Background: To date, no murine models have been reported to show the induct
ion of both antigen-specific IgE and nasal eosinophilia, two of the major h
allmarks 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 allerg
ic rhinitis.
Methods: BALB/c, CBA/J, and C57BL/6 mice were sensitized intranasally to Sc
histosoma mansoni egg antigen (SEA) solely. After repeated sensitization, s
erum Ab titers, nasal eosinophilia, and cytokine production by nasal lympho
cytes 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, whil
e 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 i
n the absence of adjuvants induces a Th2 immune reaction, reflecting the ha
llmarks of the initiation of allergic rhinitis both in vivo and in vitro, w
hich is genetically regulated.