COPD Unwound

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Abstract
In this issue of the Journal, Ito and colleagues show that the proinflammatory state in severe stages of chronic obstructive pulmonary disease (COPD) is related to chromatin unwinding.1 To review basic gene regulation quickly, the balance between histone deacetylases (HDACs) and histone acetylases determines the state of histone acetylation. Acetylated histone prompts the unwinding of chromatin, allowing transcriptional complexes to bind to DNA and generate messenger RNA. In COPD, oxidants from cigarette smoke or inflammatory cells modify and deactivate HDAC2 in lung macrophages, allowing RNA polymerase II and nuclear factor-κB (NF-κB) to bind to DNA and promote transcription of matrix . . .