https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25955 non-CF and pAEC_CF, respectively) during exposure to physiologically relevant NE. The effect of NE activity on pAEC_CF wound repair was also assessed. We report that viability after 48 hours was significantly decreased by 100 nM NE in pAEC_non-CF and pAEC_CF owing to rapid cellular detachment that was accompanied by inflammatory cytokine release. Furthermore, both phenotypes initiated an apoptotic response to 100 nM NE, whereas ≥50 nM NE activity significantly inhibited the proliferative capacity of cultures. Similar concentrations of NE also significantly inhibited wound repair of pAEC_CF, but this effect was reversed by the addition of α1AT. Collectively, our results demonstrate free NE activity is deleterious for epithelial homeostasis and support the hypothesis that proteases in the airway contribute directly to CF structural lung disease. Our results also highlight the need to investigate antiprotease therapies in early CF disease in more detail.]]> Thu 04 Nov 2021 10:39:27 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28201 Sat 24 Mar 2018 07:23:53 AEDT ]]>