Mechanisms involved in metastasis enhanced by inflammatory mediators.

Circulatory shock Pub Date : 1994-09-01
D N Männel, P Orosz, M Hafner, W Falk
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Abstract

The enhancement of tumor metastasis by concurrent inflammatory processes is mainly due to the cytokines TNF and IL-1. In the case of TNF this effect is not restricted to metastasis models as measured by in vivo colony formation but also found in experimental model systems of spontaneous metastasis. Direct effects on the tumor cells or interference with the host NK cell system did not seem to account for the observed TNF effect. Experimental evidence from different test systems rather points to TNF- or IL-1-induced enhanced adhesion of tumor cells to the endothelial cell layer as the underlying mechanism. Blocking of integrin-matrix interactions with monoclonal antibodies or competing peptides inhibited tumor cell adhesion to endothelioma cells in vitro and lung colony formation of tumor cells in vivo.

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炎症介质增强转移的机制。
并发炎症过程对肿瘤转移的增强主要是由于细胞因子TNF和IL-1的作用。在TNF的情况下,这种作用不仅限于通过体内集落形成测量的转移模型,而且在自发转移的实验模型系统中也发现。对肿瘤细胞的直接作用或对宿主NK细胞系统的干扰似乎不能解释观察到的TNF效应。来自不同测试系统的实验证据表明,TNF-或il -1诱导的肿瘤细胞与内皮细胞层的粘附增强是潜在的机制。在体外,阻断整合素基质与单克隆抗体或竞争肽的相互作用可抑制肿瘤细胞对内皮瘤细胞的粘附和体内肿瘤细胞的肺集落形成。
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