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Laboratory and Animal Investigations |

Decreased CCAAT/Enhancer Binding Protein Transcription Factor Activity in Chronic Bronchitis and COPD*

Lukas Didon, MSc; Ingemar Qvarfordt, MD, PhD; Olof Andersson, MD, PhD; Magnus Nord, MD, PhD; Gerdt C. Riise, MD, PhD
Author and Funding Information

*From the Department of Medical Nutrition (Mr. Didon and Dr. Nord), NOVUM, Karolinska Institute, Huddinge; Department of Respiratory Medicine and Allergology (Drs. Qvarfordt and Riise), Sahlgrenska University Hospital, Gothenburg; and Department of Pulmonary Medicine (Dr. Andersson), Thoracic Division, Karolinska University Hospital Solna, Stockholm, Sweden.

Correspondence to: Magnus Nord, MD, PhD, Department of Medical Nutrition, Karolinska Institute, NOVUM, Karolinska University Hospital Huddinge, SE141 86 Huddinge, Sweden; e-mail: magnus.nord@mednut.ki.se



Chest. 2005;127(4):1341-1346. doi:10.1378/chest.127.4.1341
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Background: CCAAT/enhancer binding proteins (C/EBPs) are key regulators of cell differentiation and linked processes such as proliferation, apoptosis, and gene expression in several organs. C/EBPs are also central for inflammatory responses and infectious defenses, but so far little is known of their role in lung diseases. Chronic bronchitis (CB) and COPD are common smoking-associated lung diseases involving the airway epithelium.

Methods: Gelshifts were used to study C/EBP transcription factor activity in airway epithelial cells obtained by bronchial brush biopsy in four groups: healthy never-smokers (n = 10), asymptomatic smokers (n = 7), and smokers with CB and recurrent infectious exacerbations without COPD (n = 23) and with COPD (n = 13).

Results: C/EBP-binding activity was increased 4.6-fold in airway epithelial cells of healthy smokers compared with never-smokers. In contrast, C/EBP binding activity was not increased in the epithelium of smokers with CB or COPD. C/EBP-β was the dominant C/EBP in the airway epithelium in all groups.

Conclusions: We hypothesize that this lack of increase in C/EBP-β activity renders the epithelium incompetent of efficient regeneration and more sensitive to infection, suggesting a previously unknown role for C/EBPs in the pathogenesis of CB and COPD.

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