{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Peruzzotti-Jametti L"],"funding":["Italian Ministry of Health","Austrian Science Fund FWF","ERA-Net E-rare research programme","NINDS/NIH","Biotechnology and Biological Sciences Research Council UK","NIH-OxCam","Engineering and Physical Sciences Research Council","German Excellence Initiative","Italian Multiple Sclerosis Association","European Research Council","Evelyn Trust","Medical Research Council","Wellcome Trust","Bascule Charitable Trust","United States Department of Defense (DoD) Congressionally Directed Medical Research Programs","Biotechnology and Biological Sciences Research Council"],"pagination":["355-368.e13"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5842147"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["22(3)"],"pubmed_abstract":["Neural stem cell (NSC) transplantation can influence immune responses and suppress inflammation in the CNS. Metabolites, such as succinate, modulate the phenotype and function of immune cells, but whether and how NSCs are also activated by such immunometabolites to control immunoreactivity and inflammatory responses is unclear. Here, we show that transplanted somatic and directly induced NSCs ameliorate chronic CNS inflammation by reducing succinate levels in the cerebrospinal fluid, thereby decreasing mononuclear phagocyte (MP) infiltration and secondary CNS damage. Inflammatory MPs release succinate, which activates succinate receptor 1 (SUCNR1)/GPR91 on NSCs, leading them to secrete prostaglandin E2 and scavenge extracellular succinate with consequential anti-inflammatory effects. Thus,"],"journal":["Cell stem cell"],"pubmed_title":["Macrophage-Derived Extracellular Succinate Licenses Neural Stem Cells to Suppress Chronic Neuroinflammation."],"pmcid":["PMC5842147"],"funding_grant_id":["RG 69865","MS140019","2010/R/31","2014/PMS/4","260511","MC_UU_12022/6","260511-SEM_SEM","110158/Z/15/Z","110159/Z/15/Z","I 3029","RG 75149","RRZA/057 RG79423","MC_U105663142","MC_UU_00015/3","MR/K026682/1","GR08-7"],"pubmed_authors":["Peruzzotti-Jametti L","Bicci I","Mallucci G","Braga A","Volpe G","Bernstock JD","Pluchino S","Frezza C","Vicario N","Kwok CK","Donega M","Balzarotti B","Hallenbeck JM","Iraci N","Murphy MP","Costa ASH","Leonardi T","Manferrari G","Edenhofer F","Booty LM"],"additional_accession":[]},"is_claimable":false,"name":"Macrophage-Derived Extracellular Succinate Licenses Neural Stem Cells to Suppress Chronic Neuroinflammation.","description":"Neural stem cell (NSC) transplantation can influence immune responses and suppress inflammation in the CNS. Metabolites, such as succinate, modulate the phenotype and function of immune cells, but whether and how NSCs are also activated by such immunometabolites to control immunoreactivity and inflammatory responses is unclear. Here, we show that transplanted somatic and directly induced NSCs ameliorate chronic CNS inflammation by reducing succinate levels in the cerebrospinal fluid, thereby decreasing mononuclear phagocyte (MP) infiltration and secondary CNS damage. Inflammatory MPs release succinate, which activates succinate receptor 1 (SUCNR1)/GPR91 on NSCs, leading them to secrete prostaglandin E2 and scavenge extracellular succinate with consequential anti-inflammatory effects. Thus,","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Mar","modification":"2026-05-03T17:34:05.65Z","creation":"2019-03-26T23:07:28Z"},"accession":"S-EPMC5842147","cross_references":{"pubmed":["29478844"],"doi":["10.1016/j.stem.2018.01.020"]}}