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The versatility of Shigella effectors

Abstract

When Shigella infect the intestinal epithelium, they deliver several effectors through the type III secretion system (T3SS) into the surrounding space and directly into the host-cell cytoplasm, where they can mimic and usurp host cellular functions or subvert host-cell signalling pathways and the immune response. Although bacterial strategies and mechanisms of infection vary greatly, recent studies of Shigella effectors have revealed that Shigella possess a highly evolved strategy for infection.

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Figure 1: A simplified model of membrane-ruffle production in response to the stimulation of host cellular signalling by Shigella effectors.
Figure 2: Shigella movement within the host-cell cytoplasm requires actin polymerization and microtubule degradation.
Figure 3: Shigella and the downregulation of the host inflammatory response.

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Acknowledgements

This work was supported by a Grant-in-aid for the Scientific Research on Priority Areas, Grant-in-aid-for Scientific Research (C) and Grant-in-aid-for Young Scientists (B) from the Ministry of Education, Culture, Sports, Science and Technology of Japan (MEXT) and the Special Coordination Funds for Promoting Science from Japan Science and Technology Agency (JSTA).

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Correspondence to Chihiro Sasakawa.

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DATABASES

Entrez Genome Project

Bradyrhizobium japonicum

Burkholderia pseudomallei

Campylobacter jejuni

Coxiella burnetii

Edwardsiella ictaluri

Escherichia coli

Helicobacter pylori

Legionella pneumophila

Listeria monocytogenes

Mycobacterium marinum

Mycobacterium tuberculosis

Pseudomonas syringae

Rickettsia conorii

Salmonella typhi

Shigella dysenteriae

Staphylococcus aureus

Streptococcus pyogenes

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Ogawa, M., Handa, Y., Ashida, H. et al. The versatility of Shigella effectors. Nat Rev Microbiol 6, 11–16 (2008). https://doi.org/10.1038/nrmicro1814

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