Tsai Jaw-Ji, Liu Yi-Hsia, Shen Horng-Der, Huang Shih-Hung, Han Shou-Hwa
Department of Internal Medicine, Cathay General Hospital, Taipei, Taiwan, ROC.
J Microbiol Immunol Infect. 2002 Sep;35(3):152-8.
Epidemiologic studies suggest an inverse correlation between infection and development of allergy. The purpose of this study was to test the hypothesis whether a preexisting T helper 1 (Th1)-type immune response elicited by Mycobacterium bovis-bacillus Calmette-Guerin (BCG) immunization could suppress allergic airway inflammation induced by the mite allergen Dermatophagoides pteronyssinus group 2 (Der p2) in an animal model. C57BL/6 mice were immunized with subcutaneous injection of BCG, then intraperitoneal Der p2 emulsified in alum. Der p2-specific immunoglobulin G1 and cytokine production from splenocytes were measured after Der p2 sensitization, and pulmonary function and airway inflammation were determined after inhalation challenge with Der p2. The intraperitoneal Der p2 with alum injection was able to induce Der p2-specific immunoglobulin G1 production, which could be downregulated by the pretreatment with BCG + Der p2. The inoculation of BCG + Der p2 caused splenocytes to produce more interferon-gamma, and this level was higher than that elicited by Der p2 or buffer alone. The positive interferon-gamma-staining CD4 cells were also increased after activation by phorbol myristate acetate and ionomycin. Lung pathology examination found decreased airway inflammation (associated with the best pulmonary function and least airway desquamation) in the mice inoculated with BCG + Der p2. In this Der p2-induced allergy model, BCG inoculation with Der p2 can cause a Th1-type immune response that hinders Der p2-induced allergic sensitization and the development of airway inflammation.
流行病学研究表明感染与过敏发生之间存在负相关。本研究的目的是验证以下假设:卡介苗(BCG)免疫引发的预先存在的辅助性T细胞1(Th1)型免疫反应是否能在动物模型中抑制由螨过敏原屋尘螨第2组变应原(Der p2)诱导的过敏性气道炎症。对C57BL/6小鼠进行皮下注射BCG免疫,然后腹腔注射明矾乳化的Der p2。在Der p2致敏后测量脾细胞中Der p2特异性免疫球蛋白G1和细胞因子的产生,并在用Der p2吸入激发后测定肺功能和气道炎症。腹腔注射明矾与Der p2能够诱导Der p2特异性免疫球蛋白G1的产生,而BCG + Der p2预处理可使其下调。接种BCG + Der p2使脾细胞产生更多的干扰素-γ,且该水平高于单独使用Der p2或缓冲液所引发的水平。在用佛波酯肉豆蔻酸酯和离子霉素激活后,阳性干扰素-γ染色的CD4细胞也增加。肺病理检查发现,接种BCG + Der p2的小鼠气道炎症减轻(肺功能最佳,气道脱屑最少)。在这个Der p2诱导的过敏模型中,接种BCG与Der p2可引发Th1型免疫反应,从而阻碍Der p2诱导的过敏致敏和气道炎症的发展。