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Strain‐dependent induction of allergic rhinitis without adjuvant in mice
Author(s) -
Okano M,
Harn Jr DA,
Abe M,
Wang MM,
Satoskar AR,
Nishizaki K,
Masuda Y,
Okano M,
Yoshino T
Publication year - 1999
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1034/j.1398-9995.1999.00063.x
Subject(s) - sensitization , immunology , eosinophilia , nasal administration , immunoglobulin e , medicine , adjuvant , allergy , immune system , antigen , antibody
Background: To date, no murine models have been reported to show the induction of both antigen‐specific IgE and nasal eosinophilia, two of the major hallmarks of allergic rhinitis, after local sensitization in the absence of adjuvants, a phenomenon which reflects natural exposure. In this report, we attempted to establish a murine model representing an initiation of allergic rhinitis. Methods: BALB/c, CBA/J, and C57BL/6 mice were sensitized intranasally to Schistosoma mansoni egg antigen (SEA) solely. After repeated sensitization, serum Ab titers, nasal eosinophilia, and cytokine production by nasal lymphocytes were determined. Results: BALB/c mice produced SEA‐specific IgE after repeated sensitization. High‐dose sensitization to SEA induced IgE production in CBA/J mice, while C57BL/6 mice did not show the production throughout the period observed, suggesting that IgE production was regulated genetically. BALB/c mice also exhibited nasal eosinophilia after the nasal challenge. In addition, nasal lymphocytes sensitized with SEA intranasally produced significant amount of IL‐5 in vitro . Conclusions: These results suggest that intranasal sensitization with SEA in the absence of adjuvants induces a Th2 immune reaction, reflecting the hallmarks of the initiation of allergic rhinitis both in vivo and in vitro , which is genetically regulated.