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细胞毒性/细胞抑制性巨噬细胞培养上清液在激活小鼠腹腔常驻巨噬细胞中的作用。

Role of culture supernatant of cytotoxic/cytostatic macrophages in activation of murine resident peritoneal macrophages.

作者信息

Hashimoto S, Nagaoka M, Hayashi K, Yokokura T, Mutai M

机构信息

Yakult Central Institute for Microbiological Research, Tokyo, Japan.

出版信息

Cancer Immunol Immunother. 1989;28(4):253-9. doi: 10.1007/BF00205234.

Abstract

Peritoneal macrophages elicited by Lactobacillus casei YIT9018 (LCEPM) were incubated in culture for 18 h with L. casei; the culture supernatant (LCM) was then harvested and tested for its ability to increase the cytostatic activity of resident peritoneal macrophages (RPM) and LCEPM. Treatment of RPM with LCM induced activation of macrophages to a cytostatic state against L929, Colon 26, P815, P388D1 and L1210 cells. A combination of recombinant human tumor necrosis factor (rhTNF), recombinant mouse TNF (rmTNF), recombinant human interleukin-1 (rhIL-1) or bacterial lipopolysaccharide with recombinant mouse interferon gamma (rmIFN-gamma) resulted in the synergistic induction of cytostatic activity in RPM. Recombinant mouse granulocyte-macrophage colony-stimulating factor (rmGM-CSF) plus rhTNF increased the cytostatic activity of RPM a little but rmGM-CSF or rhTNF combined with rhIL-1 or alone had no effect. The effect of LCM on RPM was not inhibited by polymyxin B, anti-mTNF antiserum or below 20 U/ml monoclonal anti-rmIFN-gamma antibody (anti-rmIFN-gamma) but was inhibited by more than 40 U/ml anti-rmIFN-gamma, and LCM did not have any interferon antiviral activity. These results suggest that the cytostatic activity of RPM was augmented by the LCM, and that the effect of the LCM may be not due to IFN-gamma, TNF, GM-CSF, IL-1 or a small amount of contaminating lipopolysaccharide.

摘要

将干酪乳杆菌YIT9018诱导产生的腹膜巨噬细胞(LCEPM)与干酪乳杆菌在培养物中孵育18小时;然后收集培养上清液(LCM),并检测其增强驻留腹膜巨噬细胞(RPM)和LCEPM细胞抑制活性的能力。用LCM处理RPM可诱导巨噬细胞激活,使其对L929、结肠26、P815、P388D1和L1210细胞处于细胞抑制状态。重组人肿瘤坏死因子(rhTNF)、重组小鼠肿瘤坏死因子(rmTNF)、重组人白细胞介素-1(rhIL-1)或细菌脂多糖与重组小鼠干扰素γ(rmIFN-γ)联合使用可协同诱导RPM产生细胞抑制活性。重组小鼠粒细胞-巨噬细胞集落刺激因子(rmGM-CSF)加rhTNF可略微增加RPM的细胞抑制活性,但rmGM-CSF或rhTNF与rhIL-1联合使用或单独使用均无作用。LCM对RPM的作用不受多粘菌素B、抗mTNF抗血清或低于20 U/ml的单克隆抗rmIFN-γ抗体(抗rmIFN-γ)的抑制,但受到超过40 U/ml抗rmIFN-γ的抑制,并且LCM没有任何干扰素抗病毒活性。这些结果表明,LCM增强了RPM的细胞抑制活性,并且LCM的作用可能不是由于IFN-γ、TNF、GM-CSF、IL-1或少量污染的脂多糖。

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Macrophage activation by Lactobacillus casei in mice.干酪乳杆菌对小鼠巨噬细胞的激活作用
Microbiol Immunol. 1983;27(7):611-8. doi: 10.1111/j.1348-0421.1983.tb00622.x.
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The cell biology of macrophage activation.巨噬细胞激活的细胞生物学
Annu Rev Immunol. 1984;2:283-318. doi: 10.1146/annurev.iy.02.040184.001435.

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