{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["7(1)"],"submitter":["Radomski N"],"pubmed_abstract":["Chlamydiae are bacterial pathogens that grow in vacuolar inclusions. Dendritic cells (DCs) disintegrate these compartments, thereby eliminating the microbes, through auto/xenophagy, which also promotes chlamydial antigen presentation via MHC I. Here, we show that TNF-α controls this pathway by driving cytosolic phospholipase (cPLA)2-mediated arachidonic acid (AA) production. AA then impairs mitochondrial function, which disturbs the development and integrity of these energy-dependent parasitic inclusions, while a simultaneous metabolic switch towards aerobic glycolysis promotes DC survival. Tubulin deacetylase/autophagy regulator HDAC6 associates with disintegrated inclusions, thereby further disrupting their subcellular localisation and stability. Bacterial remnants are decorated with def"],"journal":["Scientific reports"],"pagination":["3923"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5478671"],"repository":["biostudies-literature"],"pubmed_title":["Mito-xenophagic killing of bacteria is coordinated by a metabolic switch in dendritic cells."],"pmcid":["PMC5478671"],"pubmed_authors":["Karger A","Tews BA","Rebbig A","Muller A","Rufer E","Radomski N","Knittler MR","Nagel S","Kagebein D","Liebler-Tenorio E","Einenkel R"],"additional_accession":[]},"is_claimable":false,"name":"Mito-xenophagic killing of bacteria is coordinated by a metabolic switch in dendritic cells.","description":"Chlamydiae are bacterial pathogens that grow in vacuolar inclusions. Dendritic cells (DCs) disintegrate these compartments, thereby eliminating the microbes, through auto/xenophagy, which also promotes chlamydial antigen presentation via MHC I. Here, we show that TNF-α controls this pathway by driving cytosolic phospholipase (cPLA)2-mediated arachidonic acid (AA) production. AA then impairs mitochondrial function, which disturbs the development and integrity of these energy-dependent parasitic inclusions, while a simultaneous metabolic switch towards aerobic glycolysis promotes DC survival. Tubulin deacetylase/autophagy regulator HDAC6 associates with disintegrated inclusions, thereby further disrupting their subcellular localisation and stability. Bacterial remnants are decorated with def","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Jun","modification":"2026-05-05T09:46:38.201Z","creation":"2019-03-27T02:48:07Z"},"accession":"S-EPMC5478671","cross_references":{"pubmed":["28634388"],"doi":["10.1038/s41598-017-04142-5"]}}