Fazal N, Lammas D A, Raykundalia C, Bartlett R, Kumararatne D S
Department of Immunology, University of Birmingham, UK.
FEMS Microbiol Immunol. 1992 Dec;5(5-6):337-45. doi: 10.1111/j.1574-6968.1992.tb05919.x.
Four agents, thalidomide, oxpentifylline, dexamethasone and a polyclonal anti-TNF-alpha antibody, were all shown by specific Elisa to block endogenous TNF-alpha production by Bacillus Calmette Guerin (BCG)-infected human monocyte-derived macrophages in in vitro culture. There was however no significant enhancement of intracellular BCG growth, over a 7-day incubation, in human monocyte-derived macrophages in the presence of any of the TNF-alpha-blocking agents, as determined by both radiometric and CFU counting methods of assessing bacterial viability and growth. The result suggests that the action of TNF-alpha alone is unlikely to be an important effector mechanism in antimycobacterial immunity within human cells.
通过特异性酶联免疫吸附测定法（ELISA）表明，沙利度胺、己酮可可碱、地塞米松和一种多克隆抗TNF-α抗体这四种药物，在体外培养中均能阻断卡介苗（BCG）感染的人单核细胞衍生巨噬细胞产生内源性TNF-α。然而，通过评估细菌活力和生长的放射性测定法和菌落形成单位（CFU）计数法确定，在存在任何一种TNF-α阻断剂的情况下，人单核细胞衍生巨噬细胞在7天的培养期内，细胞内BCG的生长均未显著增强。该结果表明，仅TNF-α的作用不太可能是人体细胞内抗分枝杆菌免疫的重要效应机制。
