Presensitization to Ascaris antigens promotes induction of mite-specific IgE upon mite antigen inhalation in mice

  • Suzuki Mayu
    Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine Department of Materials and Biological Sciences, Faculty of Science, Japan Women's University
  • Hara Mutsuko
    Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine
  • Ichikawa Saori
    Department of Materials and Biological Sciences, Faculty of Science, Japan Women's University
  • Kamijo Seiji
    Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine
  • Nakazawa Takuya
    Clinical Research Center for Allergy and Rheumatology, National Hospital Organization Sagamihara National Hospital Department of Rheumatology, Allergy, and Clinical Immunology, National Hospital Organization Chiba-East National Hospital
  • Hatanaka Hideki
    National Bioscience Database Center, Japan Science and Technology Agency
  • Akiyama Kazuo
    Clinical Research Center for Allergy and Rheumatology, National Hospital Organization Sagamihara National Hospital
  • Ogawa Hideoki
    Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine
  • Okumura Ko
    Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine
  • Takai Toshiro
    Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine

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Background: Patients with house dust mite (HDM) allergy or Ascariasis produce serum IgE specific to the antigens of HDM or nematode Ascaris, respectively. Although human IgE cross-reactivity has been reported between HDM and Ascaris antigens, it remains unclear whether it contributes to the pathogenesis of allergic diseases. We herein investigated the induction of cross-reactive antibodies and T cells in mice and effects of airway exposure to HDM antigens after preimmunization with Ascaris antigens. Methods: Mice were intraperitoneally immunized with HDM or Ascaris antigens with Alum, followed by the intranasal administration of HDM antigens. Serum antigen-specific IgE and IgG were measured by ELISA. Cytokine release in splenocytes from Ascaris-immunized mice upon in vitro restimulation with HDM antigens were measured by ELISA. Results: Immunization with Ascaris or HDM antigens induced cross-reactive IgG1. Splenocytes from Ascaris-immunized mice released IL-5 and IL-13 in response to the restimulation with HDM antigens.Subsequent airway exposure to HDM antigens promoted the induction of HDM-specific IgE and upregulation of HDM-specific IgG1 in Ascaris-immunized mice, whereas these responses were not detected or smaller without the Ascaris presensitization. Conclusions: We demonstrated that the immunization of naive mice with Ascaris antigens induced production of antibodies and differentiation of Th2 cells, which were cross-reactive to HDM antigens, and accelerated induction of serum HDM-specific IgE upon subsequent airway exposure to HDM antigens in mice. These results suggest that sensitization to HDM towards IgE-mediated allergic diseases is faster in individuals with a previous history of Ascaris infection than in those without presensitization to Ascaris.

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