Format

Send to

Choose Destination
Curr Top Microbiol Immunol. 2018;416:1-26. doi: 10.1007/82_2018_104.

Shigella and Enteroinvasive Escherichia Coli.

Author information

1
Unité de Pathogénie Microbienne Moléculaire, Institut Pasteur, 28 Rue Du Dr Roux, 75724 Cedex 15, Paris, France. ilia.belotserkovsky@mail.huji.ac.il.
2
Microbiologie et Maladies Infectieuses, Collège de France, 11 Place Marcelin Berthelot, 75005, Paris, France.

Abstract

Shigella and enteroinvasive Escherichia coli (EIEC) are gram-negative bacteria responsible for bacillary dysentery (shigellosis) in humans, which is characterized by invasion and inflammatory destruction of the human colonic epithelium. Different EIEC and Shigella subgroups rose independently from commensal E. coli through patho-adaptive evolution that included loss of functional genes interfering with the virulence and/or with the intracellular lifestyle of the bacteria, as well as acquisition of genetic elements harboring virulence genes. Among the latter is the large virulence plasmid encoding for a type three secretion system (T3SS), which enables translocation of virulence proteins (effectors) from the bacterium directly into the host cell cytoplasm. These effectors enable the pathogen to subvert epithelial cell functions, promoting its own uptake, replication in the host cytosol, and dissemination to adjacent cells while concomitantly inhibiting pro-inflammatory cell death. Furthermore, T3SS effectors are directly involved in Shigella manipulation of immune cells causing their dysfunction and promoting cell death. In the current chapter, we first describe the evolution of the enteroinvasive pathovars and then summarize the overall knowledge concerning the pathogenesis of these bacteria, with a particular focus on Shigella flexneri. Subversion of host cell functions in the human gut, both epithelial and immune cells, by different virulence factors is especially highlighted.

PMID:
30218158
DOI:
10.1007/82_2018_104
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center