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Enteropathogenic and enterohaemorrhagic Escherichia coli : even more subversive elements
Author(s) -
Wong Alexander R. C.,
Pearson Jaclyn S.,
Bright Michael D.,
Munera Diana,
Robinson Keith S.,
Lee Sau Fung,
Frankel Gad,
Hartland Elizabeth L.
Publication year - 2011
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2011.07661.x
Subject(s) - biology , effector , enteropathogenic escherichia coli , virulence , secretion , microbiology and biotechnology , pathogenicity island , type three secretion system , escherichia coli , genetics , gene , biochemistry
Summary The human pathogens enteropathogenic and enterohemorrhagic Escherichia coli (EPEC and EHEC) share a unique mechanism of colonization that results from the concerted action of effector proteins translocated into the host cell by a type III secretion system (T3SS). EPEC and EHEC not only induce characteristic attaching and effacing (A/E) lesions, but also subvert multiple host cell signalling pathways during infection. Our understanding of the mechanisms by which A/E pathogens hijack host cell signalling has advanced dramatically in recent months with the identification of novel activities for many effectors. In addition to further characterization of established effectors (Tir, EspH and Map), new effectors have emerged as important mediators of virulence through activities such as mimicry of Rho guanine nucleotide exchange factors (Map and EspM), inhibition of apoptosis (NleH and NleD), interference with inflammatory signalling pathways (NleB, NleC, NleE and NleH) and phagocytosis (EspF, EspH and EspJ). The findings have highlighted the multifunctional nature of the effectors and their ability to participate in redundant, synergistic or antagonistic relationships, acting in a co‐ordinated spatial and temporal manner on different host organelles and cellular pathways during infection.