脂多糖诱导肿瘤坏死的机制：对脂多糖敏感的淋巴网状细胞的需求。
Mechanism of lipopolysaccharide-induced tumor necrosis: requirement for lipopolysaccharide-sensitive lymphoreticular cells.
作者信息
Männel D N, Rosenstreich D L, Mergenhagen S E
出版信息
Infect Immun. 1979 May;24(2):573-6. doi: 10.1128/iai.24.2.573-576.1979.
Abstract
Lipopolysaccharide (LPS) induces rapid necrosis of intradermal fibrosarcomas in mice. The mechanism(s) by which LPS produces tumor necrosis has been investigated using histocompatible LPS-sensitive (C3H/HeN) and LPS-resistant (C3H/HeJ) mouse strains. C3H/HeN- or C3H/HeJ-derived fibrosarcomas were necrotized by LPS when they were grafted onto C3H/HeN mice but were not affected when growing on C3H/HeJ mice, indicating that LPS does not act directly on the tumor itself. In contrast, lethally X-irradiated C3H/HeJ mice exhibit necrosis of their tumors when reconstituted with C3H/HeN bone marrow cells, whereas C3H/HeN mice no longer exert LPS-induced tumor necrosis after the adoptive transfer of C3H/HeJ bone marrow cells. These findings clearly indicate that LPS produces necrosis of tumors by activating host lymphoreticular cells.
摘要
脂多糖（LPS）可诱导小鼠皮内纤维肉瘤迅速坏死。利用组织相容性的LPS敏感（C3H/HeN）和LPS抗性（C3H/HeJ）小鼠品系，对LPS产生肿瘤坏死的机制进行了研究。当将源自C3H/HeN或C3H/HeJ的纤维肉瘤移植到C3H/HeN小鼠身上时，会被LPS坏死，但在C3H/HeJ小鼠身上生长时则不受影响，这表明LPS并非直接作用于肿瘤本身。相反，经致死剂量X射线照射的C3H/HeJ小鼠在用C3H/HeN骨髓细胞重建后，其肿瘤会出现坏死，而C3H/HeN小鼠在接受C3H/HeJ骨髓细胞的过继转移后，不再发生LPS诱导的肿瘤坏死。这些发现清楚地表明，LPS通过激活宿主淋巴网状细胞产生肿瘤坏死。
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