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硫酸葡聚糖增强小鼠腹腔巨噬细胞脂多糖诱导的肿瘤坏死因子-α 产生:与巨噬细胞阻断的相关性

Dextran sulphate enhancement of lipopolysaccharide-induced tumour necrosis factor-alpha production by murine peritoneal macrophages: correlation with macrophage blockade.

作者信息

Kamochi M, Ogata M, Yoshida S, Matsumoto T, Kubota E, Mizuguchi Y, Shigematsu A

机构信息

Intensive Care Unit, Hospital and School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.

出版信息

FEMS Immunol Med Microbiol. 1993 Aug;7(2):153-9. doi: 10.1111/j.1574-695X.1993.tb00394.x.

DOI:10.1111/j.1574-695X.1993.tb00394.x
PMID:8401427
Abstract

Proteose peptone-induced murine peritoneal macrophages (M phi) were preincubated with 100-800 micrograms/ml of dextran sulphate (DS) 500 (M(r) 500,000) or DS1000 (M(r) 1,000,000). After 2-24 h of the preincubation, the M phi were stimulated with 1 microgram/ml of lipopolysaccharide (LPS) in vitro for 18 h in DS-free culture medium. The culture supernatants were then collected for TNF assay. The LPS-induced TNF activity of M phi supernatant preincubated with DS500 or DS1000 for 6 h was enhanced by up to about ten-fold compared with those preincubated without DS. This enhancing effect was not observed when M phi were preincubated with 100-800 micrograms/ml of low molecular weight DS5 (M(r) 5,000) or neutral dextran (Dex) 500 (M(r) 500,000). The enhancement of LPS-induced TNF-alpha production from M phi was observed after 2 or 4 h of incubation with DS1000 or DS500, respectively. The phagocytic activity of M phi was determined in vitro by the ingestion index and phagocytic capacity using Saccharomyces cerevisiae. Treatment with DS500 or DS1000 significantly suppressed the phagocytic activity from 2 h after the incubation, but this suppression was not observed in M phi incubated with DS5 or Dex500. Our experiments indicate that DS500 and DS1000 act directly on M phi and enhance LPS-induced TNF-alpha production from M phi, and that the enhancement is closely related to the suppression of M phi phagocytic function.

摘要

将蛋白胨诱导的小鼠腹腔巨噬细胞(M phi)与100 - 800微克/毫升的硫酸葡聚糖(DS)500(相对分子质量500,000)或DS1000(相对分子质量1,000,000)预孵育。预孵育2 - 24小时后,在无DS的培养基中用1微克/毫升脂多糖(LPS)体外刺激M phi 18小时。然后收集培养上清液用于肿瘤坏死因子(TNF)检测。与未用DS预孵育的相比,用DS500或DS1000预孵育6小时的M phi上清液中LPS诱导的TNF活性增强了约10倍。当M phi与100 - 800微克/毫升的低分子质量DS5(相对分子质量5,000)或中性葡聚糖(Dex)500(相对分子质量500,000)预孵育时,未观察到这种增强作用。分别与DS1000或DS500孵育2或4小时后,观察到M phi中LPS诱导的肿瘤坏死因子 - α(TNF - α)产生增强。使用酿酒酵母通过摄取指数和吞噬能力在体外测定M phi的吞噬活性。用DS500或DS1000处理在孵育2小时后显著抑制吞噬活性,但在用DS5或Dex500孵育的M phi中未观察到这种抑制作用。我们的实验表明,DS500和DS1000直接作用于M phi并增强M phi中LPS诱导的TNF - α产生,并且这种增强与M phi吞噬功能的抑制密切相关。

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