Zhang L, Ma W, Da J
Beijing Chest Hospital, Beijing 100095, China.
Zhonghua Jie He He Hu Xi Za Zhi. 2000 Jan;23(1):43-6.
To investigate the immunoregulative mechanism of Mycobacterium vaccae by way of molecular pathology.
BALB/C mice were randomly divided into three groups: tuberculosis model (A); mice were challenged with H37Rv by their tail veins and then immunized by M. vaccae (B); control mice (N). Immunohistochemistry and pathological slices stained with HE were evaluated to investigate the correlation between the expression of IFN-gamma, IL-4 and iNOS and the type and magnitude of tissue injury.
A predominance of Th1 cells was observed manifested by a high percentage of IFN-gamma positive cells in the inflammatory infiltrate and granulomas demonstrated by immunohistology peaked 6 weeks after infection (0.058 +/- 0.010), and there was a significant increase compared with N group (0.005 +/- 0.020, P < 0.01). This was followed by a chronic advanced phase characterized by pneumonia local necrosis with a Tho balance due to an equivalent proportion of IFN-gamma and IL-4 positive cells in the lung lesions. The iNOS expression was increased in acute phase and decreased in chronic phase. B group had localized lung lesions, proliferate and lymphoid nodules were predominant, there was less necrostic change. A predominance of Th1 cells was observed during the infection changed over time and there was no Tho balance phase occurred. iNOS expression had a higher level during the wholecourse of infection.
M. vaccae can enhance the protective immunological response by inducing Th1 response and inhibiting Th2 response.
通过分子病理学方法研究母牛分枝杆菌的免疫调节机制。
将BALB/C小鼠随机分为三组:结核模型组(A);经尾静脉用H37Rv攻击后再用母牛分枝杆菌免疫的小鼠组(B);对照组小鼠(N)。采用免疫组织化学和HE染色病理切片,评估IFN-γ、IL-4和iNOS表达与组织损伤类型及程度之间的相关性。
免疫组织学显示,感染后6周炎症浸润和肉芽肿中IFN-γ阳性细胞百分比高,表明Th1细胞占优势(0.058±0.010),与N组(0.005±0.020)相比有显著增加(P<0.01)。随后进入慢性进展期,其特征为肺部局部坏死性肺炎,由于肺部病变中IFN-γ和IL-4阳性细胞比例相当而呈现Th0平衡。iNOS表达在急性期增加,在慢性期降低。B组有局限性肺部病变,以增殖和淋巴小结为主,坏死改变较少。感染过程中观察到Th1细胞占优势,且未出现Th0平衡期。iNOS表达在感染全过程中均处于较高水平。
母牛分枝杆菌可通过诱导Th1反应和抑制Th2反应增强保护性免疫反应。