Bacterial-induced cell reprogramming to stem cell-like cells: new premise in host-pathogen interactions.
Bacterial-induced cell reprogramming to stem cell-like cells: new premise in host-pathogen interactions.
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DOI：
10.1016/j.mib.2014.11.021
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发表时间：
2015-02
影响因子：
5.4
通讯作者：
Rambukkana A
中科院分区：
文献类型：
--
作者：
Hess S;Rambukkana A
细菌病原体采用多种策略来改变宿主组织细胞的功能，以在感染期间获得细菌优势。最近的进展揭示了感染生物学和干细胞生物学的融合，证明了细胞内的麻风分枝杆菌将致力于谱系的宿主神经胶质细胞重新编程为祖细胞/干细胞样细胞。获得这种重新编程细胞的迁移和免疫调节特性为促进细菌传播提供了额外的优势。这呈现了一种前所未见的复杂的细胞操纵，通过劫持宿主细胞的基因组可塑性，由人类细菌病原体。宿主细胞的这种极端命运转换的基本原理可能直接与麻风杆菌极其被动的专属生活方式有关，这种生活方式具有退化的基因组和宿主细胞对细菌生存和传播的依赖，特别是使用宿主来源的干细胞样细胞作为传播感染的媒介而不被免疫细胞检测。因此，细胞重新编程和感染之间的这种意想不到的联系打开了宿主与病原体相互作用的新前提。此外，这种细菌的独创性也可以用来开发对宿主细胞进行重新编程的自然方法，以修复感染、损伤和疾病造成的受损组织。
Bacterial pathogens employ a myriad of strategies to alter host tissue cell functions for bacterial advantage during infection. Recent advances revealed a fusion of infection biology with stem cell biology by demonstrating developmental reprogramming of lineage committed host glial cells to progenitor/stem cell-like cells by an intracellular bacterial pathogen Mycobacterium leprae. Acquisition of migratory and immunomodulatory properties of such reprogrammed cells provides an added advantage for promoting bacterial spread. This presents a previously unseen sophistication of cell manipulation by hijacking the genomic plasticity of host cells by a human bacterial pathogen. The rationale for such extreme fate conversion of host cells may be directly linked to the exceedingly passive obligate life style of M. leprae with a degraded genome and host cell dependence for both bacterial survival and dissemination, particularly the use of host-derived stem cell-like cells as a vehicle for spreading infection without being detected by immune cells. Thus, this unexpected link between cell reprogramming and infection opens up a new premise in host-pathogen interactions. Furthermore, such bacterial ingenuity could also be harnessed for developing natural ways of reprogramming host cells for repairing damaged tissues from infection, injury and diseases.
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DOI：
10.1083/jcb.200912142
发表时间：
2010-05-17
期刊：
The Journal of cell biology
影响因子：
--
作者：
Finzsch M;Schreiner S;Kichko T;Reeh P;Tamm ER;Bösl MR;Meijer D;Wegner M
通讯作者：
Wegner M
影响因子：
64.5
作者：
Bold TD;Ernst JD
通讯作者：
Ernst JD
影响因子：
64.5
作者：
Hanna JH;Saha K;Jaenisch R
通讯作者：
Jaenisch R
影响因子：
30.3
作者：
Burberry A;Zeng MY;Ding L;Wicks I;Inohara N;Morrison SJ;Núñez G
通讯作者：
Núñez G
影响因子：
56.9
作者：
Jinek, Martin;Chylinski, Krzysztof;Charpentier, Emmanuelle
通讯作者：
Charpentier, Emmanuelle