Abstract
The expression of CCAAT/enhancer-binding protein (C/EBP)β in the small airway epithelium of COPD is unknown. C/EBPβ was assessed in peripheral lung tissue of non-smoking/smoking controls and patients with GOLD I-IV COPD by quantitative immunohistochemistry. The expression of C/EBPβ was decreased in smokers compared to never smokers. Furthermore, C/EBPβ was significantly elevated in advanced COPD vs. asymptomatic smokers, and the expression correlated to lung function decline. As C/EBPβ exerts pro-inflammatory effects in the context of cigarette smoke, the elevated C/EBPβ in advanced COPD may be an indication of a breakdown of regulatory mechanisms and excessive inflammation.
Highlights
The expression of CCAAT/enhancer-binding protein (C/EBP)β in the small airway epithelium of Chronic obstructive pulmonary disease (COPD) is unknown
While glucocorticoids (GCs) and β2 agonists are mainstay in the management of COPD, these classes of drugs are, by and large, ineffective in preventing disease progression [1]
C/EBPβ is decreased in the small airway epithelium of asymptomatic smokers Strong immunoreactivity to C/EBPβ was observed in the peripheral airway epithelium, as well as in alveolar macrophages of COPD patients and asymptomatic controls (Fig. 1a-c)
Summary
The expression of CCAAT/enhancer-binding protein (C/EBP)β in the small airway epithelium of COPD is unknown. Cigarette smoke and microbial ligands, as well as GCs and β2 agonists may all activate airwayepithelial C/EBPβ in COPD, with the possibility of There is currently insufficient knowledge of the expression of C/EBPβ in the small airways of COPD, in particular in end-stage disease where GC/β2 agonist therapy is mainstay.
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