Khanna M, Srivastava L M
Department of Biochemistry, All India Institute of Medical Sciences, New Delhi, India.
Indian J Exp Biol. 1996 May;34(5):468-71.
Mouse peritoneal macrophage monolayers infected with M. tuberculosis were cultured in RPMI up to 7 days. Release of superoxide was assayed on different days in presence or absence of Phorbol myristate acetate (PMA), a known stimulator of NADPH oxidase which is involved superoxide production. Basal level of superoxide release was significantly higher in M. tuberculosis infected peritoneal mouse macrophages (P < 0.01) as compared to normal mouse macrophages. When normal and tuberculoid macrophage cultures were stimulated with PMA, increased superoxide anion release was observed in both the cultures but the increase of superoxide was significantly higher in normal macrophages as compared to tuberculoid stimulated macrophages. Superoxide release was maximum in 4 day old cultured macrophages and gradually it declined in older cultures by day 7, both in vitro and in vivo. A defective macrophage function in killing of M. tuberculosis bacilli was observed after 4 days of in vitro and in vivo cultures.
用结核分枝杆菌感染的小鼠腹膜巨噬细胞单层在RPMI培养基中培养长达7天。在存在或不存在佛波酯肉豆蔻酸酯（PMA）的情况下，于不同日期测定超氧化物的释放，PMA是已知的参与超氧化物产生的NADPH氧化酶刺激剂。与正常小鼠巨噬细胞相比，结核分枝杆菌感染的腹膜小鼠巨噬细胞中超氧化物释放的基础水平显著更高（P < 0.01）。当用PMA刺激正常和类结核巨噬细胞培养物时，在两种培养物中均观察到超氧化物阴离子释放增加，但与类结核刺激的巨噬细胞相比，正常巨噬细胞中超氧化物的增加显著更高。无论是在体外还是体内，超氧化物释放在培养4天的巨噬细胞中最高，到第7天在较老的培养物中逐渐下降。在体外和体内培养4天后，观察到巨噬细胞在杀死结核分枝杆菌方面的功能存在缺陷。
