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Previous Volume 352:2016-2019 May 12, 2005 Number 19 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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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-B (NF-B) to bind to DNA and promote transcription . . . [Full Text of this Article]

Source Information

From the Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston.

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