Douvas G S, May M H, Pearson J R, Lam E, Miller L, Tsuchida N
Department of Basic Sciences and Oral Research, School of Dentistry, University of Colorado Health, Sciences Center, Denver 80262.
J Infect Dis. 1994 Nov;170(5):1248-55. doi: 10.1093/infdis/170.5.1248.
The growth of Mycobacterium avium 7497, serovar 4, in cultured human macrophages is enhanced by Fe3+ and serum lipids over 7 days. Iron (1-80 micrograms/mL) added to macrophages cultured in normal serum resulted in 10-fold increases in growth. If iron-supplemented macrophages were cultured in serum from hypertriglyceridemic donors after infection, M. avium growth increased 10(3)- to 10(4)-fold. Without macrophages, differences in bacterial growth between sera were not seen. Removal of very low density lipoprotein (VLDL) eliminated the differences between sera. Isolated VLDL from hyperlipidemic serum resulted in 10(5)-fold increases in growth over that seen with VLDL from normal sera. Accelerated M. avium growth in macrophages cultured with hyperlipidemic serum was partly inhibited by the addition of superoxide dismutase (1000 IU/mL). Results suggest that iron stimulates O2-induced oxidation of VLDL and its subsequent accumulation in macrophages. The resultant iron- and lipid-laden cells become excellent hosts for mycobacterial growth.
在培养的人巨噬细胞中，鸟分枝杆菌7497血清型4在7天内的生长因Fe3+和血清脂质而增强。向在正常血清中培养的巨噬细胞添加铁（1 - 80微克/毫升）会使生长增加10倍。如果在感染后将补充铁的巨噬细胞置于高甘油三酯血症供体的血清中培养，鸟分枝杆菌的生长会增加10³至10⁴倍。没有巨噬细胞时，血清之间未见细菌生长差异。去除极低密度脂蛋白（VLDL）可消除血清之间的差异。从高脂血症血清中分离出的VLDL导致的生长比正常血清中的VLDL增加10⁵倍。在用高脂血症血清培养的巨噬细胞中，添加超氧化物歧化酶（1000 IU/毫升）可部分抑制鸟分枝杆菌的加速生长。结果表明，铁刺激O₂诱导的VLDL氧化及其随后在巨噬细胞中的积累。由此产生的富含铁和脂质的细胞成为分枝杆菌生长的优良宿主。
