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首页> 外文期刊>Infection and immunity >Bacterial lipopolysaccharide potentiates gamma interferon-induced cytotoxicity for normal mouse and rat fibroblasts.
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Bacterial lipopolysaccharide potentiates gamma interferon-induced cytotoxicity for normal mouse and rat fibroblasts.

机译：细菌脂多糖增强了γ-干扰素对正常小鼠和大鼠成纤维细胞的细胞毒性。

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Gamma interferon (IFN-gamma) can be cytolytic for normal mouse fibroblasts isolated from embryonic or adult tissue (R. Dijkmas, B. Decock, H. Heremans, J. Van Damme, and A. Billiau, Lymphokine Res. 8:25-34, 1989). This cytotoxicity has been shown to be transcription and translation dependent, thereby suggesting involvement of a suicidelike mechanism. The dose of IFN-gamma required for cytotoxicity is higher than that needed for antiviral and macrophage activation but can be reduced 10- to 100-fold by cotreatment of the cells with tumor necrosis factor or interleukin-1 (IL-1) or both, two cytokines that by themselves are not toxic for these cells. Here, we show that bacterial lipopolysaccharide (LPS), which alone has no effect on the viability of mouse fibroblasts, stimulates cell suicide induced by IFN-gamma. The effect was observed in cultures that were virtually free of nonfibroblastoid cells. LPS showed its toxicity-enhancing effect only if applied on the cells simultaneously with or immediately after treatment with IFN-gamma. Pretreatment of the cells with LPS was ineffective. Inclusion of antibodies directed against tumor necrosis factor alpha or IL-1 alpha in the culture medium did not block the cytotoxic effect of combined IFN-gamma plus LPS treatment. The time courses of cell toxicity appearance in fibroblasts treated with combined IFN-gamma plus LPS or IFN-gamma plus IL-1 were similar. In addition to LPS, heat-killed gram-negative (Escherichia coli) but also gram-positive (Staphylococcus aureus, Listeria monocytogenes) bacteria were found to enhance IFN-gamma-induced cell death. These findings suggest that IFN-gamma formed in vivo during infectious processes directly aggravates tissue destruction.
机译：γ干扰素（IFN-γ）可对从胚胎或成年组织分离的正常小鼠成纤维细胞进行细胞溶解（R. Dijkmas，B.Decock，H.Heremans，J.Van Damme和A. 1989年第34期）。已经证明这种细胞毒性是转录和翻译依赖性的，从而表明涉及自杀样机制。细胞毒性所需的IFN-γ剂量高于抗病毒和巨噬细胞激活所需的剂量，但可通过与肿瘤坏死因子或白介素-1（IL-1）或两者共同处理细胞，将其降低10至100倍，两种本身对这些细胞无毒的细胞因子。在这里，我们显示细菌脂多糖（LPS）单独对小鼠成纤维细胞的生存力没有影响，它会刺激IFN-γ诱导的细胞自杀。在实际上不含非成纤维细胞的培养物中观察到了这种作用。 LPS仅在与IFN-γ同时或在细胞上同时施用后才显示出增强毒性的作用。用LPS预处理细胞无效。在培养基中包含针对肿瘤坏死因子α或IL-1α的抗体不会阻止IFN-γ加LPS联合治疗的细胞毒性作用。联合IFN-γ加LPS或IFN-γ加IL-1处理的成纤维细胞中细胞毒性出现的时间过程相似。除LPS外，还发现热杀死的革兰氏阴性（大肠杆菌）但革兰氏阳性（金黄色葡萄球菌，单核细胞增生李斯特菌）细菌也可增强IFN-γ诱导的细胞死亡。这些发现表明，在感染过程中在体内形成的IFN-γ直接加剧了组织破坏。

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