Multi-omics analysis of the epigenetic effects of lipopolysaccharide-induced inflammation in Type II Pneumocytes

Chronic inflammation plays a central role in the pathogenesis of many lung diseases including asthma, SARS-COVID19, obstructive pulmonary disease (COPD), and lung cancer. Lipopolysaccharide (LPS) is an inflammatory agent produced by most Gram-negative bacteria and found in cigarette smoke. In a mouse model of inflammation, inhalation exposure to LPS induced COPD and increased the size and the multiplicity of lung tumors induced by tobacco-specific nitrosamines. In the present work, we employed a comprehensive multi-omics approach that monitored changes in DNA methylation/hydroxymethylation, gene expression, and global protein abundances in Type II pneumocytes of A/J mice following sub-chronic exposure to LPS.