Hirasawa K, Ogiso Y, Takeda M, Lee M J, Itagaki S, Doi K
Department of Biomedical Science, Faculty of Agriculture, University of Tokyo, Japan.
Lab Anim Sci. 1995 Dec;45(6):652-6.
The involvement of macrophages in protection against diabetes mellitus in mice of BALB/c (susceptible) and C57BL (resistant) strains infected with the B (non-diabetogenic) or D (highly diabetogenic) variant of encephalomyocarditis (EMC) virus was examined. Pretreatment with the B variant of EMC virus (EMC-B), avirulent interferon (IFN) inducer, or Corynebacterium parvum inhibited diabetes in BALB/c mice infected with the D variant of EMC virus (EMC-D). Treatment of C57BL mice with carrageenan to compromise macrophage function rendered C57BL mice susceptible to EMC-D-induced diabetes. In macrophage culture for BALB/c mice, EMC-B induced IFN at an earlier stage than did EMC-D. The C57BL mouse-derived macrophages produced more IFN than did BALB/c mouse-derived macrophages after stimulation with EMC-D. Moreover, C. parvum increased IFN production in macrophage cultures from BALB/c mice, whereas carrageenan inhibited that in macrophage cultures from C57BL mice. These results suggest that IFN derived from macrophages may have an important role in protecting mice against EMC virus infection.
研究了巨噬细胞在感染脑心肌炎（EMC）病毒B（非致糖尿病性）或D（高度致糖尿病性）变体的BALB/c（易感）和C57BL（抗性）品系小鼠预防糖尿病中的作用。用EMC病毒的B变体（EMC-B）、无毒干扰素（IFN）诱导剂或细小棒状杆菌预处理可抑制感染EMC病毒D变体（EMC-D）的BALB/c小鼠发生糖尿病。用角叉菜胶处理C57BL小鼠以损害其巨噬细胞功能，使C57BL小鼠易患EMC-D诱导的糖尿病。在BALB/c小鼠的巨噬细胞培养中，EMC-B比EMC-D更早诱导IFN。用EMC-D刺激后，C57BL小鼠来源的巨噬细胞产生的IFN比BALB/c小鼠来源的巨噬细胞更多。此外，细小棒状杆菌增加了BALB/c小鼠巨噬细胞培养物中的IFN产生，而角叉菜胶抑制了C57BL小鼠巨噬细胞培养物中的IFN产生。这些结果表明，巨噬细胞产生的IFN可能在保护小鼠免受EMC病毒感染中起重要作用。
