BACKGROUND: Recent studies have suggested that airway epithelial cells of atopic and nonatopic individuals may differ in their ability to produce proinflammatory cytokines. METHODS: We have cultured human nasal epithelial cells (NECs) as confluent explant cultures from nasal biopsy specimens of well-characterized nonatopic normal volunteers without rhinitis (n = 8), atopic volunteers without rhinitis (n = 9), and atopic 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 the culture medium by these cells in vitro. NECs from patients with allergic rhinitis were cultured from biopsy specimens obtained on two different occasions, during and after the pollen season. RESULTS: In general, NECs from atopic individuals released significantly greater amounts of IL-1 beta, IL-8, granulocyte-macrophage colony-stimulating factor, tumor necrosis factor-alpha, and RANTES than NECs from nonatopic individuals. IL-8 was released in greatest quantity and IL-1 beta in lowest quantity, regardless of whether the NECs were derived from atopic or nonatopic volunteers. Of the atopic individuals, NECs of atopic patients with rhinitis naturally exposed to pollen released greater quantities of all these cytokines, compared with NECs of atopic patients with rhinitis and atopic patients without rhinitis who were not exposed to allergen. CONCLUSIONS: These results suggest that NECs of atopic individuals, who are genetically predisposed to upper airway disease, release increased amounts of proinflammatory cytokines and that natural exposure to allergen enhances the release of these cytokines, exacerbating the symptoms of allergic disease.
BACKGROUND: Recent studies have suggested that airway epithelial cells of atopic and nonatopic individuals may differ in their ability to produce proinflammatory cytokines. METHODS: We have cultured human nasal epithelial cells (NECs) as confluent explant cultures from nasal biopsy specimens of well-characterized nonatopic normal volunteers without rhinitis (n = 8), atopic volunteers without rhinitis (n = 9), and atopic 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 the culture medium by these cells in vitro. NECs from patients with allergic rhinitis were cultured from biopsy specimens obtained on two different occasions, during and after the pollen season. RESULTS: In general, NECs from atopic individuals released significantly greater amounts of IL-1 beta, IL-8, granulocyte-macrophage colony-stimulating factor, tumor necrosis factor-alpha, and RANTES than NECs from nonatopic individuals. IL-8 was released in greatest quantity and IL-1 beta in lowest quantity, regardless of whether the NECs were derived from atopic or nonatopic volunteers. Of the atopic individuals, NECs of atopic patients with rhinitis naturally exposed to pollen released greater quantities of all these cytokines, compared with NECs of atopic patients with rhinitis and atopic patients without rhinitis who were not exposed to allergen. CONCLUSIONS: These results suggest that NECs of atopic individuals, who are genetically predisposed to upper airway disease, release increased amounts of proinflammatory cytokines and that natural exposure to allergen enhances the release of these cytokines, exacerbating the symptoms of allergic disease.
Authors: Maya K Nanda; Grace K LeMasters; Linda Levin; Marc E Rothenberg; Amal H Assa'ad; Nicholas Newman; David Bernstein; Gurjit Khurana-Hershey; James E Lockey; Patrick H Ryan Journal: Pediatrics Date: 2015-12-29 Impact factor: 7.124
Authors: Johanna M Gostner; Katrin Becker; Heinz Kofler; Barbara Strasser; Dietmar Fuchs Journal: Int Arch Allergy Immunol Date: 2016-05-04 Impact factor: 2.749