Production and role of Macrophage activating factor (IFN-gamma) by bacterial lipopolysaccharide and other bacterial products

(1)C3H/HeJ系小鼠脾和腹膜渗出液细胞经细菌脂多糖(LPS)刺激后产生的干扰素极少或不产生。然而，在实验前感染卡介苗(BCG)的无内毒素应答的C3H/HeJ小鼠的细胞在有内毒素存在的情况下能够在培养中产生干扰素。实验结果表明，脂多糖诱导干扰素产生的机制是贴壁细胞与非贴壁细胞直接接触，不需要贴壁细胞中的任何可溶性因子(S)参与。产生细胞主要位于非贴壁细胞群中。用抗Thy 1.2、抗Lyt-1.1、抗L3T4或抗asialo-GML抗体和补体处理非贴壁细胞可降低其借助贴壁细胞产生干扰素的能力。因此，卡介苗诱导的C3H/HeJ细胞培养上清液中的T细胞和自然杀伤细胞均可在脂多糖存在下产生干扰素-γ，且巨噬细胞的功能支持其产生。(2)检测重组干扰素-γ对小鼠感染肠炎沙门氏菌后杀菌功能的影响。低于1000U的干扰素很难显示出这种作用。而注射100u的干扰素和10 ng的内毒素对小鼠有明显的杀菌作用。(3)研究了内毒素诱导巨噬细胞产生IL-1和TSST-1诱导T细胞产生IL-2的机制。

(1) The cultured cells prepared from the spleens and peritoneal exudate cells of the C3H/HeJ strain of mice produce very little or no interferon (IFN) by stimulation of bacterial lipopolysaccharide (LPS). However, the cells taken from LPS-nonresponder C3H/Hej mice which had geen infected with mycobacterium bovis bacillus Calmette Guerin (BCG) prior to the experiment were capable of producing IFN in culture in the presence of LPS. The results in our experiments indicate that there is a mechanism of IFN- induction by LPS which rerquires the direct contact between adherent cells and nonadherent cells without the participation of any soluble factor(s) from the adherent cells. The producer cells were mainly in the nonadherent cell population. Previous treatment of nonadherent cells with anti-Thy 1.2, anti-Lyt-1.1, anti-L3T4, or anti-asialo-GMl antibody and complement diminished the ability of the cells for LPS-induced IFN production with the help of adherent cells. Therefore, it is concluded that both Tcells and natural killer cells in the BCG-primed C3H/Hej cell cultures produced IFN-gamma in the presence of LPS, and the production was supported by the function of macrophages.(2) we examined the effect of recombinant IFN-(gamma) on the bactericidal function in mice after the infection with virlent Salmonella enteritidis. Less than 1000 u of IFN could hardly show the effect. However, injection of 100 u IFN with 10 ng LPS revealed obviously bactericidal effect in the mice.(3) we examined the mechanisms of LPS-induced IL 1 production of macrophages and TSST-1-induced IL 2 prouction of T cells.