EspG, a Novel Type III System-Secreted Protein from Enteropathogenic
            <i>Escherichia coli</i>
            with Similarities to VirA of
            <i>Shigella flexneri</i>

Elliott, Simon J.; Krejany, Efrosinia O.; Mellies, Jay L.; Robins-Browne, Roy M.; Sasakawa, Chihiro; Kaper, James B.

doi:10.1128/iai.69.6.4027-4033.2001

Cited by 154 publications

(170 citation statements)

References 30 publications

(37 reference statements)

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“…To date, seven EPEC and EHEC effector molecules have been shown to be injected into the host cell by the TTSS. Five translocated effectors are encoded by LEE: Tir/EspE [35,88], Map [87], EspF [109], EspG [45] and EspH [169]. Two effectors are encoded outside the LEE by lambdoid prophages: Cif [104] and NleA/EspI [62,118].…”

Section: The Locus For Enterocyte Effacementmentioning

confidence: 99%

Enterohaemorrhagic Escherichia coli: emerging issues on virulence and modes of transmission

et al. 2005

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-Enterohaemorrhagic Escherichia coli (EHEC) constitute a subset of serotypes (E. coli O157 and some other serogroups) of Shiga toxin (Stx)-producing E. coli (STEC) firmly associated with severe human illnesses like bloody diarrhoea and haemolytic uraemic syndrome. Stx production is essential but not sufficient for EHEC virulence. Most strains are capable of colonising the intestinal mucosa of the host with the "attaching and effacing" mechanism, genetically governed by a large pathogenicity island (PAI) defined as the Locus of Enterocyte Effacement. Other virulence factors carried by mobile genetic elements like PAI and plasmids have been recently described, and their role in the pathogenic process has not been fully elucidated. EHEC are zoonotic pathogens. They rarely cause disease in animals, and ruminants are recognised as their main natural reservoir. Cattle are considered to be the most important source of human infections with EHEC O157, and the ecology of the organism in cattle farming has been extensively studied. The organism has also been reported in sheep, goats, water buffalos, and deer. Pigs and poultry are not considered to be a source of EHEC and the sporadic reports may derive from accidental exposure to ruminant dejections. The epidemiology of EHEC infections has remarkably changed during the past ten years and an increasing number of unusual food vehicles have been associated with human infections. New routes of transmission have emerged, like contact with animals during farm visits and a wide variety of environment-related exposures. As for other zoonotic agents, having animals and raw products that are free from EHEC is not possible in practice. However, their occurrence can be minimised by applying high standards of hygiene in all the steps of the food production chain.

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Section: The Locus For Enterocyte Effacementmentioning

confidence: 99%

Enterohaemorrhagic Escherichia coli: emerging issues on virulence and modes of transmission

et al. 2005

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“…The genes that are involved in the formation of the AE lesion are encoded by the locus of enterocyte effacement (LEE) chromosomal pathogenicity island 39 . The LEE region encodes a T3SS 40 , an adhesin 41 and its receptor 42 , and effector proteins [43][44][45][46][47] . The mortality that is associated with EHEC infections stems from the production and release of potent Shiga toxin.…”

Section: Ehec As a Case Study: Lessons From A Hijackermentioning

confidence: 99%

Inter-kingdom signalling: communication between bacteria and their hosts

Hughes

Sperandio²

2008

Nat Rev Microbiol

639

468

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Microorganisms and their hosts communicate with each other through an array of hormonal signals. This cross-kingdom cell-to-cell signalling involves small molecules, such as hormones that are produced by eukaryotes and hormone-like chemicals that are produced by bacteria. Cell-to-cell signalling between bacteria, usually referred to as quorum sensing, was initially described as a means by which bacteria achieve signalling in microbial communities to coordinate gene expression within a population. Recent evidence shows, however, that quorum-sensing signalling is not restricted to bacterial cell-to-cell communication, but also allows communication between microorganisms and their hosts.Prokaryotes and eukaryotes have coexisted for millions of years. It is estimated that humans have 10 13 human cells and 10 14 bacterial cells (comprising the endogenous bacterial flora). Eukaryotes have a variable relationship with prokaryotes, and these interactions can be either beneficial or detrimental. Humans maintain a symbiotic association with their intestinal microbial flora, which is crucial for nutrient assimilation and development of the innate immune system 1 . These mutually beneficial associations are possible because microorganisms and mammals can communicate with each other through various hormone and hormone-like chemical compounds. These signals, however, can be 'hijacked' by bacterial pathogens to activate their virulence genes.The hormonal communication between microorganisms and their hosts, dubbed inter-kingdom signalling, is a recent field of research. This field evolved from the initial observation that bacteria can communicate with each other through hormone-like signals 2 , a process that was later named quorum sensing (QS) 3 . This field expanded with the realization that these bacterial signals can modulate mammalian cell-signal transduction 4 and that host hormones can crosssignal with QS signals to modulate bacterial gene expression 5 .In this Review, we discuss several mechanisms that are used for hormonal communication between micro-organisms and their hosts. Owing to space constraints, we mainly consider pathogenic interactions. We focus primarily on acyl-homoserine lactones (AHLs) and aromatic (autoinducer (AI)-3) signals, because of the wealth of reports that link these signals to interkingdom communication, but it is worth noting that bacteria use an array of additional chemical

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“…Three additional proteins, EspA, EspB and EspD, are required for protein translocation into host cells but not for secretion . Five EPEC effectors were identified that are translocated by TTSS into the host cell: Tir (EspE), EspB, EspF, EspG and Map Deibel et al, 1998;Wolff et al, 1998;Kenny and Jepson, 2000;Crane et al, 2001;Elliott et al, 2001;McNamara et al, 2001). Map appears to interfere with the mitochondria membrane potential (Kenny and Jepson, 2000).…”

mentioning

confidence: 99%

“…EspF has been implicated in the disruption of tight junction structure and in the induction of apoptosis (Crane et al, 2001;McNamara et al, 2001). No apparent phenotype was identified in espG knock-out (Elliott et al, 2001). In addition to the local assembly of actin pedestals, EPEC exerts more global effects on the host cell cytoskeleton.…”

mentioning

confidence: 99%

Enteropathogenic Escherichia coli induces modification of the focal adhesions of infected host cells

et al. 2002

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SummaryEnteropathogenic Escherichia coli (EPEC) is a human-specific pathogen that causes severe diarrhoea in young children. The disease involves intimate interaction between the pathogen and the brush border of enterocytes. During infection, EPEC uses a type III secretion system (TTSS) to inject several proteins into the infected cells, and these effector proteins modify specific processes in the host cell. We show that, upon infection, EPEC induces detachment of the infected host cells from the substratum, modification of focal adhesions (FA) in the infected cells and specific dephosphorylation of focal adhesion kinase (FAK). We also show that EPEC-induced cell detachment is dependent on FAK expression by the infected cells. Finally, we demonstrate that cell detachment, FA modification and FAK dephosphorylation are dependent on functional TTSS in the infecting EPEC. These results suggest that EPEC is using its TTSS to inject protein(s) into the infected cells, which can induce FAK dephosphorylation, as well as FAK-dependent FA modification and cell detachment. These processes are specific and probably play an important role in EPEC virulence.

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EspG, a Novel Type III System-Secreted Protein from Enteropathogenic Escherichia coli with Similarities to VirA of Shigella flexneri

Cited by 154 publications

References 30 publications

Enterohaemorrhagic Escherichia coli: emerging issues on virulence and modes of transmission

Enterohaemorrhagic Escherichia coli: emerging issues on virulence and modes of transmission

Inter-kingdom signalling: communication between bacteria and their hosts

Enteropathogenic Escherichia coli induces modification of the focal adhesions of infected host cells

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