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Fig. 1 | Respiratory Research

Fig. 1

From: Acute cigarette smoke exposure activates apoptotic and inflammatory programs but a second stimulus is required to induce epithelial to mesenchymal transition in COPD epithelium

Fig. 1

Cigarette smoked induces apoptosis, proliferation and IL-8 production in normal and COPD epithelial cells. NHBEs (normal human bronchial epithelial cells) or COPD-AECs (COPD diseased human bronchial epithelial cells; Lonza) were treated with increasing concentrations of CSE (2–20% as indicated) and after 24 h CSE promoted apoptosis was increased as assessed by elevated caspase 3/7 activity (a), and cell proliferation (b) as measured using 3H-incorporation, (n = 3). CXCL8/IL8 was induced in a dose-dependent manner by CSE treatment (c), as measured by ELISA in the supernatants following stimulation for 24 h (n = 2 donors, each repeated n = 3 times).

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