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土拉弗朗西斯菌对红细胞的入侵。

Invasion of erythrocytes by Francisella tularensis.

机构信息

Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, PA, USA.

出版信息

J Infect Dis. 2011 Jul 1;204(1):51-9. doi: 10.1093/infdis/jir221.

DOI:10.1093/infdis/jir221
PMID:21628658
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3105038/
Abstract

Francisella tularensis is the causative agent of tularemia and is classified as a category A biodefense agent by the Centers for Disease Control and Prevention because of its highly infectious nature. F. tularensis infects leukocytes and exhibits an extracellular phase in the blood of the host. It is unknown, however, whether F. tularensis can infect erythrocytes; thus, we examined this possibility in vivo and in vitro. In the murine model of pulmonary type A tularemia, we showed the presence of intraerythrocytic bacteria by double-immunofluorescence microscopy and ex vivo gentamicin protection of the purified erythrocyte fraction. In vitro, F. tularensis invaded human erythrocytes, as shown in the gentamicin protection assays, double-immunofluorescence microscopy, flow cytometry, scanning electron microscopy, and transmission electron microscopy with immunogold labeling of the bacteria. Additional in vitro tests indicated that serum complement-dependent and complement-independent mechanisms contribute to erythrocyte invasion. Our results reveal a novel intraerythrocytic phase during F. tularensis infection.

摘要

土拉弗朗西斯菌是兔热病的病原体,因其高度传染性而被疾病预防控制中心归类为 A 类生物防御剂。土拉弗朗西斯菌感染白细胞,并在宿主血液中表现出细胞外阶段。然而,尚不清楚土拉弗朗西斯菌是否可以感染红细胞;因此,我们在体内和体外检查了这种可能性。在 A 型肺型兔热病的小鼠模型中,我们通过双重免疫荧光显微镜和体外庆大霉素保护纯化的红细胞部分显示了红细胞内细菌的存在。在体外,土拉弗朗西斯菌侵入人红细胞,如庆大霉素保护试验、双重免疫荧光显微镜、流式细胞术、扫描电子显微镜和用细菌免疫金标记的透射电子显微镜所示。额外的体外试验表明,血清补体依赖性和补体非依赖性机制有助于红细胞入侵。我们的结果揭示了土拉弗朗西斯菌感染期间的一个新的红细胞内阶段。

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本文引用的文献

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PLoS One. 2010 Jul 6;5(7):e11060. doi: 10.1371/journal.pone.0011060.
2
Francisella tularensis DeltapyrF mutants show that replication in nonmacrophages is sufficient for pathogenesis in vivo.土拉弗朗西斯菌 DeltapyrF 突变体表明,在非巨噬细胞中的复制足以在体内引起发病。
Infect Immun. 2010 Jun;78(6):2607-19. doi: 10.1128/IAI.00134-10. Epub 2010 Apr 12.
3
The life span of the human red blood cell.人类红细胞的寿命。
J Biol Chem. 1946 Dec;166(2):627-36.
4
The unraveling panoply of Francisella tularensis virulence attributes.弗氏柠檬酸杆菌毒力属性的逐渐显现。
Curr Opin Microbiol. 2010 Feb;13(1):11-7. doi: 10.1016/j.mib.2009.11.007. Epub 2009 Dec 23.
5
Exploring the mialome of ticks: an annotated catalogue of midgut transcripts from the hard tick, Dermacentor variabilis (Acari: Ixodidae).探索蜱的中肠转录组:美洲钝缘蜱(蜱螨亚纲:硬蜱科)中肠转录本注释目录
BMC Genomics. 2008 Nov 20;9:552. doi: 10.1186/1471-2164-9-552.
6
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Infect Immun. 2009 Feb;77(2):576-84. doi: 10.1128/IAI.00773-08. Epub 2008 Nov 17.
7
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Infect Immun. 2008 Dec;76(12):5843-52. doi: 10.1128/IAI.01176-08. Epub 2008 Oct 13.
8
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BMC Microbiol. 2008 Oct 8;8:172. doi: 10.1186/1471-2180-8-172.
9
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J Immunol. 2008 Oct 15;181(8):5568-78. doi: 10.4049/jimmunol.181.8.5568.
10
Infection-associated type IV secretion systems of Bartonella and their diverse roles in host cell interaction.巴尔通体与感染相关的IV型分泌系统及其在宿主细胞相互作用中的多种作用。
Cell Microbiol. 2008 Aug;10(8):1591-8. doi: 10.1111/j.1462-5822.2008.01171.x. Epub 2008 Jul 30.