<HashMap><database>biostudies-other</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Mr. Dominik Brokatzky</submitter><funding>Deutsche Forschungsgemeinschaft (DFG)</funding><funding>Else Kröner-Fresenius-Stiftung (EKFS)</funding><journal>The EMBO Journal</journal><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-SCDT-EMBOJ-2018-100907</full_dataset_link><abstract>Apoptosis is a frequent form of programmed cell death but the apoptotic signaling pathway can also be engaged at a low level, in the absence of cell death. We here report that such sub-lethal engagement of mitochondrial apoptosis-signaling causes the secretion of cytokines from human epithelial cells in a process controlled by the Bcl-2 family of proteins. We further show that sub-lethal signaling of the mitochondrial apoptosis pathway is initiated by infections with all tested viral, bacterial and protozoan pathogens and causes damage to the genomic DNA. Epithelial cells infected with these pathogens secreted cytokines, and this cytokine-secretion upon microbial infection was substantially reduced if mitochondrial sub-lethal apoptosis-signaling was blocked. In the absence of mitochondrial</abstract><repository>biostudies-other</repository><pubmed_authors>Dr. Tobias Steinfeldt</pubmed_authors><pubmed_authors>Juliane Vier</pubmed_authors><pubmed_authors>Dr. Arnim Weber</pubmed_authors><pubmed_authors>Dr. Ian, E. Gentle</pubmed_authors><pubmed_authors>Julia Henschel</pubmed_authors><pubmed_authors>Arlena Metz</pubmed_authors><pubmed_authors>Mr. Dominik Brokatzky</pubmed_authors><pubmed_authors>Dr. Susanne Kirschnek</pubmed_authors><pubmed_authors>Mr. Benedikt Dörflinger</pubmed_authors><pubmed_authors>Dr. Aladin Haimovici</pubmed_authors><pubmed_authors>Prof. Georg Häcker</pubmed_authors></additional><is_claimable>false</is_claimable><name>A non-death function of the mitochondrial apoptosis apparatus in immunity</name><description>Apoptosis is a frequent form of programmed cell death but the apoptotic signaling pathway can also be engaged at a low level, in the absence of cell death. We here report that such sub-lethal engagement of mitochondrial apoptosis-signaling causes the secretion of cytokines from human epithelial cells in a process controlled by the Bcl-2 family of proteins. We further show that sub-lethal signaling of the mitochondrial apoptosis pathway is initiated by infections with all tested viral, bacterial and protozoan pathogens and causes damage to the genomic DNA. Epithelial cells infected with these pathogens secreted cytokines, and this cytokine-secretion upon microbial infection was substantially reduced if mitochondrial sub-lethal apoptosis-signaling was blocked. In the absence of mitochondrial</description><dates><release>2020-04-01T00:00:00Z</release><modification>2020-04-01T12:31:49Z</modification><creation>2020-04-01T12:31:49Z</creation></dates><accession>S-SCDT-EMBOJ-2018-100907</accession><cross_references><doi>10.15252/embj.2018100907</doi></cross_references></HashMap>