{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zierfuss B"],"funding":["Austrian Science Fund FWF"],"pagination":["305"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9759912"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["19(1)"],"pubmed_abstract":["Saturated very long-chain fatty acids (VLCFA, ≥ C22), enriched in brain myelin and innate immune cells, accumulate in X-linked adrenoleukodystrophy (X-ALD) due to inherited dysfunction of the peroxisomal VLCFA transporter ABCD1. In its severest form, X-ALD causes cerebral myelin destruction with infiltration of pro-inflammatory skewed monocytes/macrophages. How VLCFA levels relate to macrophage activation is unclear. Here, whole transcriptome sequencing of X-ALD macrophages indicated that VLCFAs prime human macrophage membranes for inflammation and increased expression of factors involved in chemotaxis and invasion. When added externally to mimic lipid release in demyelinating X-ALD lesions, VLCFAs did not activate toll-like receptors in primary macrophages. In contrast, VLCFAs provoked pr"],"journal":["Journal of neuroinflammation"],"pubmed_title":["Saturated very long-chain fatty acids regulate macrophage plasticity and invasiveness."],"pmcid":["PMC9759912"],"funding_grant_id":["KLI 837","DOC 33-B27","DOC 33","KLI 837-B"],"pubmed_authors":["Vandersteene S","Waidhofer-Sollner P","Weinhofer I","Grabmeier-Pfistershammer K","Berger J","Villoria-Gonzalez A","Kemp S","Buda A","Forss-Petter S","Fabjan J","Battin C","Zierfuss B","Steinberger P","Logist M","Dijkstra IME","Parzer P"],"additional_accession":[]},"is_claimable":false,"name":"Saturated very long-chain fatty acids regulate macrophage plasticity and invasiveness.","description":"Saturated very long-chain fatty acids (VLCFA, ≥ C22), enriched in brain myelin and innate immune cells, accumulate in X-linked adrenoleukodystrophy (X-ALD) due to inherited dysfunction of the peroxisomal VLCFA transporter ABCD1. In its severest form, X-ALD causes cerebral myelin destruction with infiltration of pro-inflammatory skewed monocytes/macrophages. How VLCFA levels relate to macrophage activation is unclear. Here, whole transcriptome sequencing of X-ALD macrophages indicated that VLCFAs prime human macrophage membranes for inflammation and increased expression of factors involved in chemotaxis and invasion. When added externally to mimic lipid release in demyelinating X-ALD lesions, VLCFAs did not activate toll-like receptors in primary macrophages. In contrast, VLCFAs provoked pr","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Dec","modification":"2026-05-28T21:28:25.839Z","creation":"2025-02-19T03:24:45.745Z"},"accession":"S-EPMC9759912","cross_references":{"pubmed":["36528616"],"doi":["10.1186/s12974-022-02664-y"]}}