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结核分枝杆菌与宿主细胞之间的相互作用：分枝杆菌糖类是关键所在吗？

Interactions between Mycobacterium tuberculosis and host cells: are mycobacterial sugars the key?

作者信息

Ehlers M R, Daffé M

机构信息

BioNebraska Inc., Lincoln, NE 68524, USA.

出版信息

Trends Microbiol. 1998 Aug;6(8):328-35. doi: 10.1016/s0966-842x(98)01301-8.

DOI:10.1016/s0966-842x(98)01301-8
PMID:9746944
Abstract

Mycobacterium tuberculosis has evolved successful strategies to invade and persist within macrophages. Intimate pathogen-macrophage contacts dictate receptor choice and probably specify the intracellular fate of these microorganisms. Binding to specific receptors, such as complement receptor type 3, could provide an advantage. These interactions appear to involve surface polysaccharides and glycolipids.

摘要

结核分枝杆菌已经进化出成功的策略来侵入巨噬细胞并在其中持续存在。病原体与巨噬细胞的紧密接触决定了受体的选择，并可能决定这些微生物在细胞内的命运。与特定受体（如3型补体受体）结合可能具有优势。这些相互作用似乎涉及表面多糖和糖脂。

相似文献

1
Interactions between Mycobacterium tuberculosis and host cells: are mycobacterial sugars the key?结核分枝杆菌与宿主细胞之间的相互作用：分枝杆菌糖类是关键所在吗？
Trends Microbiol. 1998 Aug;6(8):328-35. doi: 10.1016/s0966-842x(98)01301-8.
2
The 19-kDa antigen of Mycobacterium tuberculosis is a major adhesin that binds the mannose receptor of THP-1 monocytic cells and promotes phagocytosis of mycobacteria.结核分枝杆菌的19-kDa抗原是一种主要黏附素，可与THP-1单核细胞的甘露糖受体结合并促进分枝杆菌的吞噬作用。
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DC-SIGN and mannosylated surface structures of Mycobacterium tuberculosis: a deceptive liaison.DC-SIGN 与结核分枝杆菌的甘露糖化表面结构：一场欺骗性的勾结。
Eur J Cell Biol. 2010 Jan;89(1):95-101. doi: 10.1016/j.ejcb.2009.10.004. Epub 2009 Nov 4.
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Absence of complement receptor 3 results in reduced binding and ingestion of Mycobacterium tuberculosis but has no significant effect on the induction of reactive oxygen and nitrogen intermediates or on the survival of the bacteria in resident and interferon-gamma activated macrophages.补体受体3的缺失导致结核分枝杆菌的结合和摄取减少，但对活性氧和氮中间体的诱导或细菌在驻留巨噬细胞和干扰素-γ激活的巨噬细胞中的存活没有显著影响。
Microb Pathog. 2005 Sep;39(3):57-67. doi: 10.1016/j.micpath.2005.05.001.
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Activation of human neutrophils by mycobacterial phenolic glycolipids.分枝杆菌酚糖脂对人中性粒细胞的激活作用。
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The glycan-rich outer layer of the cell wall of Mycobacterium tuberculosis acts as an antiphagocytic capsule limiting the association of the bacterium with macrophages.结核分枝杆菌细胞壁富含聚糖的外层起着抗吞噬荚膜的作用，限制了该细菌与巨噬细胞的结合。
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PstS-1, the 38-kDa Mycobacterium tuberculosis glycoprotein, is an adhesin, which binds the macrophage mannose receptor and promotes phagocytosis.结核分枝杆菌38千道尔顿糖蛋白PstS-1是一种黏附素，它能结合巨噬细胞甘露糖受体并促进吞噬作用。
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Surfactant protein D binds to Mycobacterium tuberculosis bacilli and lipoarabinomannan via carbohydrate-lectin interactions resulting in reduced phagocytosis of the bacteria by macrophages.表面活性蛋白D通过碳水化合物-凝集素相互作用与结核分枝杆菌及脂阿拉伯甘露聚糖结合，导致巨噬细胞对细菌的吞噬作用减弱。
J Immunol. 1999 Jul 1;163(1):312-21.
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Selective receptor blockade during phagocytosis does not alter the survival and growth of Mycobacterium tuberculosis in human macrophages.吞噬作用期间的选择性受体阻断不会改变结核分枝杆菌在人类巨噬细胞中的存活和生长。
Am J Respir Cell Mol Biol. 1996 Dec;15(6):760-70. doi: 10.1165/ajrcmb.15.6.8969271.
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Overexpression of Mycobacterium tuberculosis manB, a phosphomannomutase that increases phosphatidylinositol mannoside biosynthesis in Mycobacterium smegmatis and mycobacterial association with human macrophages.结核分枝杆菌manB的过表达，manB是一种磷酸甘露糖变位酶，可增加耻垢分枝杆菌中磷脂酰肌醇甘露糖苷的生物合成以及分枝杆菌与人类巨噬细胞的关联。
Mol Microbiol. 2005 Nov;58(3):774-90. doi: 10.1111/j.1365-2958.2005.04862.x.

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