Document Detail


Intranasal administration of eotaxin increases nasal eosinophils and nitric oxide in patients with allergic rhinitis.
MedLine Citation:
PMID:  10629453     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
CONCLUSION: 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:
T Hanazawa; J D Antuni; S A Kharitonov; P J Barnes
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of allergy and clinical immunology     Volume:  105     ISSN:  0091-6749     ISO Abbreviation:  J. Allergy Clin. Immunol.     Publication Date:  2000 Jan 
Date Detail:
Created Date:  2000-02-08     Completed Date:  2000-02-08     Revised Date:  2011-10-27    
Medline Journal Info:
Nlm Unique ID:  1275002     Medline TA:  J Allergy Clin Immunol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  58-64     Citation Subset:  AIM; IM    
Affiliation:
Department of Thoracic Medicine, Imperial College School of Medicine at the National Heart and Lung Institute, London, United Kingdom.
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MeSH Terms
Descriptor/Qualifier:
Administration, Intranasal
Adult
Chemokine CCL11
Chemokines, CC*
Cytokines / pharmacology*
Dose-Response Relationship, Drug
Eosinophils / pathology*
Female
Humans
Male
Nasal Mucosa / metabolism*,  pathology*
Nitric Oxide / metabolism*
Nitric Oxide Synthase / metabolism
Nitric Oxide Synthase Type II
Rhinitis, Allergic, Perennial / metabolism*,  pathology*
Therapeutic Irrigation
Tyrosine / analogs & derivatives,  metabolism
Chemical
Reg. No./Substance:
0/CCL11 protein, human; 0/Chemokine CCL11; 0/Chemokines, CC; 0/Cytokines; 10102-43-9/Nitric Oxide; 3604-79-3/3-nitrotyrosine; 55520-40-6/Tyrosine; EC 1.14.13.39/NOS2 protein, human; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type II

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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