Pourshafie M R, Sonnenfeld G
Department of Microbiology, Pasteur Institute of Iran, Tehran, Iran.
J Interferon Cytokine Res. 1997 Feb;17(2):69-75. doi: 10.1089/jir.1997.17.69.
In the present study, we evaluated whether the activation of a murine macrophage cell line (J774.1A) by treatment with recombinant murine tumor necrosis factor-alpha (rTNF-alpha) or recombinant murine interferon-gamma (rIFN-gamma) before or simultaneous with infection with Mycobacterium intracellulare would affect their ability to express lymphocyte function-associated antigen-1 (LFA-1) and to restrict growth and kill the ingested M. intracellulare. The data showed that the effect of lipopolysaccharide (LPS) in increasing the level of LFA-1 was the same in the presence or absence of M. intracellulare. The inability of M. intracellulare to affect the level of expression of LFA-1 was irrespective of the M. intracellulare to J774A.1 ratio. A significant increase in the expression of LFA-1 was observed when J774A.1 cells were prestimulated with IFN-gamma 1 day before the addition of the bacteria. The addition of IFN-gamma with M. intracellulare simultaneously, however, did not affect the expression of the adhesion molecules as compared with the IFN-gamma alone. Our results indicated no change in the level of LFA-1 on J774A.1 following exposure with TNF-alpha. We observed that preexposure with 10-10(4) IU/ml of TNF-alpha can significantly decrease the number of ingested M. intracellulare. Simultaneous addition of 10(3) and 10(4) IU/ml of TNF-alpha, however, did not have any mycobactericidal effect. This indicates that the TNF-alpha-induced killing by J774A.1 cells was relatively selective, depending on the concentration and the time of presence of TNF-alpha. The data may suggest that the uptake of M. intracellulare is carried out via other adhesion receptors when M. intracellulare and IFN-alpha are present simultaneously and that in the presence of TNF-alpha other surface receptors are involved in the uptake of M. intracellulare. Flow cytometry analysis of the spleen cells removed at various times from M. intracellulare-infected mice also indicated no change in the level of LFA-1 beta or MAC-1, a finding comparable with that of the J774A.1 cells.
在本研究中，我们评估了在用重组鼠肿瘤坏死因子-α（rTNF-α）或重组鼠干扰素-γ（rIFN-γ）处理小鼠巨噬细胞系（J774.1A）之前或与细胞内分枝杆菌感染同时进行处理时，是否会影响其表达淋巴细胞功能相关抗原-1（LFA-1）以及限制细胞内分枝杆菌生长和杀伤所摄入的细胞内分枝杆菌的能力。数据显示，脂多糖（LPS）在增加LFA-1水平方面的作用，在有或无细胞内分枝杆菌存在的情况下是相同的。细胞内分枝杆菌无法影响LFA-1的表达水平，这与细胞内分枝杆菌与J774A.1的比例无关。当在添加细菌前1天用IFN-γ对J774A.1细胞进行预刺激时，观察到LFA-1的表达显著增加。然而，与单独使用IFN-γ相比，将IFN-γ与细胞内分枝杆菌同时添加并不影响黏附分子的表达。我们的结果表明，用TNF-α处理后J774A.1上LFA-1的水平没有变化。我们观察到，用10 - 10⁴IU/ml的TNF-α进行预暴露可显著减少摄入的细胞内分枝杆菌数量。然而，同时添加10³和10⁴IU/ml的TNF-α并没有任何杀菌作用。这表明J774A.1细胞由TNF-α诱导的杀伤作用具有相对选择性，这取决于TNF-α的浓度和存在时间。数据可能表明，当细胞内分枝杆菌和IFN-α同时存在时，细胞内分枝杆菌的摄取是通过其他黏附受体进行的，并且在TNF-α存在的情况下，其他表面受体参与了细胞内分枝杆菌的摄取。对从细胞内分枝杆菌感染小鼠在不同时间取出的脾细胞进行的流式细胞术分析也表明，LFA-1β或MAC-1的水平没有变化，这一发现与J774A.1细胞的情况相当。
