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炎症增强了人腹膜巨噬细胞的抗肿瘤细胞生长抑制作用。

Inflammation amplifies the antitumor cytostasis by human peritoneal macrophages.

作者信息

Ben-Efraim S, Tak C, Fieren M J, Van den Bemd G J, Bonta I L

机构信息

Department of Pharmacology, Erasmus University, Rotterdam, The Netherlands.

出版信息

Med Oncol Tumor Pharmacother. 1991;8(2):87-94. doi: 10.1007/BF02988859.

DOI:10.1007/BF02988859
PMID:1749305
Abstract

The effect of an inflammatory environment on the antitumor cytostatic ability of human macrophages was examined. Peritoneal macrophages of patients on continuous ambulatory peritoneal dialysis (CAPD) were collected, when CAPD was without complication, during an intercurrent infectious inflammation and after recovery. Inhibition of 3H-thymidine uptake served as a measure of cytostasis by macrophages co-cultured with target murine cells MOPC-315 plasmacytoma, WEHI-3B myelomonocytic leukemia and L929 transformed fibroblasts. Macrophages from inflammatory peritoneum expressed a markedly enhanced cytostasis, irrespective of the nature of the tumor cell. Endotoxin (LPS) challenge of inflammatory macrophages failed to further reinforce the cytostasis towards MOPC-315 plasmacytoma, but reinforced the cytostasis towards WEHI-3B leukemia (sensitive to inhibition by IL-1) and towards L929 (sensitive to TNF alpha). Cytostasis by supernatants of human peritoneal macrophages against L929 was markedly inhibited by anti-rHuTNF alpha and against WEHI-3B by anti-rHuIL-1 beta. The results suggest a link between inflammatory function and antitumor cytostasis by macrophages. This link is constituted by mediators involved in the activation process of macrophages.

摘要

研究了炎性环境对人巨噬细胞抗肿瘤细胞生长抑制能力的影响。收集持续非卧床腹膜透析(CAPD)患者的腹膜巨噬细胞,分别在CAPD无并发症时、并发感染性炎症期间及恢复后采集。以抑制³H-胸腺嘧啶核苷摄取作为与靶小鼠细胞MOPC-315浆细胞瘤、WEHI-3B骨髓单核细胞白血病及L929转化成纤维细胞共培养的巨噬细胞细胞生长抑制的指标。来自炎性腹膜的巨噬细胞表现出明显增强的细胞生长抑制作用,而与肿瘤细胞的性质无关。炎性巨噬细胞经内毒素(LPS)刺激后,对MOPC-315浆细胞瘤的细胞生长抑制作用未进一步增强,但增强了对WEHI-3B白血病(对IL-1抑制敏感)及L929(对TNFα敏感)的细胞生长抑制作用。人腹膜巨噬细胞上清液对L929的细胞生长抑制作用被抗rHuTNFα明显抑制,对WEHI-3B的细胞生长抑制作用被抗rHuIL-1β抑制。结果提示巨噬细胞的炎性功能与抗肿瘤细胞生长抑制之间存在联系。这种联系由参与巨噬细胞激活过程的介质构成。

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Indomethacin stimulation of macrophage cytostasis against MOPC-315 tumor cells is inhibited by both prostaglandin E2 and nordihydroguaiaretic acid, a lipoxygenase inhibitor.吲哚美辛对巨噬细胞抑制MOPC - 315肿瘤细胞作用的刺激,受到前列腺素E2和脂氧合酶抑制剂去甲二氢愈创木酸的抑制。
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