[Humoral mucosal immunity in allergic rhinitis].
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.
Kramer
M F
MF
Klinik und Poliklinik für Hals-, Nasen-, und Ohrenheilkunde am Klinikum Grosshadern, Ludwig-Maximilians-Universität München. Matthias. Kramer@med.uni-muenchen.de
Jordan
T R
TR
Pfrogner
E
E
Rasp
G
G
D000328:Adult; D000918:Antibody Specificity / Q000276:immunology; D000941:Antigens / Q000276:immunology; D047150:Eosinophil Cationic Protein / Q000378:metabolism; D004802:Eosinophilia / Q000276:immunology; D004804:Eosinophils / Q000276:immunology; D005260:Female; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000276:immunology; D018928:Immunity, Mucosal / Q000276:immunology*; D007070:Immunoglobulin A / Q000378:metabolism; D007071:Immunoglobulin A, Secretory / Q000378:metabolism; D007074:Immunoglobulin G / Q000378:metabolism; D008297:Male; D008407:Mast Cells / Q000276:immunology; D008875:Middle Aged; D009297:Nasal Mucosa / Q000276:immunology; D012221:Rhinitis, Allergic, Perennial / Q000276:immunology*; D006255:Rhinitis, Allergic, Seasonal / Q000276:immunology*; D012697:Serine Endopeptidases / Q000378:metabolism; D053802:Tryptases
D000941:Antigens; D007070:Immunoglobulin A; D007071:Immunoglobulin A, Secretory; D007074:Immunoglobulin G; D047150:Eosinophil Cationic Protein; D012697:Serine Endopeptidases; D053802:Tryptases