title: Upregulation of nasal mucosal eotaxin in patients with allergic rhinitis during grass pollen season: effect of a local glucocorticoid.
abstract: BACKGROUND
  Allergic rhinitis is a common disease characterized by infiltration of eosinophils into the nasal mucosa during the periods of symptoms. Among chemokines, which attract cells to the site of inflammation, eotaxin is relatively specific for eosinophils.
  
  
  OBJECTIVE
  We examined the influence of grass pollen season on nasal eotaxin expression in patients with seasonal allergic rhinitis, as well as the effect of a nasal glucocorticoid on this eotaxin expression.
  
  
  METHODS
  Nineteen patients with allergic rhinitis received treatment with either nasal beclomethasone (400 microgram/day) or placebo over a grass pollen season. In these patients, nasal biopsies were taken prior to and during the peak of the pollen season and stained immunohistochemically for eotaxin and EG2 + eosinophils. Five healthy subjects served as controls and gave nasal biopsies once prior to the pollen season.
  
  
  RESULTS
  Prior to pollen season, there was no significant difference in nasal eotaxin expression between patients with allergic rhinitis and healthy subjects. Grass pollen season induced significant increase in eotaxin expression in placebo-treated (P = 0.04; n = 9) but not in beclomethasone-treated rhinitis patients (P = 0.8; n = 10). During peak grass pollen season, the eotaxin expression in placebo-treated patients was significantly higher compared with healthy subjects outside season (P = 0.03). There was no significant correlation between the expression of eotaxin and the number of EG2 + eosinophils in nasal mucosa. The serum levels of eotaxin in rhinitis patients remained stable over the pollen season.
  
  
  CONCLUSIONS
  Expression of eotaxin in nasal mucosa of grass-pollen allergic rhinitis patients is upregulated during pollen season and treatment with a nasal glucocorticoid protects against this upregulation.
authors.affiliation: Lung Pharmacology Group, Institute of Heart and Lung Diseases, Department of Respiratory Medicine and Allergology, Göteborg University, Gothenburg, Sweden.
authors.forename: T
authors.initials: T
authors.lastname: Pullerits
authors.forename: A
authors.initials: A
authors.lastname: Lindén
authors.forename: L
authors.initials: L
authors.lastname: Praks
authors.forename: L O
authors.initials: LO
authors.lastname: Cardell
authors.forename: J
authors.initials: J
authors.lastname: Lötvall
mesh_terms: D000287:Administration, Topical; D000293:Adolescent; D000328:Adult; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001507:Beclomethasone / Q000627:therapeutic use*; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines / Q000096:biosynthesis* / Q000097:blood; D004311:Double-Blind Method; D004804:Eosinophils / Q000502:physiology; D005260:Female; D005938:Glucocorticoids; D006801:Humans; D008297:Male; D009297:Nasal Mucosa / Q000378:metabolism*; D006255:Rhinitis, Allergic, Seasonal / Q000188:drug therapy* / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D000893:Anti-Inflammatory Agents; C515456:CCL11 protein, human; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines; D005938:Glucocorticoids; D001507:Beclomethasone