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在感染杜氏利什曼原虫的小鼠脾脏和骨髓中,寄生虫增殖伴随着造血活性增强。

Enhanced hematopoietic activity accompanies parasite expansion in the spleen and bone marrow of mice infected with Leishmania donovani.

作者信息

Cotterell S E, Engwerda C R, Kaye P M

机构信息

Department of Infectious Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom.

出版信息

Infect Immun. 2000 Apr;68(4):1840-8. doi: 10.1128/IAI.68.4.1840-1848.2000.

DOI:10.1128/IAI.68.4.1840-1848.2000
PMID:10722572
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC97356/
Abstract

In this study, we have analyzed hematopoietic activity in the spleen, bone marrow, and blood of BALB/c and scid mice infected with Leishmania donovani. Our analysis demonstrates that infection induces a rapid but transient mobilization of progenitor cells into the circulation, associated with elevated levels of granulocyte/macrophage colony-stimulating factor (GM-CSF) and MIP-1alpha. From 14 to 28 days postinfection, when parasite expansion begins in the spleen and bone marrow, both the frequency and cell cycle activity of hematopoietic progenitors, particulary CFU-granulocyte, monocyte, are dramatically increased in these organs. This is associated with increased accumulation of mRNA for GM-CSF, M-CSF, and G-CSF, but not interleukin-3. Our data also illustrate that hematopoietic activity, as assessed by changes in the frequency of progenitor cell populations and their levels of cell cycle activity, can be regulated in both a T-cell-independent and T-cell-dependent, as well as in an organ-specific, manner. Collectively, these data add to our knowledge of the long-term changes which occur in organs in which L. donovani is able to persist.

摘要

在本研究中,我们分析了感染杜氏利什曼原虫的BALB/c小鼠和重度联合免疫缺陷(scid)小鼠的脾脏、骨髓及血液中的造血活性。我们的分析表明,感染会诱导祖细胞迅速但短暂地进入循环,这与粒细胞/巨噬细胞集落刺激因子(GM-CSF)和MIP-1α水平升高有关。感染后14至28天,当寄生虫在脾脏和骨髓中开始增殖时,这些器官中造血祖细胞,尤其是CFU-粒细胞、单核细胞的频率和细胞周期活性显著增加。这与GM-CSF、M-CSF和G-CSF的mRNA积累增加有关,但与白细胞介素-3无关。我们的数据还表明,通过祖细胞群体频率及其细胞周期活性水平的变化评估的造血活性,可以通过T细胞非依赖性和T细胞依赖性以及器官特异性方式进行调节。总体而言,这些数据增加了我们对杜氏利什曼原虫能够持续存在的器官中发生的长期变化的认识。

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本文引用的文献

1
Leishmania donovani infection of bone marrow stromal macrophages selectively enhances myelopoiesis, by a mechanism involving GM-CSF and TNF-alpha.杜氏利什曼原虫感染骨髓基质巨噬细胞可通过一种涉及粒细胞-巨噬细胞集落刺激因子(GM-CSF)和肿瘤坏死因子-α(TNF-α)的机制选择性增强骨髓生成。
Blood. 2000 Mar 1;95(5):1642-51.
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Leishmania donovani infection initiates T cell-independent chemokine responses, which are subsequently amplified in a T cell-dependent manner.杜氏利什曼原虫感染引发非T细胞依赖性趋化因子反应,随后以T细胞依赖性方式进行放大。
Eur J Immunol. 1999 Jan;29(1):203-14. doi: 10.1002/(SICI)1521-4141(199901)29:01<203::AID-IMMU203>3.0.CO;2-B.
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Anti-LFA-1 blocking antibodies prevent mobilization of hematopoietic progenitor cells induced by interleukin-8.
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Transcription factors that regulate monocyte/macrophage differentiation.调节单核细胞/巨噬细胞分化的转录因子。
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Neutralization of IL-12 demonstrates the existence of discrete organ-specific phases in the control of Leishmania donovani.白细胞介素-12的中和作用证明了在杜氏利什曼原虫的控制中存在离散的器官特异性阶段。
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Essential roles for granulocyte-macrophage colony-stimulating factor (GM-CSF) and G-CSF in the sustained hematopoietic response of Listeria monocytogenes-infected mice.粒细胞巨噬细胞集落刺激因子(GM-CSF)和粒细胞集落刺激因子(G-CSF)在单核细胞增生李斯特菌感染小鼠的持续造血反应中的重要作用。
Blood. 1998 Feb 1;91(3):863-9.
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Adhesion molecules in haemopoiesis.造血过程中的黏附分子。
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Biology and mechanisms of action of synergistically stimulated myeloid progenitor cell proliferation and suppression by chemokines.趋化因子协同刺激髓系祖细胞增殖和抑制的生物学及作用机制
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Impaired host defense, hematopoiesis, granulomatous inflammation and type 1-type 2 cytokine balance in mice lacking CC chemokine receptor 1.缺乏CC趋化因子受体1的小鼠的宿主防御、造血功能、肉芽肿性炎症及1型-2型细胞因子平衡受损。
J Exp Med. 1997 Jun 2;185(11):1959-68. doi: 10.1084/jem.185.11.1959.