Zhang L, Goren M B, Holzer T J, Andersen B R
Department of Medicine, University of Illinois College of Medicine, Chicago.
Infect Immun. 1988 Nov;56(11):2876-83. doi: 10.1128/iai.56.11.2876-2883.1988.
Experiments were performed to determine the effects of Mycobacterium tuberculosis-derived sulfolipid I on phagocytic cells. Sulfolipid I was taken up in significant amounts by human neutrophils and in lesser amounts by monocytes and lymphocytes. Superoxide (O2-) production by neutrophils was significantly increased by sulfolipid I, but the rate of production was slower than that reported previously for other stimuli. The optimal concentration of sulfolipid I for stimulation of O2- production was 27 micrograms/ml, while higher concentrations produced less. At substimulatory levels sulfolipid I caused enhancement of O2- release from neutrophils when it was subsequently stimulated by other agents. Nonadherent monocytes from most normal donors failed to produce O2- when treated with sulfolipid I; however, adherent monocytes pretreated with gamma interferon did produce O2- with sulfolipid I stimulation. Priming for an enhanced oxidative response of activated monocytes was also observed. These sulfolipid I-induced changes in phagocytic cell function may be important in altering the ability of phagocytes to respond effectively to M. tuberculosis and may also cause exaggerated inflammatory responses.
开展实验以确定结核分枝杆菌来源的硫脂I对吞噬细胞的影响。硫脂I被人类中性粒细胞大量摄取，被单核细胞和淋巴细胞少量摄取。硫脂I显著增加了中性粒细胞超氧化物（O2-）的产生，但产生速率比先前报道的其他刺激物要慢。刺激O2-产生的硫脂I最佳浓度为27微克/毫升，而更高浓度产生的量较少。在亚刺激水平，当硫脂I随后被其他试剂刺激时，它会导致中性粒细胞O2-释放增强。大多数正常供体的非贴壁单核细胞在用硫脂I处理时不产生O2-；然而，用γ干扰素预处理的贴壁单核细胞在用硫脂I刺激时确实产生了O2-。还观察到对活化单核细胞增强氧化反应的启动作用。这些硫脂I诱导的吞噬细胞功能变化可能在改变吞噬细胞有效应对结核分枝杆菌的能力方面很重要，也可能导致过度的炎症反应。
