{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Nosaka N"],"funding":["National Heart, Lung, and Blood Institute","NHLBI NIH HHS"],"pagination":["207"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7033480"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11"],"pubmed_abstract":["Targeting inflammasome activation to modulate interleukin (IL)-1β is a promising treatment strategy against acute respiratory distress syndrome and ventilator-induced lung injury (VILI). Autophagy is a key regulator of inflammasome activation in macrophages. Here, we investigated the role of autophagy in the development of acute lung injury (ALI) induced by lipopolysaccharide (LPS) and mechanical ventilation (MV). Two hours before starting MV, 0.2 mg/kg LPS was administered to mice intratracheally. Mice were then placed on high-volume MV (30 ml/kg with 3 cmH<sub>2</sub>O positive end-expiratory pressure for 2.5 h without additional oxygen application). Mice with myeloid-specific deletion of the autophagic protein ATG16L1 (<i>Atg16l1</i> <sup>fl/fl</sup> <i>LysM</i> <sup>Cre</sup>) suffered"],"journal":["Frontiers in immunology"],"pubmed_title":["Autophagy Protects Against Developing Increased Lung Permeability and Hypoxemia by Down Regulating Inflammasome Activity and IL-1β in LPS Plus Mechanical Ventilation-Induced Acute Lung Injury."],"pmcid":["PMC7033480"],"funding_grant_id":["R01 HL130353"],"pubmed_authors":["Martinon D","Moreira D","Nosaka N","Arditi M","Shimada K","Crother TR"],"additional_accession":[]},"is_claimable":false,"name":"Autophagy Protects Against Developing Increased Lung Permeability and Hypoxemia by Down Regulating Inflammasome Activity and IL-1β in LPS Plus Mechanical Ventilation-Induced Acute Lung Injury.","description":"Targeting inflammasome activation to modulate interleukin (IL)-1β is a promising treatment strategy against acute respiratory distress syndrome and ventilator-induced lung injury (VILI). Autophagy is a key regulator of inflammasome activation in macrophages. Here, we investigated the role of autophagy in the development of acute lung injury (ALI) induced by lipopolysaccharide (LPS) and mechanical ventilation (MV). Two hours before starting MV, 0.2 mg/kg LPS was administered to mice intratracheally. Mice were then placed on high-volume MV (30 ml/kg with 3 cmH<sub>2</sub>O positive end-expiratory pressure for 2.5 h without additional oxygen application). Mice with myeloid-specific deletion of the autophagic protein ATG16L1 (<i>Atg16l1</i> <sup>fl/fl</sup> <i>LysM</i> <sup>Cre</sup>) suffered","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020","modification":"2025-04-05T16:10:50.183Z","creation":"2020-05-22T11:58:56Z"},"accession":"S-EPMC7033480","cross_references":{"pubmed":["32117318"],"doi":["10.3389/fimmu.2020.00207"]}}