Nakazawa T, Umegae Y
College of Medical Care and Technology, Gunma University, Japan.
Ann Allergy. 1992 Apr;68(4):319-23.
This study was undertaken to investigate the effect of histamine, its receptor antagonists and agonists on IgE antibody production in mice. BALB/c mice were immunized intraperitoneally with 1 mg alum plus 30 micrograms of Ag90, the antigen of Japanese occupational asthma. Histamine receptor antagonists were administered before the immunization and simultaneous injection of histamine. The mice were bled 14 days after immunization and anti-Ag90 IgE antibody was obtained. Titers of the antisera were measured by passive cutaneous anaphylaxis reaction in Sprague-Dawley rats. Treatment with histamine only did not affect the level of specific IgE antibody. Administration of H1 antagonist or H2 agonist suppressed IgE production significantly. In contrast, treatment with H2 antagonist or H1 agonist augmented the IgE antibody production. Injection of H1 + H2 antagonists had no effect on the antibody production. These results suggest that histamine suppressed specific IgE production via H2 receptors and enhanced it through H1 receptors in the induction phase of the system.
本研究旨在探讨组胺及其受体拮抗剂和激动剂对小鼠IgE抗体产生的影响。将BALB/c小鼠腹腔注射1mg明矾加30μg日本职业性哮喘抗原Ag90进行免疫。在免疫前及同时注射组胺时给予组胺受体拮抗剂。免疫14天后采集小鼠血液,获得抗Ag90 IgE抗体。通过在斯普拉格-道利大鼠中进行被动皮肤过敏反应来测定抗血清的滴度。仅用组胺处理不影响特异性IgE抗体水平。给予H1拮抗剂或H2激动剂可显著抑制IgE产生。相反,用H2拮抗剂或H1激动剂处理可增强IgE抗体产生。注射H1 + H2拮抗剂对抗体产生无影响。这些结果表明,在该系统的诱导阶段,组胺通过H2受体抑制特异性IgE产生,并通过H1受体增强其产生。