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驻留和活化的小鼠巨噬细胞产生肿瘤坏死因子α。

Production of tumor necrosis factor alpha by resident and activated murine macrophages.

作者信息

Tachibana K, Chen G J, Huang D S, Scuderi P, Watson R R

机构信息

Department of Fishery Food Sciences, Faculty of Fisheries, Nagasaki University, Japan.

出版信息

J Leukoc Biol. 1992 Mar;51(3):251-5. doi: 10.1002/jlb.51.3.251.

DOI:10.1002/jlb.51.3.251
PMID:1541908
Abstract

Alveolar macrophages (Am phi s), resident peritoneal macrophages (RPm phi s), and thioglycolate-elicited peritoneal macrophages (TGPm phi s) were isolated from C57BL/6 mice and incubated with lipopolysaccharide (LPS), stimulated cell supernatant, or recombinant interferon gamma (IFN-gamma) for 24 h. Tumor necrosis factor (TNF) in cell-free supernatants was measured by enzyme-linked immunosorbent assay. Amo phi s incubated with 10(3) ng/ml LPS produced 50 times more TNF than RPm phi s and 5 times more than TGPm phi s, and LPS alone induced maximum TNF production by Am phi s. Stimulated cell supernatant or recombinant IFN-gamma alone did not induce TNF production. A combination of LPS with stimulated cell supernatant or IFN-gamma had only a limited synergistic effect on TNF production by Am phi s. However, both LPS and stimulated cell supernatant or recombinant IFN-gamma induced maximum TNF production by RPm phi s and TGPm phi s. TGPm phi s showed greater sensitivity to LPS and stimulated cell supernatant or IFN-gamma with regard to TNF production than the other macrophage populations investigated.

摘要

从C57BL/6小鼠中分离出肺泡巨噬细胞(Am phi s)、常驻腹膜巨噬细胞(RPm phi s)和巯基乙酸盐诱导的腹膜巨噬细胞(TGPm phi s),并与脂多糖(LPS)、刺激细胞上清液或重组干扰素γ(IFN-γ)一起孵育24小时。通过酶联免疫吸附测定法测量无细胞上清液中的肿瘤坏死因子(TNF)。与10(3) ng/ml LPS孵育的Am phi s产生的TNF比RPm phi s多50倍,比TGPm phi s多5倍,并且单独的LPS诱导Am phi s产生最大量的TNF。单独的刺激细胞上清液或重组IFN-γ不会诱导TNF产生。LPS与刺激细胞上清液或IFN-γ的组合对Am phi s产生TNF的协同作用有限。然而,LPS和刺激细胞上清液或重组IFN-γ均诱导RPm phi s和TGPm phi s产生最大量的TNF。就TNF产生而言,TGPm phi s对LPS、刺激细胞上清液或IFN-γ的敏感性高于所研究的其他巨噬细胞群体。

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