Sex-related differences in the initiation of allergic rhinitis in mice

T. Yamatomo, M. Okano, Toshiro Ono, E. Nakayama, Tadashi Yoshino, A. R. Satoskar, D. A. Harn, Kazunori Nishizaki

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

Background: Several clinical and epidemiologic studies have investigated sex differences in the prevalence of allergic rhinitis. At present, however, no reports have demonstrated such differences in experimental models with local, but not parenteral, sensitization with antigens that may reflect natural exposure to allergens. We have recently developed murine models of allergic rhinitis after repeated intranasal sensitization with antigens in the absence of adjuvants. In this study, we investigated the role of sex in the initiation of the disease in vivo. Methods: Male and female CBA/J and BALB/c mice were sensitized intranasally with phospholipase A2 (PLA2) and Schistosoma mansoni egg antigen (SEA), respectively, in the absence of adjuvants. After the repeated sensitization, serum Ab titers against the sensitizing antigen and nasal eosinophilia were determined. In addition, the involvement of androgen in IgE synthesis was investigated in castrated CBA/J male mice with or without testosterone administration. Results: Females produced significantly higher levels of PLA2-specific IgE than males in CBA/J mice sensitized with PLA2. On the other hand, both titers of PLA2-specific IgG1 and nasal eosinophilia did not significantly differ between the two groups. Castrated male mice produced significantly higher amounts of PLA2-specific IgE than sham-treated male mice. In addition, PLA2-specific IgE production decreased in castrated mice treated with testosterone. Sexual differences in the production of Ag-specific IgE were not seen in BALB/c mice after the sensitization with SEA. Conclusions: These results suggest that sex is responsible for the production of Ag-specific IgE, but not IgG1 or nasal eosinophilia, and that androgen appears to be involved in the in vivo production of specific IgE in male mice.

Original languageEnglish
Pages (from-to)525-531
Number of pages7
JournalAllergy: European Journal of Allergy and Clinical Immunology
Volume56
Issue number6
DOIs
Publication statusPublished - 2001

Fingerprint

Phospholipases A2
Sex Characteristics
Immunoglobulin E
Eosinophilia
Antigens
Nose
Schistosoma mansoni
Androgens
Ovum
Testosterone
Immunoglobulin G
Safe Sex
Inbred CBA Mouse
Allergic Rhinitis
Allergens
Epidemiologic Studies
Theoretical Models
Serum

Keywords

  • Allergic rhinitis
  • Eosinophil
  • IgE
  • Mice
  • Sex

ASJC Scopus subject areas

  • Immunology

Cite this

Sex-related differences in the initiation of allergic rhinitis in mice. / Yamatomo, T.; Okano, M.; Ono, Toshiro; Nakayama, E.; Yoshino, Tadashi; Satoskar, A. R.; Harn, D. A.; Nishizaki, Kazunori.

In: Allergy: European Journal of Allergy and Clinical Immunology, Vol. 56, No. 6, 2001, p. 525-531.

Research output: Contribution to journalArticle

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abstract = "Background: Several clinical and epidemiologic studies have investigated sex differences in the prevalence of allergic rhinitis. At present, however, no reports have demonstrated such differences in experimental models with local, but not parenteral, sensitization with antigens that may reflect natural exposure to allergens. We have recently developed murine models of allergic rhinitis after repeated intranasal sensitization with antigens in the absence of adjuvants. In this study, we investigated the role of sex in the initiation of the disease in vivo. Methods: Male and female CBA/J and BALB/c mice were sensitized intranasally with phospholipase A2 (PLA2) and Schistosoma mansoni egg antigen (SEA), respectively, in the absence of adjuvants. After the repeated sensitization, serum Ab titers against the sensitizing antigen and nasal eosinophilia were determined. In addition, the involvement of androgen in IgE synthesis was investigated in castrated CBA/J male mice with or without testosterone administration. Results: Females produced significantly higher levels of PLA2-specific IgE than males in CBA/J mice sensitized with PLA2. On the other hand, both titers of PLA2-specific IgG1 and nasal eosinophilia did not significantly differ between the two groups. Castrated male mice produced significantly higher amounts of PLA2-specific IgE than sham-treated male mice. In addition, PLA2-specific IgE production decreased in castrated mice treated with testosterone. Sexual differences in the production of Ag-specific IgE were not seen in BALB/c mice after the sensitization with SEA. Conclusions: These results suggest that sex is responsible for the production of Ag-specific IgE, but not IgG1 or nasal eosinophilia, and that androgen appears to be involved in the in vivo production of specific IgE in male mice.",
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AU - Okano, M.

AU - Ono, Toshiro

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AU - Satoskar, A. R.

AU - Harn, D. A.

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AB - Background: Several clinical and epidemiologic studies have investigated sex differences in the prevalence of allergic rhinitis. At present, however, no reports have demonstrated such differences in experimental models with local, but not parenteral, sensitization with antigens that may reflect natural exposure to allergens. We have recently developed murine models of allergic rhinitis after repeated intranasal sensitization with antigens in the absence of adjuvants. In this study, we investigated the role of sex in the initiation of the disease in vivo. Methods: Male and female CBA/J and BALB/c mice were sensitized intranasally with phospholipase A2 (PLA2) and Schistosoma mansoni egg antigen (SEA), respectively, in the absence of adjuvants. After the repeated sensitization, serum Ab titers against the sensitizing antigen and nasal eosinophilia were determined. In addition, the involvement of androgen in IgE synthesis was investigated in castrated CBA/J male mice with or without testosterone administration. Results: Females produced significantly higher levels of PLA2-specific IgE than males in CBA/J mice sensitized with PLA2. On the other hand, both titers of PLA2-specific IgG1 and nasal eosinophilia did not significantly differ between the two groups. Castrated male mice produced significantly higher amounts of PLA2-specific IgE than sham-treated male mice. In addition, PLA2-specific IgE production decreased in castrated mice treated with testosterone. Sexual differences in the production of Ag-specific IgE were not seen in BALB/c mice after the sensitization with SEA. Conclusions: These results suggest that sex is responsible for the production of Ag-specific IgE, but not IgG1 or nasal eosinophilia, and that androgen appears to be involved in the in vivo production of specific IgE in male mice.

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