Beschreibung:
<jats:p><i>Background:</i> Chronic obstructive pulmonary disease (COPD) is characterized by chronic airway inflammation. Nuclear factor-ĸB (NF-ĸB) is a transcription factor that mediates proinflammatory gene expression. NF-ĸB is activated when its inhibitor, IĸBα, is phosphorylated and degraded. <i>Objectives:</i> The aims of this study were to compare the number of phosphorylated IĸBα-immunopositive airway epithelial cells (AECs) in the peripheral airways of patients with COPD, asymptomatic smokers and asymptomatic nonsmokers. <i>Methods:</i> We examined lung tissues obtained from 10 smokers with COPD, 7 asymptomatic smokers and 10 asymptomatic nonsmokers. Paraffin-embedded sections and immunohistochemical techniques were used to assess the number of phosphorylated IĸBα-positive AECs as well as the numbers of tumor necrosis factor (TNF)α-positive, 8-hydroxy-2′-deoxyguanosine (8-OHdG)-positive and 4-hydroxy-2-nonenal (4-HNE)-positive AECs in the peripheral airway specimens. <i>Results:</i> The percentages of phosphorylated IĸBα-positive AECs and TNFα-positive AECs out of the total number of AECs were significantly higher in patients with COPD than in asymptomatic nonsmokers (p < 0.05). The percentage of phosphorylated IĸBα-positive AECs was positively correlated with the percentage of TNFα-positive AECs (r = 0.82, p < 0.01), but not with the percentage of 8-OHdG-positive AECs or the percentage of 4-HNE-positive AECs. <i>Conclusions:</i> The activation of NF-ĸB, which was evaluated by measuring the level of phosphorylated IĸBα, was enhanced in the peripheral airway epithelia of the COPD patients in this study. The activation of NF-ĸB in the peripheral airway epithelium is associated with an elevated level of TNFα and seems to occur through a mechanism independent of oxidative stress.</jats:p>