Sakuma T, Suenaga T, Yoshida I, Azuma M
Infect Immun. 1983 Nov;42(2):567-73. doi: 10.1128/iai.42.2.567-573.1983.
The mechanism of enhanced resistance of Mycobacterium bovis BCG-treated mice to ectromelia virus infection was investigated by determining the effect of splenectomy, antithymocyte serum, and antimacrophage serum on resistance. It was greatly reduced by these treatments, not only in normal mice, but also in mice treated with live or heat-inactivated BCG. Production of circulating interferon by ectromelia virus and Newcastle disease virus was augmented in BCG-treated mice and was markedly depressed by splenectomy and antithymocyte and antimacrophage serum treatments in both BCG-treated and normal mice. Carbon clearance activity was activated in BCG-treated mice, but splenectomy did not influence phagocytic activity. These results suggest that augmented interferon production in the spleens of BCG-treated mice plays a major role in enhanced resistance. Other possible mechanisms are discussed.
通过确定脾切除、抗胸腺细胞血清和抗巨噬细胞血清对抵抗力的影响,研究了卡介苗处理的小鼠对痘苗病毒感染抵抗力增强的机制。这些处理不仅在正常小鼠中,而且在经活卡介苗或热灭活卡介苗处理的小鼠中,都极大地降低了抵抗力。痘苗病毒和新城疫病毒在卡介苗处理的小鼠中诱导产生的循环干扰素增加,并且在卡介苗处理的小鼠和正常小鼠中,脾切除、抗胸腺细胞血清和抗巨噬细胞血清处理均显著抑制了干扰素的产生。卡介苗处理的小鼠的碳清除活性被激活,但脾切除不影响吞噬活性。这些结果表明,卡介苗处理的小鼠脾脏中干扰素产生增加在增强抵抗力中起主要作用。还讨论了其他可能的机制。