SCNN1B and chronic obstructive pulmonary disease: However, despite finding an almost ‘normal lung’ in Cftr mutants, there is evidence for alterations in the cellular uptake of inhaled TiO2NP similar to findings we recently obtained for the uptake of inhaled 20-nm gold (Au) NP in Scnn1b transgenic mice (airway targeted overexpression of the epithelial Na + channel β subunit Scnn1b), which mimic key aspects of chronic obstructive lung diseases in humans [20]: (i) The uptake of a substantial part of the NP (26%) by alveolar epithelial cells in Cftr mutants points to less efficient TiO2NP uptake by surface macrophages in these mice.