Laryngorhinootologie 2005; 84(7): 503-510
DOI: 10.1055/s-2005-861402
Allergologie
© Georg Thieme Verlag KG Stuttgart · New York

Humorale Mukosa-Immunantwort bei der Rhinitis allergica

Humoral Mucosal Immunity in Allergic RhinitisM.  F.  Kramer1 , T.  R.  Jordan1 , E.  Pfrogner1 , G.  Rasp1
  • 1 Klinik und Poliklinik für Hals-, Nasen-, und Ohrenheilkunde am Klinikum Großhadern, Ludwig-Maximilians-Universität München (Direktor: Prof. Dr. med. A. Berghaus)
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Publikationsverlauf

Eingegangen: 22. Juni 2004

Angenommen: 10. Januar 2005

Publikationsdatum:
23. Mai 2005 (online)

Zusammenfassung

Hintergrund: Ziel der vorliegenden Arbeit war die Untersuchung allergen-spezifischer Immunglobuline (Ig) der Klassen IgA und IgG im Nasensekret als Ausdruck einer eigenständigen Mukosa-Immunantwort bei der Rhinitis allergica.

Methoden: Nasensekrete von 40 Allergikern wurden auf allergen-spezifisches IgA, IgG und IgE sowie auf ECP und Tryptase untersucht. 43 nicht-atopische Individuen dienten als Kontrolle. Um mögliche Einflüsse der aktuellen Pollenbelastung auf die untersuchten Parameter zu evaluieren, verglichen wir Pollinotiker co- (n = 28) versus extra-saisonal (n = 41). Weiterhin untersuchten wir 5 Patienten nach nasaler Allergenprovokation, um einen möglichen Einfluss des allergen-spezifischen IgA bei der Degranulation von Eosinophilen zu erfassen.

Ergebnisse: Im Vergleich zu den nicht-atopischen Kontrollen fanden wir signifikant erhöhte allergen-spezifische Ig aller untersuchten Klassen und Antigene bei den Allergikern. Co-saisonal fanden wir erhöhte Konzentrationen von allergen-spezifischem IgE, ECP und Tryptase, jedoch niedrigere Konzentrationen von allergen-spezifischem IgA und IgG. Es fand sich keine Assoziation zwischen der Eosinophilie in der allergischen Spätphase nach Provokation und dem allergen-spezifischen IgA.

Diskussion: Den Nachweis von allergen-spezifischem IgA und IgG im Nasensekret von Patienten mit allergischer Rhinitis interpretieren wir als Ausdruck einer eigenständigen, humoralen Mukosa-Immunantwort.

Abstract

Background: Mucosa-immunologic aspects are gaining an increasing awareness in the pathophysiology of type I allergies. Humoral mucosal immune responses are dominated by secretory IgA, but there is evidence for a relevant role of IgG in nasal mucosa-associated lymphoid tissue.

Objective: was to measure allergen-specific immunoglobulins (IgA and IgG) in nasal secretions as an expression of a humoral mucosal immune response in allergic rhinitis. For tissue eosinophilia we studied nasal Eosinophilic Cationic Protein (ECP) and for mast cell activation nasal tryptase.

Methods: Nasal secretions of 40 patients suffering from allergic rhinitis were analyzed for allergen-specific IgA, IgG, and IgE, and for ECP and tryptase. Patients were highly sensitized against the major allergens of house dust mites, timothy, and birch pollen. 43 non-atopic individuals served as controls. In order to study possible effects of the actual pollen season on the studied parameter we secondly compared patients allergic to seasonal allergens co- (n = 28) and extra-seasonally (n = 41). In order to determine a possible influence of allergen-specific IgA in eosinophilic degranulation we additionally studied 5 patients after nasal allergen challenge.

Results: In allergic rhinitis we found significantly increased levels of allergen-specific immunoglobulins of all studied subclasses and allergens in nasal secretions. Comparison of nasal ECP and tryptase showed significantly increased concentrations in allergic individuals as well. Co-seasonally we found elevated allergen-specific IgE, ECP, and tryptase but lower concentrations of allergen-specific IgA and IgG. There was no association between late phase eosinophilia and IgA concentrations after local allergen challenge.

Conclusions: The occurrence of allergen-specific immunoglobulins in nasal secretions is interpreted as a local humoral mucosal immune response. The physiologic role of local allergen-specific immunoglobulins is not clear to date. Involvement in degranulation of eosinophils or mast cells, like suggested before, seems unlikely.

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Dr. med. Matthias F. Kramer

Klinik und Poliklinik für Hals-, Nasen-, Ohrenheilkunde am Klinikum Großhadern, Ludwig-Maximilians-Universität München

Marchioninistraße 15 · 81377 München ·

eMail: Matthias. Kramer@med. uni-muenchen. de

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