Fig. 3.

Epigenetic regulation of inflammation. A number of epigenetic events can regulate inflammation. Modulators such as methylation and acetylation maintain a balance between heterochromatin and euchromatin with the relaxed euchromatin favoring transcription of genes. Histone acetyltransferases (HATs) and other proteins with similar activity such as bromodomain-containing protein 4 (BRD4) acetylate histones while histone deacetylases (HDACs) remove acetyl groups from histones. Methylation of DNA and histones is carried out by methyltransferases while demethylases are responsible for demethylating action. Finally, regulation through non-coding RNAs (both long non-coding RNAs ‘lncRNAs’ and microRNAs ‘miRNAs’) also comprises epigenetic regulation of inflammation. The overall result of such epigenetic events is either induction or resolution of inflammation with induction of inflammation manifested by release of pro-inflammatory cytokines, chemokines and chemokine receptors along with mobilization of neutrophils/ macrophages, elevated neutrophils-to-lymphocytes ratio (NLR) and coagulation. All these manifestations finally result in lung injury and pulmonary diseases characterized by chronic obstructive pulmonary disease (COPD) and/or acute respiratory distress syndrome (ARDS).