],"funding_grant_id":["I01 BX002297","P30 CA016059"],"pubmed_authors":["Ghosh S","Yannie PJ","Ghosh SS","Wang J"],"additional_accession":[]},"is_claimable":false,"name":"Regulation of interleukin-1 beta secretion from macrophages via modulation of potassium ion (K<sup>+</sup> ) channel activity.","description":"A causal relationship exists between macrophage cholesterol levels and inflammation, for example, Interleukin-1β (IL-1β) secretion. A decrease in intracellular K<sup>+</sup> is essential for inflammasome activation/IL-1β secretion and, herein, we examined the hypothesis that cellular cholesterol affects K<sup>+</sup> -channel activity and K<sup>+</sup> -efflux using mouse peritoneal macrophages (MPMs) and human/THP1 macrophages. An increase in cellular cholesterol led to a significant increase in K<sup>+</sup> currents (> 350% in both MPM and THP1). Enhancing cholesterol efflux returned K<sup>+</sup> currents back to basal levels with corresponding increase in intracellular K<sup>+</sup> (11.2-14.5%) and reduced IL-1β secretion (32-62%). These data demonstrate a novel mechanism by which ce","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Jun","modification":"2025-04-19T14:24:33.42Z","creation":"2020-10-29T16:40:21Z"},"accession":"S-EPMC6557664","cross_references":{"pubmed":["31026357"],"doi":["10.1002/1873-3468.13395"]}}