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Mechanism of lipopolysaccharide-induced tumor necrosis: requirement for lipopolysaccharide-sensitive lymphoreticular cells.

机译:脂多糖诱导的肿瘤坏死的机制:对脂多糖敏感的淋巴网状细胞的需求。

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摘要

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.
机译:脂多糖(LPS)诱导小鼠皮内纤维肉瘤快速坏死。已使用组织相容性LPS敏感(C3H / HeN)和LPS抗性(C3H / HeJ)小鼠品系研究了LPS产生肿瘤坏死的机制。 C3H / HeN或C3H / HeJ衍生的纤维肉瘤在移植到C3H / HeN小鼠时被LPS坏死,但在C3H / HeJ小鼠上生长时不受影响,这表明LPS并不直接作用于肿瘤本身。相比之下,致命的X射线照射的C3H / HeJ小鼠在用C3H / HeN骨髓细胞重建时表现出肿瘤坏死,而C3H / HeN小鼠在过继转移C3H / HeJ骨髓细胞后不再表现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而产生肿瘤坏死。

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