Cystic fibrosis airway epithelia fail to kill bacteria because of abnormal airway surface fluid.
摘要：
Despite an increased understanding of the cellular and molecular biology of the CFTR Cl channel, it is not known how defective Cl transport across airway epithelia causes chronic bacterial infections in cystic fibrosis (CF) airways. Here, we show that common CF pathogens were killed when added to the apical surface of normal airway epithelia. In contrast, these bacteria multiplied on CF epithelia. We found that bactericidal activity was present in airway surface fluid of both normal and CF epithelia. However, because bacterial killing required a low NaCl concentration and because CF surface fluid has a high NaCl concentration, CF epithelia failed to kill bacteria. This defect was corrected by reducing the NaCl concentration on CF epithelia. These data explain how the loss of CFTR Cl channels may lead to lung disease and suggest new approaches to therapy.
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关键词：
Humans Epithelium Lung Pseudomonas aeruginosa Cystic Fibrosis Chlorides Bacteriocins Chloride Channels Biological Transport Dose-Response Relationship, Drug
DOI：
10.1016/S0092-8674(00)81099-5
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年份：
1996
Elsevier
BMJ
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万方医学
掌桥科研
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