title: [Airway inflammation in COPD].
abstract: COPD is characterized by chronic and persistent inflammation in the small airways and lung parenchyma, which lead to airway remodeling and parenchymal destruction. This inflammation is mediated by the increased expression of multiple inflammatory genes. For the initiation of the transcription of inflammatory genes, the acetylation of core histones is necessary to open up the chromatin structure, that allow transcription factors and RNA polymerase to bind to DNA. Conversely, deacetylation of these histones switches off for the gene transcription. In the COPD lung, the reduced expression of histone deacetylases (HDACs), particularly HDAC-2 is thought to be a key mechanism for the persistence of airway inflammation and corticosteroid resistance.
authors.affiliation: Department of Respiratory Medicine, Kyoto University Hospital.
authors.forename: Shigeo
authors.initials: S
authors.lastname: Muro
mesh_terms: D000107:Acetylation; D006655:Histone Deacetylases / Q000378:metabolism; D006657:Histones / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000473:pathology / Q000503:physiopathology; D029424:Pulmonary Disease, Chronic Obstructive / Q000503:physiopathology*
chemical_list: D006657:Histones; D006655:Histone Deacetylases