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重症监护病房细菌感染患者刺激血培养中细胞因子的差异产生

Differential cytokine production in stimulated blood cultures from intensive care patients with bacterial infections.

作者信息

Mitov I G, Kropec A, Benzing A, Just H, Garotta G, Galanos C, Freudenberg M

机构信息

Max-Planck-Institut für Immunbiologie, Germany.

出版信息

Infection. 1997 Jul-Aug;25(4):206-12. doi: 10.1007/BF01713144.

DOI:10.1007/BF01713144
PMID:9266258
Abstract

Mice infected with bacteria develop an interferon-gamma (IFN-gamma) dependent hypersensitivity to lipopolysaccharide (LPS) and other bacterial components. The broader aim of this study is to find out whether such hypersensitivity also occurs in patients suffering from bacterial infections. The capacity of stimulated peripheral blood cells from infected, intensive-care patients to produce cytokines (IFN-gamma, tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6)) was compared to that of healthy donors. Culturing of the cells was carried out preferentially in whole blood diluted 1:3. Whole blood cultures (WBC) were stimulated with lipopolysaccharide (LPS), whole killed Salmonella typhimurium and Staphylococcus aureus and concanavalin A (ConA), and the cytokine production was determined. Two main findings emerged from this study: The IFN-gamma production by WBC of patients was, compared to healthy donors, markedly suppressed, regardless of stimulus used. Further, patients' WBC exhibited a suppressed TNF-alpha production after stimulation with LPS. Surprisingly, following stimulation with bacteria (S. typhimurium and S. aureus) an elevated TNF-alpha and IL-6 response was obtained. Thus, in severely infected patients the cytokine responses of peripheral blood cells to LPS may be suppressed, while the response to other bacterial components is enhanced.

摘要

感染细菌的小鼠会对脂多糖(LPS)和其他细菌成分产生依赖干扰素-γ(IFN-γ)的超敏反应。本研究的更广泛目标是查明这种超敏反应是否也发生在患有细菌感染的患者身上。将感染的重症监护患者的外周血刺激细胞产生细胞因子(IFN-γ、肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6))的能力与健康供体的进行比较。细胞培养优先在1:3稀释的全血中进行。用脂多糖(LPS)、全灭活的鼠伤寒沙门氏菌和金黄色葡萄球菌以及伴刀豆球蛋白A(ConA)刺激全血培养物(WBC),并测定细胞因子的产生。本研究得出两个主要发现:与健康供体相比,患者WBC产生的IFN-γ明显受到抑制,无论使用何种刺激物。此外,患者的WBC在用LPS刺激后TNF-α产生受到抑制。令人惊讶的是,在用细菌(鼠伤寒沙门氏菌和金黄色葡萄球菌)刺激后,TNF-α和IL-6反应升高。因此,在严重感染的患者中,外周血细胞对LPS的细胞因子反应可能受到抑制,而对其他细菌成分的反应则增强。

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