title: Effect of anti-immunoglobulin E on nasal inflammation in patients with seasonal allergic rhinoconjunctivitis.
abstract: BACKGROUND
  Binding of allergens to IgE on mast cells and basophils causes release of inflammatory mediators in nasal secretions.
  
  
  OBJECTIVE
  The combined effect of specific immunotherapy (SIT) and omalizumab, a humanized monoclonal anti-IgE antibody, on release of eosinophilic cationic protein (ECP), tryptase, IL-6, and IL-8 in nasal secretion was evaluated.
  
  
  METHODS
  Two hundred and twenty five children (aged 6-17 years) with a history of seasonal allergic rhinoconjunctivitis induced by birch and grass pollen were randomized into four groups: either birch- or grass-pollen SIT in combination with either anti-IgE or placebo. Complete sets of nasal secretion samples before treatment Visit 1 (V1), during birch- (V2) and grass (V3)-pollen season and after the pollen season (V4) were collected from 53 patients.
  
  
  RESULTS
  A significant reduction in tryptase only was seen in the anti-IgE-treated group at V2 (P<0.05) and V4 (P<0.05) compared with the placebo group. During the pollen season, patients with placebo showed an increase of ECP compared with baseline (V2: +30.3 microg/L; V3: +134.2 microg/L, P< 0.005; V4: +79.0 microg/L, P< 0.05), and stable levels of tryptase, IL-6 and IL-8. Treatment with anti-IgE resulted in stable ECP values and a significant decrease of tryptase compared with V1 (baseline): V2: -80.0 microg/L (P< 0.05); V3: -56.3 microg/L, which persisted after the pollen season with V4: -71.6 microg/L (P< 0.05). After the pollen season, a decrease of IL-6 was observed in both groups (V4 placebo group: -37.5 ng/L; V4 anti-IgE group: -42.9 ng/L, P< 0.01).
  
  
  CONCLUSIONS
  The combination of SIT and anti-IgE is associated with prevention of nasal ECP increase and decreased tryptase levels in nasal secretions.
authors.affiliation: University Children's Hospital, Frankfurt, Germany.
authors.forename: C
authors.initials: C
authors.lastname: Bez
authors.forename: R
authors.initials: R
authors.lastname: Schubert
authors.forename: M
authors.initials: M
authors.lastname: Kopp
authors.forename: Y
authors.initials: Y
authors.lastname: Ersfeld
authors.forename: M
authors.initials: M
authors.lastname: Rosewich
authors.forename: J
authors.initials: J
authors.lastname: Kuehr
authors.forename: W
authors.initials: W
authors.lastname: Kamin
authors.forename: A V
authors.initials: AV
authors.lastname: Berg
authors.forename: U
authors.initials: U
authors.lastname: Wahu
authors.forename: S
authors.initials: S
authors.lastname: Zielen
mesh_terms: D000293:Adolescent; D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D029662:Betula; D001798:Blood Proteins / Q000032:analysis; D001826:Body Fluids / Q000737:chemistry; D002648:Child; D003888:Desensitization, Immunologic / Q000379:methods*; D004311:Double-Blind Method; D047091:Eosinophil Granule Proteins; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000276:immunology*; D015850:Interleukin-6 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D008297:Male; D009297:Nasal Mucosa / Q000276:immunology* / Q000378:metabolism; D000069444:Omalizumab; D006109:Poaceae; D011058:Pollen; D006255:Rhinitis, Allergic, Seasonal / Q000276:immunology / Q000628:therapy*; D012260:Ribonucleases / Q000032:analysis; D012697:Serine Endopeptidases / Q000032:analysis; D053802:Tryptases
chemical_list: D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D015850:Interleukin-6; D016209:Interleukin-8; D000069444:Omalizumab; D007073:Immunoglobulin E; D012260:Ribonucleases; D012697:Serine Endopeptidases; D053802:Tryptases