title: 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.
abstract: 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.affiliation: Department of Respiratory Medicine and Allergy, St. Bartholomew's Hospital, London, England.
authors.forename: M A
authors.initials: MA
authors.lastname: Calderón
authors.forename: J L
authors.initials: JL
authors.lastname: Devalia
authors.forename: A J
authors.initials: AJ
authors.lastname: Prior
authors.forename: R J
authors.initials: RJ
authors.lastname: Sapsford
authors.forename: R J
authors.initials: RJ
authors.lastname: Davies
mesh_terms: D000293:Adolescent; D000328:Adult; D001706:Biopsy; D002478:Cells, Cultured; D018946:Chemokine CCL5 / Q000378:metabolism; D003470:Culture Media; D016207:Cytokines / Q000378:metabolism*; D004847:Epithelial Cells; D004848:Epithelium / Q000378:metabolism; D005260:Female; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000378:metabolism; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000473:pathology / Q000503:physiopathology*; D007375:Interleukin-1 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D008297:Male; D009297:Nasal Mucosa / Q000166:cytology / Q000378:metabolism*; D006255:Rhinitis, Allergic, Seasonal / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D018946:Chemokine CCL5; D003470:Culture Media; D016207:Cytokines; D007375:Interleukin-1; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D016178:Granulocyte-Macrophage Colony-Stimulating Factor