title: Intranasal administration of eotaxin increases nasal eosinophils and nitric oxide in patients with allergic rhinitis.
abstract: BACKGROUND
  Nitric oxide (NO) plays an important role as an inflammatory mediator in the airways. Inducible NO synthase in the nasal mucosa is upregulated in perennial allergic rhinitis, and nasal NO is reduced after treatment with topical corticosteroids. A previous study has suggested that there is a significant correlation between exhaled NO and sputum eosinophils in patients with asthma.
  
  
  OBJECTIVE
  We investigated the ability of intranasal administration of eotaxin, a potent chemoattractant for eosinophils, to induce eosinophil accumulation and the relationship between eosinophil recruitment in the nasal mucosa and nasal NO production in patients with allergic rhinitis.
  
  
  METHODS
  Nine patients with allergic rhinitis were studied. Eotaxin or diluent was delivered intranasally in patients by using a metered spray pump. Nasal NO, symptom scores, and the influx of inflammatory cells in nasal lavage fluid were assessed before and after the challenge. Immunoreactivity for inducible NO synthase and nitrotyrosine was evaluated in nasal lavage cells.
  
  
  RESULTS
  Eotaxin induced a significant influx of eosinophils (P <.05) with mild symptoms of rhinitis. There was neither significant migration of lymphocytes, basophils, and macrophages into nasal lavage fluid nor a shedding of nasal epithelial cells after eotaxin challenge. Nasal NO was increased significantly (P <.05) 8 hours after eotaxin challenge compared with diluent challenge. Nitrotyrosine immunoreactivity was moderately elevated in nasal epithelial cells after the challenge.
  
  
  CONCLUSIONS
  We have shown that eotaxin causes chemotaxis of eosinophils with a clinically symptomatic inflammatory response in the nasal mucosa and that eosinophil recruitment accompanies an increase in nasal NO, contributing to oxidative stress.
authors.affiliation: Department of Thoracic Medicine, Imperial College School of Medicine at the National Heart and Lung Institute, London, United Kingdom.
authors.forename: T
authors.initials: T
authors.lastname: Hanazawa
authors.forename: J D
authors.initials: JD
authors.lastname: Antuni
authors.forename: S A
authors.initials: SA
authors.lastname: Kharitonov
authors.forename: P J
authors.initials: PJ
authors.lastname: Barnes
mesh_terms: D000281:Administration, Intranasal; D000328:Adult; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004804:Eosinophils / Q000473:pathology*; D005260:Female; D006801:Humans; D008297:Male; D009297:Nasal Mucosa / Q000378:metabolism* / Q000473:pathology*; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D012221:Rhinitis, Allergic, Perennial / Q000378:metabolism* / Q000473:pathology*; D007507:Therapeutic Irrigation; D014443:Tyrosine / Q000031:analogs & derivatives / Q000378:metabolism
chemical_list: C515456:CCL11 protein, human; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines; D009569:Nitric Oxide; C002744:3-nitrotyrosine; D014443:Tyrosine; C496319:NOS2 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II