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This Article Full Text Full Text (PDF) All Versions of this Article: 297/5/L816    most recent 90466.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Johnson, M. Articles by Dobbs, L. PubMed PubMed Citation Articles by Johnson, M. Articles by Dobbs, L.

Editorial Focus

Characteristics of Cl^– uptake in rat alveolar type I cells

¹Department of Medicine, ; ²Cardiovascular Research Institute, ; ³Department of Pediatrics, University of California, San Francisco, and ; ⁴San Francisco Veterans Affairs Medical Center, San Francisco, California

Submitted 2 September 2008 ; accepted in final form 8 August 2009

Although Cl^– transport in fetal lung is important for fluid secretion and normal lung development, the role of Cl^– transport in adult lung is not well understood. In physiological studies, the cystic fibrosis transmembrane regulator (CFTR) plays a role in fluid absorption in the distal air spaces of adult lung, and alveolar type II cells cultured for 5 days have the capacity to transport Cl^–. Although both alveolar type I and type II cells express CFTR, it has previously not been known whether type I cells transport Cl^–. We studied Cl^– uptake in isolated type I cells directly, using either radioisotopic tracers or halide-sensitive fluorescent indicators. By both methods, type I cells take up Cl^–. In the presence of β-adrenergic agonist stimulation, Cl^– uptake can be inhibited by CFTR antagonists. Type I cells express both the Cl^–/HCO₃^– anion exchanger AE2 and the voltage-gated Cl^– channels CLC5 and CLC2. Inhibitors of AE2 also block Cl^– uptake in type I cells. Together, these results demonstrate that type I cells are capable of Cl^– uptake and suggest that the effects seen in whole lung studies establishing the importance of Cl^– movement in alveolar fluid clearance may be, in part, the result of Cl^– transport across type I cells.

chloride transport; cystic fibrosis transmembrane regulator; CLC5