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金黄色葡萄球菌诱导性关节炎中的粒细胞巨噬细胞集落刺激因子

Granulocyte-macrophage colony-stimulating factor in Staphylococcus aureus-induced arthritis.

作者信息

Verdrengh M, Tarkowski A

机构信息

Department of Rheumatology, University of Göteborg, Sweden.

出版信息

Infect Immun. 1998 Feb;66(2):853-5. doi: 10.1128/IAI.66.2.853-855.1998.

Abstract

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a cytokine that is able to increase not only the production of phagocytic cells but also their efficacy with respect to, e.g., bactericidal properties. In this study, we wanted to analyze the impact of GM-CSF on experimental Staphylococcus aureus-induced arthritis. For that purpose, mice were administered GM-CSF before and after bacterial inoculation. Although there was an increase in the total number of leukocytes as well as in the granulocyte fraction, there was no favorable effect on the severity of arthritis or on survival rates. There were no obvious differences between the GM-CSF-pretreated animals and controls with regard to growth of staphylococci in joints and kidneys 4 days after the bacterial inoculation. In contrast, mice that had been pretreated with GM-CSF prior to bacterial inoculation showed approximately four times lower numbers of bacteria in their blood 24 h later. These results, along with those of our previous studies, suggest that on the one hand the granulocyte is the main protective cell during the course of S. aureus infection but that on the other hand, upregulation of granulocyte-macrophage production will not exert any additional protective effects with respect to tissue injury.

摘要

粒细胞-巨噬细胞集落刺激因子(GM-CSF)是一种细胞因子,它不仅能够增加吞噬细胞的产生,还能提高其在杀菌特性等方面的效能。在本研究中,我们想要分析GM-CSF对实验性金黄色葡萄球菌诱导的关节炎的影响。为此,在细菌接种前后给小鼠施用GM-CSF。尽管白细胞总数以及粒细胞比例有所增加,但对关节炎的严重程度或存活率没有产生有利影响。在细菌接种4天后,GM-CSF预处理动物与对照在关节和肾脏中葡萄球菌的生长方面没有明显差异。相反,在细菌接种前用GM-CSF预处理的小鼠在24小时后血液中的细菌数量大约低四倍。这些结果,连同我们之前研究的结果表明,一方面粒细胞是金黄色葡萄球菌感染过程中的主要保护细胞,但另一方面,粒细胞-巨噬细胞产生的上调不会对组织损伤产生任何额外的保护作用。

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Potential role of colony-stimulating factors in the prevention and treatment of infectious diseases.
Clin Infect Dis. 1994 Feb;18 Suppl 2:S180-8. doi: 10.1093/clinids/18.supplement_2.s180.

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