{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lu B"],"funding":["NIGMS NIH HHS"],"pagination":["350-8"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4153835"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["20"],"pubmed_abstract":["The mammalian immune system and the nervous system coevolved under the influence of cellular and environmental stress. Cellular stress is associated with changes in immunity and activation of the NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome, a key component of innate immunity. Here we show that α7 nicotinic acetylcholine receptor (α7 nAchR)-signaling inhibits inflammasome activation and prevents release of mitochondrial DNA, an NLRP3 ligand. Cholinergic receptor agonists or vagus nerve stimulation significantly inhibits inflammasome activation, whereas genetic deletion of α7 nAchR significantly enhances inflammasome activation. Acetylcholine accumulates in macrophage cytoplasm after adenosine triphosphate (ATP) stimulation in an α7 nAchR-independent manner. Acetylch"],"journal":["Molecular medicine (Cambridge, Mass.)"],"pubmed_title":["α7 nicotinic acetylcholine receptor signaling inhibits inflammasome activation by preventing mitochondrial DNA release."],"pmcid":["PMC4153835"],"funding_grant_id":["R01 GM098446"],"pubmed_authors":["Yang H","Kwan K","Li J","Levine YA","Andersson U","Tracey KJ","Olofsson PS","Wang H","Chavan SS","Joshi S","Lu B"],"additional_accession":[]},"is_claimable":false,"name":"α7 nicotinic acetylcholine receptor signaling inhibits inflammasome activation by preventing mitochondrial DNA release.","description":"The mammalian immune system and the nervous system coevolved under the influence of cellular and environmental stress. Cellular stress is associated with changes in immunity and activation of the NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome, a key component of innate immunity. Here we show that α7 nicotinic acetylcholine receptor (α7 nAchR)-signaling inhibits inflammasome activation and prevents release of mitochondrial DNA, an NLRP3 ligand. Cholinergic receptor agonists or vagus nerve stimulation significantly inhibits inflammasome activation, whereas genetic deletion of α7 nAchR significantly enhances inflammasome activation. Acetylcholine accumulates in macrophage cytoplasm after adenosine triphosphate (ATP) stimulation in an α7 nAchR-independent manner. Acetylch","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Aug","modification":"2025-04-19T04:19:04.473Z","creation":"2019-03-27T01:35:07Z"},"accession":"S-EPMC4153835","cross_references":{"pubmed":["24849809"],"doi":["10.2119/molmed.2013.00117"]}}