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Nasal Epithelial Cells as Surrogates for Bronchial Epithelial Cells in Airway Inflammation Studies

¹ School of Medicine, University of Aberdeen; ² Department of Respiratory Medicine, Aberdeen Royal Infirmary; and ³ Department of Medical Paediatrics, Royal Aberdeen Children's Hospital, Aberdeen, United Kingdom

Correspondence and requests for reprints should be addressed to Catherine McDougall, MRCPCH, PhD, Department of Child Health, University of Aberdeen, Royal Aberdeen Children's Hospital, Westburn Road, Aberdeen AB25 2ZG, UK. E-mail: catherine.mcdougall{at}luht.scot.nhs.uk

The nose is an attractive source of airway epithelial cells, particularly in populations in which bronchoscopy may not be possible. However, substituting nasal cells for bronchial epithelial cells in the study of airway inflammation depends upon comparability of responses, and evidence for this is lacking. Our objective was to determine whether nasal epithelial cell inflammatory mediator release and receptor expression reflect those of bronchial epithelial cells. Paired cultures of undifferentiated nasal and bronchial epithelial cells were obtained from brushings from 35 subjects, including 5 children. Cells were subject to morphologic and immunocytochemical assessment. Mediator release from resting and cytokine-stimulated cell monolayers was determined, as was cell surface receptor expression. Nasal and bronchial cells had identical epithelial morphology and uniform expression of cytokeratin 19. There were no differences in constitutive expression of CD44, intercellular adhesion molecule-1, vβ3, and vβ5. Despite significantly higher constitutive release of IL-8, IL-6, RANTES (regulated on activation, normal T cell expressed and secreted), and matrix metalloproteinase (MMP)-9 from nasal compared with bronchial cells, the increments in release of all studied mediators in response to stimulation with IL-1β and TNF- were similar, and there were significant positive correlations between nasal and bronchial cell secretion of IL-6, RANTES, vascular endothelial growth factor, monocyte chemoattractant protein-1, MMP-9, and tissue inhibitor of metalloproteinase-1. Despite differences in absolute mediator levels, the responses of nasal and bronchial epithelial cells to cytokine stimulation were similar, expression of relevant surface receptors was comparable, and there were significant correlations between nasal and bronchial cell mediator release. Therefore, nasal epithelial cultures constitute an accessible surrogate for studying lower airway inflammation.

Key Words: airway epithelium • cultured cells • mediator release • adult • child

CLINICAL RELEVANCE The airway epithelium has many important functions. Study of bronchial epithelial cells is hampered by difficulties obtaining suitable samples. Evidence that inflammatory responses of nasal epithelial cells reflect those of bronchial cells is limited. Nasal epithelial cells can be used as surrogates for lower airway cells, facilitating more detailed study of the epithelium in airway inflammation in hitherto largely inaccessible populations, including children.