Rossol S, Voth R, Brunner S, Müller W E, Büttner M, Gallati H, Meyer zum Büschenfelde K H, Hess G
I. Medizinische Klinik und Poliklinik, Johannes Gutenberg Universität Mainz, FRG.
Eur J Immunol. 1990 Aug;20(8):1761-5. doi: 10.1002/eji.1830200821.
The present study investigates the potential capacity of the immunostimulant Corynebacterium parvum (C.p.) to induce tumor necrosis factor-alpha (TNF-alpha) in human peripheral blood mononuclear cells (PBMC) and blood monocytes (BMo) in vitro. Both at the mRNA and protein level, stimulation of PBMC and BMo upon C.p. induces TNF-alpha. Compared to the hitherto used TNF-alpha inducers in vitro such as Sendai virus, phytohemagglutinin or lipopolysaccharide the C.p. stimulus displayed a threefold stronger induction of TNF-alpha production (p less than 0.001). Using C.p. as an inducer it was possible to demonstrate that TNF-alpha production is regulated by prostaglandin E2; preincubation of the cells with prostaglandin E2 resulted in a reduced C.p.-mediated TNF-alpha production (p less than 0.001). Coincubation of interferon-gamma (IFN-gamma) together with C.p. led to an enhanced release of TNF-alpha, supporting the assumption that C.p. is a potent TNF-alpha inducer. The additive effect of IFN-gamma and TNF-alpha on the receptor level was demonstrated by addition of IFN-gamma antibodies to the PBMC cultures. Under these conditions TNF-alpha production, stimulated by C.p. and IFN-gamma, was decreased by 30%, compared to the production in assays supplemented with C.p. alone. From these data we conclude that C.p. is a new inducer of TNF-alpha in vitro and a useful tool to study TNF-alpha production of PBMC and BMo from either healthy donors or from patients.
本研究调查了免疫刺激剂短小棒状杆菌（C.p.）在体外诱导人外周血单核细胞（PBMC）和血液单核细胞（BMo）产生肿瘤坏死因子-α（TNF-α）的潜在能力。在mRNA和蛋白质水平上，C.p.刺激PBMC和BMo均能诱导TNF-α产生。与迄今为止体外使用的TNF-α诱导剂如仙台病毒、植物血凝素或脂多糖相比，C.p.刺激显示出对TNF-α产生的诱导作用强三倍（p<0.001）。使用C.p.作为诱导剂能够证明TNF-α的产生受前列腺素E2调节；细胞与前列腺素E2预孵育导致C.p.介导的TNF-α产生减少（p<0.001）。干扰素-γ（IFN-γ）与C.p.共同孵育导致TNF-α释放增加，支持C.p.是一种有效的TNF-α诱导剂的假设。通过向PBMC培养物中添加IFN-γ抗体证明了IFN-γ和TNF-α在受体水平上的相加作用。在这些条件下，与仅添加C.p.的试验中的产生相比，由C.p.和IFN-γ刺激的TNF-α产生减少了30%。从这些数据我们得出结论，C.p.是体外TNF-α的一种新诱导剂，也是研究来自健康供体或患者的PBMC和BMo产生TNF-α的有用工具。
