Cigarette smoke-triggered inflammation is important in the pathophysiology of chronic obstructive pulmonary disease, and involves overexpression of many proinflammatory genes. Transcription factors regulating expression of inflammatory mediators may play a key role in characterizing the disease. To observe alterations in pulmonary function, observe pathological changes in lung tissues, and detect changes in transcriptional factors, mice were exposed to 30 days of cigarette smoke. Pulmonary function was measured by pressure sensors, and pathological changes were observed in lung tissue sections. Nuclear factor (NF)-κB and AP-1 activities were detected by electrophoretic mobility shift assay (EMSA). The levels of inflammatory mediators tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-8 in bronchoalveolar lavage fluid (BALF) were measured using enzyme-linked immunosorbent assay (ELISA). Pulmonary function was not markedly decreased after 30 days of smoke exposure. Exposure to this regimen of cigarette smoke induced peribronchial and perivascular lymphocytic aggregates and parenchymal accumulation of macrophages in mice. EMSA demonstrated that smoke exposure enhanced activator protein (AP)-1 DNA binding activation, but only slightly changed NF-κB activation in mouse lung. Compared to the control group, smoke exposure induced a notable increase in TNF-α in BALF. These data demonstrated that subacute smoke-triggered lung inflammation was accompanied by inflammatory cell influx, AP-1 activation, and proinflammatory gene overexpression in mouse lungs.

Biomarkers for the progression of lung function in COPD are currently scarce. Plasma fetuin-B (FETUB) was identified by iTRAQ-based proteomics and was verified by ELISA in another group. Information regarding acute exacerbation (AE) was collected in a one-year follow-up programme. FETUB concentrations (1652 ± 427 ng/ml) were greater in COPD patients than in controls (1237 ± 77 ng/ml). The concentrations of FETUB in GOLD II (1762 ± 427 ng/ml), III (1650 ± 375 ng/ml) and IV (1800 ± 451 ng/ml) groups were greater than those in the controls (1257 ± 414 ng/ml) and the GOLD I (1345 ± 391 ng/ml) group. ROCs indicated that FETUB distinguished COPD patients from controls (AUC 0.747, 95% CI: 0.642–0.834) and also GOLD II, III and IV from GOLD I COPD patients (AUC: 0.770, 95% CI: 0.634–0.874). The combination of FETUB and fibrinogen performed better (AUC: 0.804, 95% CI: 0.705–0.881). FETUB also predicted the occurrence of AE (AUC: 0.707, 95% CI: 0.566–0.824) or frequent AE (AUC: 0.727, 95% CI: 0.587–0.840). FETUB concentrations were negatively correlated with FEV1%pred (r = −0.446, p = 0.000) and positively correlated with RV%pred (r = 0.317, p = 0.004), RV/TLC% (r = 0.360, p = 0.004), CT emphysema% (r = 0.322, p = 0.008) and grades of lung function (r = 0.437, p = 0.000). In conclusion, FETUB is likely to assist the diagnosis and management of COPD as a complement for other markers.