TY - JOUR
T1 - Signals through CD40 play a critical role in the pathophysiology of Schistosoma mansoni egg antigen-induced allergic rhinitis in mice
AU - Hattori, Hisashi
AU - Okano, Mitsuhiro
AU - Kariya, Shin
AU - Nishizaki, Kazunori
AU - Satoskar, Abhay R.
PY - 2006
Y1 - 2006
N2 - Background: Interaction between CD40 and CD40L is thought to regulate immune responses in several allergic diseases. However, little is known about its in vivo role in the pathophysiology of allergic rhinitis. We sought to determine whether the lack of signals through CD40 affects the pathophysiology of allergic rhinitis using a murine model. Methods: Wild type (WT) and CD40-deficient BALB/c (CD40-/-) mice were sensitized intranasally to Schistosoma mansoni egg antigen (SEA). After repeated sensitization, histamine responsiveness, serum antibody titer including immunoglobunin E (IgE), nasal eosinophilia, and cytokine production by nasal mononuclear cells were determined in each group. Results: Intranasal sensitization with SEA in WT mice elicited a strong Th2 response including SEA-specific IgE production, nasal eosinophilia, and interleukin (IL)-4, and IL-5 production by nasal mononuclear cells after antigen challenge. Production of SEA-specific IgE and IgG1 was abolished in SEA-sensitized CD40-/- mice. These mice showed impaired nasal eosinophilia and displayed markedly reduced histamine-induced nasal hyperresponsiveness as compared with WT mice. Furthermore, reduced production of IL-4 and IL-5 by nasal mononuclear cells was seen in CD40-/- mice. Conclusion: These results show that signals through CD 40 play a critical role in not only IgE production but also pathophysiology of allergic rhinitis such as nasal hyperresponsiveness and nasal eosinophilia.
AB - Background: Interaction between CD40 and CD40L is thought to regulate immune responses in several allergic diseases. However, little is known about its in vivo role in the pathophysiology of allergic rhinitis. We sought to determine whether the lack of signals through CD40 affects the pathophysiology of allergic rhinitis using a murine model. Methods: Wild type (WT) and CD40-deficient BALB/c (CD40-/-) mice were sensitized intranasally to Schistosoma mansoni egg antigen (SEA). After repeated sensitization, histamine responsiveness, serum antibody titer including immunoglobunin E (IgE), nasal eosinophilia, and cytokine production by nasal mononuclear cells were determined in each group. Results: Intranasal sensitization with SEA in WT mice elicited a strong Th2 response including SEA-specific IgE production, nasal eosinophilia, and interleukin (IL)-4, and IL-5 production by nasal mononuclear cells after antigen challenge. Production of SEA-specific IgE and IgG1 was abolished in SEA-sensitized CD40-/- mice. These mice showed impaired nasal eosinophilia and displayed markedly reduced histamine-induced nasal hyperresponsiveness as compared with WT mice. Furthermore, reduced production of IL-4 and IL-5 by nasal mononuclear cells was seen in CD40-/- mice. Conclusion: These results show that signals through CD 40 play a critical role in not only IgE production but also pathophysiology of allergic rhinitis such as nasal hyperresponsiveness and nasal eosinophilia.
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U2 - 10.1177/194589240602000208
DO - 10.1177/194589240602000208
M3 - Article
C2 - 16686380
AN - SCOPUS:33646269502
VL - 20
SP - 165
EP - 169
JO - American Journal of Rhinology and Allergy
JF - American Journal of Rhinology and Allergy
SN - 1945-8924
IS - 2
ER -