title: Increased eosinophil transmigration after nasal allergen challenge in children with allergic asthma and rhinitis.
abstract: BACKGROUND
  Eotaxin and interleukin-5 together provide the signal essential for eosinophil transmigration to airway tissue in allergic reactions. However, it is not known whether peripheral blood eosinophils (PBE) possess an increased transmigration capacity in vitro after allergen challenge in vivo before they leave the circulation. We aimed to determine whether PBE in cat-sensitized children have increased spontaneous and/or eotaxin-induced transmigration capacity in vitro, and to what extent allergen challenge alters this feature.
  
  
  METHODS
  Fourteen cat-allergic children and four healthy controls underwent nasal challenge with cat-allergen. Blood samples were drawn prechallenge and at 2 h and 24 h postchallenge. We analyzed the in vitro transmigration of PBE, with and without eotaxin as a chemoattractant. We used a transmigration assay with fibronectin-coated membranes. Eosinophil cationic protein (ECP) and PBE counts were run in parallel.
  
  
  RESULTS
  The spontaneous transmigration capacity of eosinophils in vitro was significantly higher at 2 h after allergen challenge (P < 0.01 vs. prechallenge) and returned to prechallenge levels at 24 h postchallenge (P < 0.02 vs. 2 h postchallenge). Addition of eotaxin further augmented the increased transmigration. In concordance, no accompanying changes were measured in the levels of eosinophils in blood or ECP in serum. Furthermore no spontaneous or eotaxin-induced eosinophil transmigration was detected in healthy controls.
  
  
  CONCLUSIONS
  PBE possess increased spontaneous (and eotaxin-induced) capacity to transmigrate as early as 2 h after allergen challenge in allergic children, without accompanying signs of eosinophil activation in terms of increased PBE count or ECP level. This is probably due to the increased stage of activation of the eosinophil, often referred to as "priming".
authors.affiliation: Astrid Lindgren Children's Hospital, Karolinska Hospital, Karolinska Institutet, Stockholm, Sweden.
authors.forename: K
authors.initials: K
authors.lastname: Lönnkvist
authors.forename: A
authors.initials: A
authors.lastname: Moshfegh
authors.forename: C
authors.initials: C
authors.lastname: Pedroletti
authors.forename: G
authors.initials: G
authors.lastname: Hedlin
authors.forename: G
authors.initials: G
authors.lastname: Halldén
authors.forename: J
authors.initials: J
authors.lastname: Lundahl
mesh_terms: D000293:Adolescent; D000485:Allergens / Q000276:immunology* / Q000494:pharmacology*; D000818:Animals; D001249:Asthma / Q000097:blood / Q000276:immunology*; D002415:Cats; D002465:Cell Movement / Q000187:drug effects / Q000276:immunology; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000276:immunology / Q000494:pharmacology; D002648:Child; D002669:Child Welfare; D004804:Eosinophils / Q000166:cytology* / Q000276:immunology*; D005260:Female; D006801:Humans; D006967:Hypersensitivity / Q000097:blood; D007958:Leukocyte Count; D008297:Male; D009299:Nasal Provocation Tests; D012221:Rhinitis, Allergic, Perennial / Q000097:blood / Q000276:immunology*; D012882:Skin Tests; D013997:Time Factors
chemical_list: D000485:Allergens; C515456:CCL11 protein, human; D054413:Chemokine CCL11; D019742:Chemokines, CC