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侵袭性细菌对宿主信号转导通路和细胞骨架功能的利用。

Exploitation of host signal transduction pathways and cytoskeletal functions by invasive bacteria.

作者信息

Rosenshine I, Finlay B B

机构信息

Department of Biochemistry, University of British Columbia, Vancouver, Canada.

出版信息

Bioessays. 1993 Jan;15(1):17-24. doi: 10.1002/bies.950150104.

Abstract

Many bacteria that cause disease have the capacity to enter into and live within eukaryotic cells such as epithelial cells and macrophages. The mechanisms used by these organisms to achieve and maintain this intracellular lifestyle vary considerably, but most mechanisms involve subversion and exploitation of host cell functions. Entry into non-phagocytic cells involves triggering host signal transduction mechanisms to induce rearrangement of the host cytoskeleton, thereby facilitating bacterial uptake. Once inside the host cell, intracellular pathogens either remain within membrane bound inclusions or escape to the cytoplasm. Those living in the cytoplasm can further pirate the host actin system, using actin as a mechanism to facilitate movement within and between host cells. Organisms remaining within the vacuole have specialized mechanisms for intracellular survival and growth which involve additional communication with the host cell. Some of the processes involved in the various steps of facultative intracellular parasitism are discussed in the context of subverting the host cell cytoskeleton and signal transduction pathways for bacterial benefit.

摘要

许多致病细菌能够进入真核细胞(如上皮细胞和巨噬细胞)并在其中生存。这些微生物实现并维持这种细胞内生活方式所采用的机制差异很大,但大多数机制都涉及对宿主细胞功能的颠覆和利用。进入非吞噬细胞需要触发宿主信号转导机制,以诱导宿主细胞骨架重排,从而促进细菌摄取。一旦进入宿主细胞,细胞内病原体要么留在膜结合的内含物中,要么逃逸到细胞质中。那些生活在细胞质中的病原体可以进一步盗用宿主肌动蛋白系统,利用肌动蛋白作为在宿主细胞内和细胞间移动的机制。留在液泡内的生物体具有专门的细胞内存活和生长机制,这涉及与宿主细胞的额外通讯。本文将在为细菌谋利而颠覆宿主细胞骨架和信号转导途径的背景下,讨论兼性细胞内寄生各个步骤中涉及的一些过程。

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