Dahl K E, Shiratsuchi H, Hamilton B D, Ellner J J, Toossi Z
Department of Medicine, Case Western Reserve University, Cleveland, Ohio, USA.
Infect Immun. 1996 Feb;64(2):399-405. doi: 10.1128/iai.64.2.399-405.1996.
The induction of macrophage-deactivating (interleukin-10 [IL-10] and transforming growth factor beta [TGF-beta] and macrophage-activating (IL-1, IL-6, and tumor necrosis factor alpha [TNF-alpha] cytokines by lipoarabinomannan (LAM) from pathogenic Mycobacterium tuberculosis Erdman and H37Rv strains (ManLAM) and nonpathogenic mycobacteria (AraLAM) in human blood monocytes was examined. ManLAM was significantly less potent in induction of TNF-alpha, IL-1, IL-6, and IL-10 protein and mRNA, whereas its ability to induce TGF-beta was similar to that of AraLAM. Differences in induction of TNF-alpha mRNA by the two LAM preparations only became apparent at late time points of culture (24 h). The induction of TNF-alpha and IL-1 by purified protein derivative of M. tuberculosis was significantly stronger than that by ManLAM. Pretreatment of monocytes with ManLAM did not, however, interfere with cytokine induction by lipopolysaccharide or AraLAM. The extensive mannosyl capping of arabinose termini of ManLAM may underlie the lack of ability to induce some cytokines (IL-1, TNF-alpha, and IL-10) and the retained ability to induce TGF-beta. The latter may have a role in shifting the cytokine milieu in favor of survival of M. tuberculosis.
研究了来自致病性结核分枝杆菌 Erdman 和 H37Rv 菌株（甘露糖脂阿拉伯甘露聚糖 [ManLAM]）以及非致病性分枝杆菌（阿拉伯糖脂阿拉伯甘露聚糖 [AraLAM]）的脂阿拉伯甘露聚糖（LAM）对人血单核细胞中巨噬细胞失活细胞因子（白细胞介素 -10 [IL-10] 和转化生长因子β [TGF-β]）以及巨噬细胞激活细胞因子（IL-1、IL-6 和肿瘤坏死因子α [TNF-α]）的诱导作用。ManLAM 在诱导 TNF-α、IL-1、IL-6 和 IL-10 蛋白及 mRNA 方面的效力显著较低，而其诱导 TGF-β 的能力与 AraLAM 相似。两种 LAM 制剂诱导 TNF-α mRNA 的差异仅在培养后期（24 小时）才变得明显。结核分枝杆菌纯蛋白衍生物诱导 TNF-α 和 IL-1 的能力明显强于 ManLAM。然而，用 ManLAM 预处理单核细胞并不干扰脂多糖或 AraLAM 诱导细胞因子。ManLAM 阿拉伯糖末端广泛的甘露糖封端可能是其缺乏诱导某些细胞因子（IL-1、TNF-α 和 IL-10）的能力以及保留诱导 TGF-β 能力的原因。后者可能在改变细胞因子环境以利于结核分枝杆菌存活方面发挥作用。
