Alveolar epithelial cells mitigate neutrophilic inflammation in acute lung injury through regulating mitochondrial fatty acid oxidation. Alveolar epithelial cells mitigate neutrophilic inflammation in acute lung injury through regulating mitochondrial fatty acid oxidation

Carnitine palmitoyltransferase 1a (CPT1a) is the key regulator of mitochondrial long-chain fatty acid beta-oxidation (LCFAO). However, the functional significance of AT2 cell-specific LCFAO at baseline and during acute lung injury (ALI) is not fully understood. In this study, Murine models of AT2 cell-specific Cpt1a deletion were generated for investigating the role of CPT1a in regulating AT2 cell function and the severity of lipopolysaccharide-induced murine ALI models. Overall design: AT2 cells were isolated from the lungs from mice with AT2 cell-specific Cpt1a deletion (Cpt1a-KO) and the control (Sftpc-CreERt2 +/-) at baseline and 24 hours after intra-tracheal LPS administration. To investigate whether impaired LCFAO in AT2 cells regulates the responses of alveolar macrophages in ALI, we also isolated alveolar macrophages from Cpt1a-KO and control mice at 4 hours after intra-tracheal LPS administration, and alveolar macrophages from control mice at baseline. Alveolar macrophages from 2 mice were pooled to make one sample for trancriptomic analysis.