Rationale: The nose is an attractive source of airway epithelial cells, particularly in populations where 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. Objectives: To determine whether nasal epithelial cell inflammatory mediator release and receptor expression reflect those of bronchial epithelial cells. Methods: 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. Results: Nasal and bronchial cells had identical epithelial morphology and uniform expression of cytokeratin 19. There were no differences in constitutive expression of CD44, ICAM-1, v3 and v5. Despite significantly higher constitutive release of IL-8, IL-6, RANTES and MMP-9 from nasal compared to bronchial cells, the increments in release of all studied mediators in response to stimulation with IL-1 and TNF were similar and there were significant positive correlations between nasal and bronchial cell secretion of IL-6, RANTES, VEGF, MCP-1, MMP-9 and TIMP-1. Conclusions: 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.