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1
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80052690031
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The chronic bronchitic phenotype of copd: an analysis of the copdgene study
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Kim, V., Han, M.K., Vance, G.B., Make, B.J., Newell, J.D., Hokanson, J.E., Hersh, C.P., Stinson, D., Silverman, E.K., Criner, G.J., Investigators, C.O., The chronic bronchitic phenotype of copd: an analysis of the copdgene study. Chest 140 (2011), 626–633.
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Hersh, C.P.7
Stinson, D.8
Silverman, E.K.9
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Kim, V., Criner, G.J., Chronic bronchitis and chronic obstructive pulmonary disease. Am J Respir Crit Care Med 187 (2013), 228–237.
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Kim, V., Sternberg, A.L., Washko, G., Make, B.J., Han, M.K., Martinez, F., Criner, G.J., National Emphysema Treatment Trial Research G. Severe chronic bronchitis in advanced emphysema increases mortality and hospitalizations. COPD 10 (2013), 667–678.
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Kim, V.1
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Martinez, F.6
Criner, G.J.7
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4
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84959476027
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Acquired cystic fibrosis transmembrane conductance regulator dysfunction in chronic bronchitis and other diseases of mucus clearance
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Review that describes the mechanistic basis for acquired CFTR dysfunction in chronic bronchitis.
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Raju, S.V., Solomon, G.M., Dransfield, M.T., Rowe, S.M., Acquired cystic fibrosis transmembrane conductance regulator dysfunction in chronic bronchitis and other diseases of mucus clearance. Clin Chest Med 37 (2016), 147–158 Review that describes the mechanistic basis for acquired CFTR dysfunction in chronic bronchitis.
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Clin Chest Med
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, pp. 147-158
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Raju, S.V.1
Solomon, G.M.2
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5
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84863090252
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A pharmacologic approach to acquired cystic fibrosis transmembrane conductance regulator dysfunction in smoking related lung disease
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Sloane, P.A., Shastry, S., Wilhelm, A., Courville, C., Tang, L.P., Backer, K., Levin, E., Raju, S.V., Li, Y., Mazur, M., Byan-Parker, S., et al. A pharmacologic approach to acquired cystic fibrosis transmembrane conductance regulator dysfunction in smoking related lung disease. PLoS ONE, 7, 2012, e39809.
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Sloane, P.A.1
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Mazur, M.10
Byan-Parker, S.11
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6
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First evidence that CFTR expression was decreased by exposure to cigarette smoke in vitro and in vivo. They showed that acquired CFTR deficiency occurs in the nasal respiratory epithelium of cigarette smokers and suggested that CFTR deficiency contributed to cigarette-induced diseases such as chronic bronchitis.
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Cantin, A.M., Hanrahan, J.W., Bilodeau, G., Ellis, L., Dupuis, A., Liao, J., Zielenski, J., Durie, P., Cystic fibrosis transmembrane conductance regulator function is suppressed in cigarette smokers. Am J Respir Crit Care Med 173 (2006), 1139–1144 First evidence that CFTR expression was decreased by exposure to cigarette smoke in vitro and in vivo. They showed that acquired CFTR deficiency occurs in the nasal respiratory epithelium of cigarette smokers and suggested that CFTR deficiency contributed to cigarette-induced diseases such as chronic bronchitis.
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Am J Respir Crit Care Med
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Cantin, A.M.1
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7
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84881494429
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This important study compared lower airway CFTR activity in current and former smokers with COPD, current smokers without COPD, and nonsmokers and found that smokers with and without COPD had reduced lower airway activity compared with nonsmokers and suggested that CFTR dysfunction contributed to COPD pathogenesis.
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Dransfield, M.T., Wilhelm, A.M., Flanagan, B., Courville, C., Tidwell, S.L., Raju, S.V., Gaggar, A., Steele, C., Tang, L.P., Liu, B., Rowe, S.M., Acquired cystic fibrosis transmembrane conductance regulator dysfunction in the lower airways in COPD. Chest 144 (2013), 498–506 This important study compared lower airway CFTR activity in current and former smokers with COPD, current smokers without COPD, and nonsmokers and found that smokers with and without COPD had reduced lower airway activity compared with nonsmokers and suggested that CFTR dysfunction contributed to COPD pathogenesis.
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Chest
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Dransfield, M.T.1
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Gaggar, A.7
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8
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Zhao, R., Liang, X., Zhao, M., Liu, S.L., Huang, Y., Idell, S., Li, X., Ji, H.L., Correlation of apical fluid-regulating channel proteins with lung function in human copd lungs. PLOS ONE, 9, 2014, e109725.
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Zhao, R.1
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9
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Courville, C.A., Tidwell, S., Liu, B., Accurso, F.J., Dransfield, M.T., Rowe, S.M., Acquired defects in CFTR-dependent beta-adrenergic sweat secretion in chronic obstructive pulmonary disease. Respir Res, 15, 2014, 25.
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10
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Courville, C.A., Raju, S.V., Liu, B., Accurso, F.J., Dransfield, M.T., Rowe, S.M., Recovery of acquired cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction following smoking cessation. Am J Respir Crit Care Med 192:12 (2015), 1521–1524.
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Rennolds, J., Butler, S., Maloney, K., Boyaka, P.N., Davis, I.C., Knoell, D.L., Parinandi, N.L., Cormet-Boyaka, E., Cadmium regulates the expression of the CFTR chloride channel in human airway epithelial cells. Toxicol Sci 116 (2010), 349–358.
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Rennolds, J.1
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12
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This significant paper illustrated that cigarette smoke affected other organ systems such as intestinal epithelium and showed that acrolein, a component of cigarette smoke, was higher in smokers and inhibited CFTR channel gating, and that a scavenger of acrolein, N-acetylcysteine, could reverse these effects.
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Raju, S.V., Jackson, P.L., Courville, C.A., McNicholas, C.M., Sloane, P.A., Sabbatini, G., Tidwell, S., Tang, L.P., Liu, B., Fortenberry, J.A., Jones, C.W., et al. Cigarette smoke induces systemic defects in cystic fibrosis transmembrane conductance regulator function. Am J Respir Crit Care Med 188 (2013), 1321–1330 This significant paper illustrated that cigarette smoke affected other organ systems such as intestinal epithelium and showed that acrolein, a component of cigarette smoke, was higher in smokers and inhibited CFTR channel gating, and that a scavenger of acrolein, N-acetylcysteine, could reverse these effects.
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Raju, S.V.1
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13
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Bodas, M., Van Westphal, C., Carpenter-Thompson, R., D, K.M., Vij, N., Nicotine exposure induces bronchial epithelial cell apoptosis and senescence via ros mediated autophagy-impairment. Free Radic Biol Med 97 (2016), 441–453.
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Bodas, M.1
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Rasmussen, J.E., Sheridan, J.T., Polk, W., Davies, C.M., Tarran, R., Cigarette smoke-induced Ca2+ release leads to cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction. J Biol Chem 289 (2014), 7671–7681.
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Rowell, T.R., Tarran, R., Will chronic e-cigarette use cause lung disease?. Am J Physiol Lung Cell Mol Physiol 309 (2015), L1398–L1409.
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Rowell, T.R.1
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In this mechanistic study, the authors demonstrate that cigarette exposure directly leads to loss of CFTR from the cell surface and results in airway surface dehydration, leading to mucus stasis, and suggested that stategies for rehydrating the surface could provide a therapy for chronic bronchitis.
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Clunes, L.A., Davies, C.M., Coakley, R.D., Aleksandrov, A.A., Henderson, A.G., Zeman, K.L., Worthington, E.N., Gentzsch, M., Kreda, S.M., Cholon, D., Bennett, W.D., et al. Cigarette smoke exposure induces CFTR internalization and insolubility, leading to airway surface liquid dehydration. FASEB J 26 (2012), 533–545 In this mechanistic study, the authors demonstrate that cigarette exposure directly leads to loss of CFTR from the cell surface and results in airway surface dehydration, leading to mucus stasis, and suggested that stategies for rehydrating the surface could provide a therapy for chronic bronchitis.
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Clunes, L.A.1
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Leopold, P.L., O'Mahony, M.J., Lian, X.J., Tilley, A.E., Harvey, B.G., Crystal, R.G., Smoking is associated with shortened airway cilia. PLoS ONE, 4, 2009, e8157.
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18
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This manuscipt provides a novel a link between neutrophil elastase-calpain activation and CFTR loss of function in bacterial lung infections relevant to CF. They demonstrate that neutrophil elastase degrades CFTR through activation of intracellular calpains.
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Le Gars, M., Descamps, D., Roussel, D., Saussereau, E., Guillot, L., Ruffin, M., Tabary, O., Hong, S.S., Boulanger, P., Paulais, M., Malleret, L., et al. Neutrophil elastase degrades cystic fibrosis transmembrane conductance regulator via calpains and disables channel function in vitro and in vivo. Am J Respir Crit Care Med 187 (2013), 170–179 This manuscipt provides a novel a link between neutrophil elastase-calpain activation and CFTR loss of function in bacterial lung infections relevant to CF. They demonstrate that neutrophil elastase degrades CFTR through activation of intracellular calpains.
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Le Gars, M.1
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Robinson, D.S., Hamid, Q., Ying, S., Tsicopoulos, A., Barkans, J., Bentley, A.M., Corrigan, C., Durham, S.R., Kay, A.B., Predominant th2-like bronchoalveolar t-lymphocyte population in atopic asthma. N Engl J Med 326 (1992), 298–304.
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Sheehan, J.K., Richardson, P.S., Fung, D.C., Howard, M., Thornton, D.J., Analysis of respiratory mucus glycoproteins in asthma: a detailed study from a patient who died in status asthmaticus. Am J Respir Cell Mol Biol 13 (1995), 748–756.
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Nakagome, K., Matsushita, S., Nagata, M., Neutrophilic inflammation in severe asthma. Int Arch Allergy Immunol 158:Suppl. 1 (2012), 96–102.
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Evans, C.M., Kim, K., Tuvim, M.J., Dickey, B.F., Mucus hypersecretion in asthma: causes and effects. Curr Opin Pulm Med 15 (2009), 4–11.
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Galietta, L.J., Pagesy, P., Folli, C., Caci, E., Romio, L., Costes, B., Nicolis, E., Cabrini, G., Goossens, M., Ravazzolo, R., Zegarra-Moran, O., Il-4 is a potent modulator of ion transport in the human bronchial epithelium in vitro. J Immunol 168 (2002), 839–845.
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Bergougnoux, A., Viart, V., Miro, J., Bommart, S., Molinari, N., des Georges, M., Claustres, M., Chiron, R., Taulan-Cadars, M., Should diffuse bronchiectasis still be considered a CFTR-related disorder?. J Cyst Fibros 14 (2015), 646–653.
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