Release of superoxide anion from resident and activated mouse peritoneal macrophages infected with Mycobacterium intracellulare.
Release of superoxide anion from resident and activated mouse peritoneal macrophages infected with Mycobacterium intracellulare.
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感染细胞内分枝杆菌的常驻和激活的小鼠腹腔巨噬细胞释放超氧阴离子。
DOI：
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发表时间：
1984
期刊：
影响因子：
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通讯作者：
C. Edwards
中科院分区：
文献类型：
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作者：
P. Gangadharam;C. Edwards
胞内分枝杆菌吞噬触发小鼠腹膜巨噬细胞释放超氧阴离子（O-2）；bcg活化细胞的释放量明显大于常驻细胞。超氧阴离子释放量与吞噬菌数量成正比。当估计细菌攻击后O-2释放时，观察到最佳吞噬时间为4小时。同时，O-2释放量与胞内支原体毒力呈反比关系。与不透明和光滑的菌落变体相比，透明和粗糙的菌落变体触发的O-2释放量明显降低。血清型4和8在人类中导致预后较差的疾病，其触发的O-2明显低于对化疗方案反应更有利的血清型9、12、13、14、16、18和19。
Phagocytosis of Mycobacterium intracellulare triggered the release of superoxide anion (O-2) from mouse peritoneal macrophages; the amount release from BCG-activated cells was significantly greater than that from resident cells. Superoxide anion release was proportional to the number of phagocytes ingesting bacilli. An optimal phagocytic time course of 4 h was observed when estimating O-2 release consequent to bacterial challenge. Also, an inverse relationship between the amount of O-2 released and the virulence of M. intracellulare in mice was shown. Transparent and rough colony variants triggered the release of significantly lower amounts of O-2 as compared with the opaque and smooth colony variants. Serovars 4 and 8, which cause a disease with a poor prognosis in humans, triggered significantly less O-2 than did serovars 9, 12, 13, 14, 16, 18, and 19, which respond more favorably to chemotherapeutic regimens.