LATE ASTHMATIC RESPONSE BY RECRUITMENT OF HOMOCYTOTROPIC ANTIBODY FROM CIRCULATING BLOOD TO THE AIRWAY WALL IN GUINEA PIG

DOI
  • Saito Motoyasu
    The Third Department of Internal Medicine, Kanazawa University, School of Medicine
  • Fujimura Masaki
    The Third Department of Internal Medicine, Kanazawa University, School of Medicine
  • Miyake Yasushi
    The Third Department of Internal Medicine, Kanazawa University, School of Medicine
  • Sakamoto Sayuri
    The Third Department of Internal Medicine, Kanazawa University, School of Medicine
  • Yasui Masahide
    The Third Department of Internal Medicine, Kanazawa University, School of Medicine
  • Kurashima Kazuki
    The Third Department of Internal Medicine, Kanazawa University, School of Medicine
  • Mastuda Tamotsu
    The Third Department of Internal Medicine, Kanazawa University, School of Medicine

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Other Title
  • 同種細胞親和性抗体の動員による Late Asthmatic Response の発現

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Abstract

Many reports have been published about the late asthmatic response (LAR) of animal model. But most of the animals used were sensitized actively and it is considered generally that it is impossible to generate LAR in passively sensitized animals, especially in guinea pig. About the mechanism of LAR, most discussion are focused on airway hyperreactivity, inflammation and chemical mediators. But little is known about the direct initiator of the late phase bronchoconstriction. Instead of the circulating antibody which is generated by antibody producing cells in actively sensitized animals, anti-serum was administered to guinea pigs intravenously as passive sensitization fifteen minutes prior to antigen inhalation. Four to eight hours after antigen inhalation, we investigated bronchoconstriction. Eight hours after antigen challenge, bronchoalveolar lavage (BAL) were performed. In the BAL fluid, macrophages decreased and neutrophils increased significantly. These results suggest that LAR can occur without airway inflammation and the inflammation might be the result of antigen-antibody reaction at the airway wall, and that the direct initiator of late phase bronchoconstriction might be the recruitment of homocytotropic antibody from circulating blood to the airway wall.

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