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重组粒细胞-巨噬细胞集落刺激因子(GM-CSF)或肿瘤坏死因子-α(TNF-α)可激活人肺泡巨噬细胞,以抑制鸟分枝杆菌复合体的生长。

Recombinant granulocyte-macrophage colony-stimulating factor (GM-CSF) or tumour necrosis factor-alpha (TNF-alpha) activate human alveolar macrophages to inhibit growth of Mycobacterium avium complex.

作者信息

Suzuki K, Lee W J, Hashimoto T, Tanaka E, Murayama T, Amitani R, Yamamoto K, Kuze F

机构信息

Department of Infection and Inflammation, Kyoto University, Japan.

出版信息

Clin Exp Immunol. 1994 Oct;98(1):169-73. doi: 10.1111/j.1365-2249.1994.tb06625.x.

Abstract

We investigated the effects of certain macrophage-active cytokines on the phagocytosis and growth inhibition of Mycobacterium avium complex (MAC) by human alveolar macrophages (AM). We also evaluated the effects of pretreatment with each cytokine on the superoxide anion release (O2-) from AM. The cytokines that we used were recombinant GM-CSF, natural type TNF-alpha, recombinant interferon-gamma (IFN-gamma), and recombinant IL-2. We found that phagocytosis by the various cytokine-stimulated AM was similar to that of unstimulated AM. On the other hand, significant growth inhibition of MAC was observed in the macrophages treated with GM-CSF or TNF-alpha, while no growth inhibition of MAC was observed in the macrophages treated with IFN-gamma or IL-2. Pretreatment with all cytokines tested enhanced the O2- release from AM, but there was no correlation between the enhancement of O2- release and the growth inhibition of MAC. Thus, we concluded that GM-CSF or TNF-alpha could activate AM to inhibit growth of MAC, probably not through the enhanced production of reactive oxygen intermediates.

摘要

我们研究了某些巨噬细胞活性细胞因子对人肺泡巨噬细胞(AM)吞噬鸟分枝杆菌复合群(MAC)及生长抑制的影响。我们还评估了用每种细胞因子预处理对AM释放超氧阴离子(O2-)的影响。我们使用的细胞因子有重组粒细胞-巨噬细胞集落刺激因子(GM-CSF)、天然型肿瘤坏死因子-α(TNF-α)、重组干扰素-γ(IFN-γ)和重组白细胞介素-2(IL-2)。我们发现,各种细胞因子刺激的AM的吞噬作用与未刺激的AM相似。另一方面,在用GM-CSF或TNF-α处理的巨噬细胞中观察到MAC有显著的生长抑制,而在用IFN-γ或IL-2处理的巨噬细胞中未观察到MAC的生长抑制。用所有测试的细胞因子预处理均可增强AM释放O2-,但O2-释放的增强与MAC的生长抑制之间无相关性。因此,我们得出结论,GM-CSF或TNF-α可能通过不依赖活性氧中间体产生增加的途径激活AM以抑制MAC的生长。

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