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短期系统性低氧对外周血细胞吞噬作用、细胞因子产生和转录因子激活的影响。

Impact of short-term systemic hypoxia on phagocytosis, cytokine production, and transcription factor activation in peripheral blood cells.

机构信息

Department of Internal Medicine I, Division of Cardiology, Friedrich-Schiller-University, Erlanger Allee 101, 07740 Jena, Germany.

出版信息

Mediators Inflamm. 2011;2011:429501. doi: 10.1155/2011/429501. Epub 2011 Jun 2.

Abstract

Hypoxia frequently associated with certain physiologic and pathologic conditions influences numerous cellular functions. Because the effects of short-term hypoxia are incompletely understood, we examined phagocytosis and cytokine production as well as the activation of the transcription factors HIF-1 and NFκB in peripheral blood cells of healthy volunteers exposed to an oxygen concentration equivalent to that found at a height of 5500 m. Furthermore, we analysed plasma HIF-1 and serum concentrations of various HIF-1-dependent genes. Results showed that short-term hypoxia increased phagocytosis in neutrophils without affecting monocyte phagocytosis. Hypoxia decreased basal TNFα concentration in monocytes and basal interferon γ concentration in CD4(+) T lymphocytes. In contrast, plasma HIF and serum VEGF concentrations were not affected by hypoxia, although serum EPO concentration was raised. In PBMC, hypoxia increased cytosolic HIF-1 concentration without affecting nuclear HIF-1 concentration and led to a rise in the nuclear NFκB in PBMC. Our results show that short-term hypoxia affects immune functions in healthy individuals. Furthermore, we speculate that the effects of hypoxia are not due to HIF-1, but are caused by the activation of NFκB .

摘要

缺氧常与某些生理和病理状况相关,影响着众多的细胞功能。由于人们对短期缺氧的影响还不完全了解,我们检测了健康志愿者外周血细胞在暴露于相当于 5500 米高处氧气浓度下时的吞噬作用和细胞因子产生情况,以及转录因子 HIF-1 和 NFκB 的激活情况。此外,我们分析了血浆 HIF-1 和血清中各种 HIF-1 依赖基因的浓度。结果表明,短期缺氧增加了中性粒细胞的吞噬作用,而不影响单核细胞的吞噬作用。缺氧降低了单核细胞中的基础 TNFα 浓度和 CD4+T 淋巴细胞中的基础干扰素 γ 浓度。相反,尽管血清 EPO 浓度升高,但血浆 HIF 和血清 VEGF 浓度不受缺氧影响。在 PBMC 中,缺氧增加了胞质 HIF-1 浓度,而不影响核 HIF-1 浓度,并导致 PBMC 中核 NFκB 的增加。我们的研究结果表明,短期缺氧会影响健康个体的免疫功能。此外,我们推测缺氧的影响不是由 HIF-1 引起的,而是由 NFκB 的激活引起的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c97/3134261/a31094c31886/MI2011-429501.001.jpg

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