caa a22 4500 606174931 CHVBK 20210128100740.0 cr unu---uuuuu 210128e20151001xx s 000 0 eng 10.1007/s00018-015-1946-7 doi (NATIONALLICENCE)springer-10.1007/s00018-015-1946-7 Airway hydration and COPD [Elektronische Daten] [Arunava Ghosh, R. Boucher, Robert Tarran] Chronic obstructive pulmonary disease (COPD) is one of the prevalent causes of worldwide mortality and encompasses two major clinical phenotypes, i.e., chronic bronchitis (CB) and emphysema. The most common cause of COPD is chronic tobacco inhalation. Research focused on the chronic bronchitic phenotype of COPD has identified several pathological processes that drive disease initiation and progression. For example, the lung's mucociliary clearance (MCC) system performs the critical task of clearing inhaled pathogens and toxic materials from the lung. MCC efficiency is dependent on: (1) the ability of apical plasma membrane ion channels such as the cystic fibrosis transmembrane conductance regulator (CFTR) and the epithelial Na+ channel (ENaC) to maintain airway hydration; (2) ciliary beating; and (3) appropriate rates of mucin secretion. Each of these components is impaired in CB and likely contributes to the mucus stasis/accumulation seen in CB patients. This review highlights the cellular components responsible for maintaining MCC and how this process is disrupted following tobacco exposure and with CB. We shall also discuss existing therapeutic strategies for the treatment of chronic bronchitis and how components of the MCC can be used as biomarkers for the evaluation of tobacco or tobacco-like-product exposure. Springer Basel, 2015 Airway surface liquid nationallicence Cystic fibrosis nationallicence CFTR nationallicence ENaC nationallicence Mucus nationallicence Tobacco smoke nationallicence Ghosh Arunava Cystic Fibrosis Center/Marsico Lung Institute and the Department of Cell Biology and Physiology, The University of North Carolina, 7102 Marsico Hall, 27599-7248, Chapel Hill, NC, USA aut Boucher R. Cystic Fibrosis Center/Marsico Lung Institute and the Department of Cell Biology and Physiology, The University of North Carolina, 7102 Marsico Hall, 27599-7248, Chapel Hill, NC, USA aut Tarran Robert Cystic Fibrosis Center/Marsico Lung Institute and the Department of Cell Biology and Physiology, The University of North Carolina, 7102 Marsico Hall, 27599-7248, Chapel Hill, NC, USA aut Cellular and Molecular Life Sciences Springer Basel 72/19(2015-10-01), 3637-3652 1420-682X 72:19<3637 2015 72 18 https://doi.org/10.1007/s00018-015-1946-7 text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 review-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s00018-015-1946-7 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Ghosh Arunava Cystic Fibrosis Center/Marsico Lung Institute and the Department of Cell Biology and Physiology, The University of North Carolina, 7102 Marsico Hall, 27599-7248, Chapel Hill, NC, USA aut NATIONALLICENCE 700 1- Boucher R. Cystic Fibrosis Center/Marsico Lung Institute and the Department of Cell Biology and Physiology, The University of North Carolina, 7102 Marsico Hall, 27599-7248, Chapel Hill, NC, USA aut NATIONALLICENCE 700 1- Tarran Robert Cystic Fibrosis Center/Marsico Lung Institute and the Department of Cell Biology and Physiology, The University of North Carolina, 7102 Marsico Hall, 27599-7248, Chapel Hill, NC, USA aut NATIONALLICENCE 773 0- Cellular and Molecular Life Sciences Springer Basel 72/19(2015-10-01), 3637-3652 1420-682X 72:19<3637 2015 72 18