title: Effects of rhinovirus infection on the expression and function of cystic fibrosis transmembrane conductance regulator and epithelial sodium channel in human nasal mucosa.
abstract: BACKGROUND
  Changes in expression and function of the cystic fibrosis transmembrane conductance regulator (CFTR) and epithelial sodium channel (ENaC) have been found to cause airway surface liquid (ASL) derangement and to impair mucociliary clearance, both of which have been linked to the pathogenesis of rhinovirus (RV) infection.
  
  
  OBJECTIVE
  The effects of RV infection on the expression and function of CFTR and ENaC in nasal epithelial cells were investigated.
  
  
  METHODS
  Nasal epithelial cells obtained from 14 turbinoplasty patients were infected with RV serotype 16 (RV-16) for 4 hours. Expression of CFTR, α-ENaC, β-ENaC, and γ-ENaC was determined by real-time polymerase chain reaction, Western blot analysis, and confocal immunofluorescence microscopy. Functional changes in the CFTR and ENaC proteins were assessed by measuring transepithelial resistance (TER) using a voltmeter combined with ion channel modulators.
  
  
  RESULTS
  Rhinovirus infection increased expression of CFTR, α-ENaC, β-ENaC, and γ-ENaC messenger RNA (mRNA) and protein compared with controls (P < .05 each) and increased the expression of all 4 proteins on confocal immunofluorescence microscopy. Treatment of cells with the ENaC blocker amiloride and the CFTR activator forskolin increased TER in RV-infected cells, whereas forskolin decreased TER in uninfected cells. The CFTR inhibitor NPPB, however, blocked CFTR more in RV-infected than in noninfected cells.
  
  
  CONCLUSIONS
  Rhinovirus increased the expression of CFTR and appeared to alter its function. In contrast, ENaC expression and function were increased by RV infection. Therefore, RV infection may impair mucociliary transport of nasal epithelium by these alterations.
authors.affiliation: Department of Otorhinolaryngology-Head and Neck Surgery, Chuncheon Sacred Heart Hospital, Hallym University College of Medicine, Chuncheon, South Korea.
authors.forename: Ji Heui
authors.initials: JH
authors.lastname: Kim
authors.forename: Hyun Ja
authors.initials: HJ
authors.lastname: Kwon
authors.forename: Yong Ju
authors.initials: YJ
authors.lastname: Jang
mesh_terms: D000584:Amiloride / Q000494:pharmacology; D002478:Cells, Cultured; D005576:Colforsin / Q000494:pharmacology; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000096:biosynthesis / Q000378:metabolism*; D004847:Epithelial Cells / Q000378:metabolism; D062686:Epithelial Sodium Channel Blockers; D053503:Epithelial Sodium Channels / Q000096:biosynthesis / Q000378:metabolism*; D006801:Humans; D017136:Ion Transport; D009297:Nasal Mucosa / Q000378:metabolism* / Q000821:virology; D018408:Patch-Clamp Techniques; D010850:Picornaviridae Infections / Q000378:metabolism*; D012229:Rhinovirus; D014420:Turbinates / Q000378:metabolism
chemical_list: D062686:Epithelial Sodium Channel Blockers; D053503:Epithelial Sodium Channels; C507045:SCNN1A protein, human; C507051:SCNN1D protein, human; C507052:SCNN1G protein, human; D019005:Cystic Fibrosis Transmembrane Conductance Regulator; D005576:Colforsin; D000584:Amiloride