A COMPARISON OF CYTOKINE RELEASE FROM EPITHELIAL-CELLS CULTURED FROM NASAL BIOPSY SPECIMENS OF ATOPIC PATIENTS WITH AND WITHOUT RHINITIS AND NONATOPIC SUBJECTS WITHOUT RHINITIS
Ma. Calderon et al., A COMPARISON OF CYTOKINE RELEASE FROM EPITHELIAL-CELLS CULTURED FROM NASAL BIOPSY SPECIMENS OF ATOPIC PATIENTS WITH AND WITHOUT RHINITIS AND NONATOPIC SUBJECTS WITHOUT RHINITIS, Journal of allergy and clinical immunology, 99(1), 1997, pp. 65-76
Background: Recent studies have suggested that airway epithelial cells
of atopic and nonatopic individuals may differ in their ability to pr
oduce proinflammatory cytokines. Methods: We have cultured human nasal
epithelial cells (NECs) as confluent explant cultures from nasal biop
sy specimens of well-characterized nonatopic normal volunteers without
rhinitis (n = 8), atopic volunteers without rhinitis (n = 9), and ato
pic patient volunteers with rhinitis (n = 10) and measured the amounts
of IL-1 beta, IL-8, granulocyte-macrophage colony-stimulating factor,
tumor necrosis factor-alpha, and RANTES released spontaneously into t
he culture medium by these cells in vitro. NECs from patients with all
ergic rhinitis were cultured from biopsy specimens obtained on two dif
ferent occasions, during and after the pollen season. Results: In gene
ral, NECs from atopic individuals released significantly greater amoun
ts of IL-1 beta, IL-8, granulocyte-macrophage colony-stimulating facto
r, tumor necrosis factor-alpha, and RANTES than NECs from nonatopic in
dividuals. IL-8 was released iir greatest quantity and IL-1 beta in lo
west quantity, regardless of whether the NECs were derived from atopic
or nonatopic volunteers. Of the atopic individuals, NECs of atopic pa
tients with rhinitis naturally exposed to pollen released greater quan
tities of all these cytokines, compared with NECs of atopic patients w
ith rhinitis and atopic patients without rhinitis who were not exposed
To allergen. Conclusions: These results suggest that NECs of atopic i
ndividuals, who are genetically predisposed to upper airway disease, r
elease increased amounts of proinflammatory cytokines and that natural
exposure to allergen enhances the release of these cytokines, exacerb
ating the symptoms of allergic disease.