The lactoperoxidase system links anion transport to host defense in cystic fibrosis

Gregory E. Conner, Corinne Wijkstrom-Frei, Scott H. Randell, Vania E. Fernandez, Matthias Salathe

Research output: Contribution to journalArticle

85 Scopus citations

Abstract

Chronic respiratory infections in cystic fibrosis result from CFTR channel mutations but how these impair antibacterial defense is less clear. Airway host defense depends on lactoperoxidase (LPO) that requires thiocyanate (SCN-) to function and epithelia use CFTR to concentrate SCN- at the apical surface. To test whether CFTR mutations result in impaired LPO-mediated host defense, CF epithelial SCN- transport was measured. CF epithelia had significantly lower transport rates and did not accumulate SCN- in the apical compartment. The lower CF [SCN-] did not support LPO antibacterial activity. Modeling of airway LPO activity suggested that reduced transport impairs LPO-mediated defense and cannot be compensated by LPO or H2O2 upregulation.

Original languageEnglish (US)
Pages (from-to)271-278
Number of pages8
JournalFEBS letters
Volume581
Issue number2
DOIs
StatePublished - Jan 23 2007

Keywords

  • CFTR
  • Cystic fibrosis
  • Host defense
  • Hydrogen peroxide
  • Lactoperoxidase
  • Thiocyanate

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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