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. Author manuscript; available in PMC: 2017 Jul 1.
Published in final edited form as: Expert Opin Ther Targets. 2016 Feb 11;20(7):869–883. doi: 10.1517/14728222.2016.1139084

Figure 2. CC16 protects murine lungs from developing several lung pathologies when exposed to cigarette smoke.

Figure 2

Left panel: In acute CS exposure models (up to 12 week of CS exposure) CC16−/− mice develop greater increased bronchial and alveolar epithelial apoptosis (second and third panel), lung inflammation (increases in lung macrophage and PMN counts and lung levels of pro-inflammatory cytokines) and greater mucus metaplasia (increased numbers of Muc5ac positive airway epithelial cells) than WT mice. Right panel: In mice exposed chronically to CS (24 weeks) CC16−/− mice had greater increases in lung compliance, and greater airspace enlargement (a readout of emphysema) and greater fibrosis around small airways (with increased deposition of type-I collagen and fibronectin) than WT mice.