Chronic obstructive pulmonary disease (COPD) is a respiratory disorder characterized by progressive dyspnea. Damage to the lung air‑blood barrier is a major cause of progressive dyspnea observed in COPD. Although cigarette smoke inhalation and repetitive bacterial infection cause and exacerbate COPD, their specific effects on the air‑blood barrier remain to be fully elucidated. The present study explored the effects of the air‑blood barrier in a COPD rat model induced by cigarette smoke inhalation and repetitive bacterial infection. From weeks 1‑8, Sprague‑Dawley rats were treated with cigarette smoke inhalation and repeated Klebsiella pneumoniae exposure. At the end of week 8, lung function, pulmonary pathology, mucin content, inflammation, oxidative stress and MAPK/NF‑κB/IκBα pathway indicators were detected in rats. Lung function parameters, including tidal volume, peak expiratory flow and 50% tidal volume expiratory flow showed significant decreases in COPD model rats. The pulmonary organizational structure and ultrastructure of the air‑blood barrier were also markedly damaged in COPD model rats. Due to cigarette smoke and Klebsiella pneumoniae exposure, the expression of IL‑6, malondialdehyde, mucoprotein (MUC)5AC, MUC5B, matrix metallopeptidase‑9 and angiopoietin‑2 increased in COPD rats, while the expression of IL‑10, tissue inhibitor of metalloproteinases‑1, heme oxygenase‑1, zonula occludens‑1, claudin‑5, aquaporin‑5, surfactant protein‑D and superoxide dismutase significantly decreased. Subsequently, cigarette smoke exposure and Klebsiella pneumoniae infection increased the levels of phosphorylated‑(p‑)p38, p‑ERK, p‑JNK, p‑p65 and p‑IκBα. The present study provided notable evidence that cigarette smoke and Klebsiella pneumoniae exposure exacerbated the destruction of the air‑blood barrier in COPD via the MAPK/NF‑κB/IκBα pathway. .
Tian et al. (Sun,) studied this question.