The Interacting Cra and KdpE Regulators Are Involved in the Expression of Multiple Virulence Factors in Enterohemorrhagic Escherichia coli

Njoroge, Jacqueline W.; Gruber, Charley C.; Sperandio, Vanessa

doi:10.1128/jb.02252-12

Cited by 42 publications

(36 citation statements)

References 66 publications

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“…However, we also reported that in the presence of E. coli MG1655, E. coli EDL933 switches, at least in part, to gluconeogenesis in order to maintain itself in the intestine, while E. coli MG1655 continues to use glycolytic nutrients exclusively (15). These findings are of extreme interest in view of recent reports showing that E. coli 86-24, also an O157:H7 strain, activates the expression of virulence genes under gluconeogenic conditions (16,17), because this suggests the possibility that precolonization of the intestine with a probiotic E. coli strain that starves E. coli O157:H7 strains of gluconeogenic nutrients might render them nonpathogenic.…”

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confidence: 38%

“…It was reported recently that E. coli 86-24, an O157:H7 strain, activates the expression of virulence genes under gluconeogenic conditions (16,17). The present study was undertaken to determine whether E. coli Nissle 1917, routinely used as a probiotic agent, depletes gluconeogenic nutrients by using them for growth in the mouse intestine, thereby preventing E. coli EDL933, also an O157:H7 strain, from activating virulence gene expression.…”

Section: Discussionmentioning

confidence: 99%

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Escherichia coli EDL933 Requires Gluconeogenic Nutrients To Successfully Colonize the Intestines of Streptomycin-Treated Mice Precolonized with E. coli Nissle 1917

et al. 2015

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bEscherichia coli MG1655, a K-12 strain, uses glycolytic nutrients exclusively to colonize the intestines of streptomycin-treated mice when it is the only E. coli strain present or when it is confronted with E. coli EDL933, an O157:H7 strain. In contrast, E. coli EDL933 uses glycolytic nutrients exclusively when it is the only E. coli strain in the intestine but switches in part to gluconeogenic nutrients when it colonizes mice precolonized with E. -12) reported that E. coli 86-24, an O157:H7 strain, activates the expression of virulence genes under gluconeogenic conditions, suggesting that colonization of the intestine with a probiotic E. coli strain that outcompetes O157:H7 strains for gluconeogenic nutrients could render them nonpathogenic. Here we report that E. coli Nissle 1917, a probiotic strain, uses both glycolytic and gluconeogenic nutrients to colonize the mouse intestine between 1 and 5 days postfeeding, appears to stop using gluconeogenic nutrients thereafter in a large, long-term colonization niche, but continues to use them in a smaller niche to compete with invading E. coli EDL933. Evidence is also presented suggesting that invading E. coli EDL933 uses both glycolytic and gluconeogenic nutrients and needs the ability to perform gluconeogenesis in order to colonize mice precolonized with E. coli Nissle 1917. The data presented here therefore rule out the possibility that E. coli Nissle 1917 can starve the O157:H7 E. coli strain EDL933 of gluconeogenic nutrients, even though E. coli Nissle 1917 uses such nutrients to compete with E. coli EDL933 in the mouse intestine. While much attention has been paid to the role of specific virulence factors in bacterial pathogenesis, until recently little attention has been paid to the roles of specific metabolic pathways in the ability of bacterial pathogens to initiate the pathogenic process. Yet clearly, if a bacterial pathogen is unable to initiate pathogenesis because nutrients essential for its growth are unavailable in the host, it will be unable to establish itself and cause disease. Therefore, it is important to determine whether pathogens require glycolytic nutrients, gluconeogenic nutrients, or both for success in invading and subsequently colonizing the host. Indeed, recent studies have suggested that some pathogens use glycolytic nutrients, some use gluconeogenic nutrients, and some use both to adapt to diverse host habitats (1-7).We are interested in the nutritional basis of Escherichia coli colonization of the intestine and particularly in whether precolonization by commensal E. coli strains can be used to prevent invading E. coli intestinal pathogens from colonizing. Commensal E. coli strains colonize the human intestine in the presence of a dense and diverse intestinal microbiota comprising at least 500 cultivable species and 10 13 to 10 14 total bacteria (8). Unfortunately, E. coli colonization cannot be studied experimentally in conventional animals due to colonization resistance, which occurs when all niches are filled by the microbiota (9)....

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confidence: 38%

Section: Discussionmentioning

confidence: 99%

Escherichia coli EDL933 Requires Gluconeogenic Nutrients To Successfully Colonize the Intestines of Streptomycin-Treated Mice Precolonized with E. coli Nissle 1917

et al. 2015

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“…In addition, ethanolamine, a cell membrane component, stimulates ler production through EutR and QseC (38). Gluconeogenic conditions of the large intestine activate the ler activators KdpE and Cra, and butyrate directly activates LEE transcriptional activity (37,125). The RNA chaperone Hfq affects LEE expression through interactions with Ler mRNA but has negative or positive effects depending on the strain of EHEC, as indicated by a dashed arrow (71)(72)(73).…”

Section: Figure 4 Stimulation Of Lee and Non-lee Effector Molecules Rmentioning

confidence: 99%

“…The genes espFu and espJ are influenced by changes in temperature, pH, osmolarity, and oxygen pressure (124). The regulators KdpE and Cra act to increase expression of espFu (125). The QseEF two-component, quorumsensing system controls expression of EspFu through AI-3, epinephrine, and norepinephrine signaling (85) (Fig.…”

Section: Injection Of Effectorsmentioning

confidence: 99%

Enterohemorrhagic Escherichia coli Virulence Gene Regulation

Mellies

Lorenzen

2014

Microbiol Spectr

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Coordinated expression of enterohemorrhagic Escherichia coli virulence genes enables the bacterium to cause hemorrhagic colitis and the complication known as hemolytic-uremic syndrome. Horizontally acquired genes and those common to E. coli contribute to the disease process, and increased virulence gene expression is correlated with more severe disease in humans. Researchers have gained considerable knowledge about how the type III secretion system, secreted effectors, adhesin molecules, and the Shiga toxins are regulated by environmental signals and multiple genetic pathways. Also emergent from the data is an understanding of how enterohemorrhagic E. coli regulates response to acid stress, the role of flagellar motility, and how passage through the human host and bovine intestinal tract causes disease and supports carriage in the cattle reservoir, respectively. Particularly exciting areas of discovery include data suggesting how expression of the myriad effectors is coordinately regulated with their cognate type III secretion system and how virulence is correlated with bacterial metabolism and gut physiology.As a species, Escherichia coli is highly successful, adapting to inhabit the lower intestine of warm-blooded animals. Commensal E. coli, part of the normal biota, resides harmlessly in the gut, producing vitamin K. However, E. coli also causes three types of disease in humans: urinary tract infections, sepsis in newborns, and diarrheal disease. Enterohemorrhagic E. coli (EHEC) plays a prominent role in the third type of illness. It has been estimated that, for the pan genome of E. coli, the nonpathogenic and pathogenic strains only contain a core set of genes comprising approximately 20% of any one genome (1, 2). Much of the horizontally acquired genetic information is clustered within genomic islands in pathogens. As for EHEC, this has allowed the organism to not only attach and colonize the large intestine of humans and other animals, to outcompete commensal E. coli and other bacteria at the site of infection, but also to cause serious disease.Horizontally acquired genetic information in EHEC results in evolution into a specific pathotype-genotype dictates phenotype. How this genetic information is controlled is of equal importance for the success and virulence of the organism. Indeed, investigated differences in virulence gene regulation in two distinct EHEC isolate lineages, clade 8 and clade 2. A clade is a group of EHEC isolates with one ancestor and all its descendants. Eight clades of E. coli O157 isolates were defined by single nucleotide polymorphism (SNP) analyses, where clade 8 was a group of hypervirulent bacteria compared to the other seven clades (4). By examining multiple strains per lineage, the investigators found increased expression of horizontally acquired virulence genes in clade 8 versus clade 2. Genes expressed to higher levels in clade 8, which is associated with a greater number of cases of E. coli hemorrhagic

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“…Simi-larly, GI genes can be regulated by proteins encoded by the same GI, another GI, or the bacterial host genome, indicating that GIs are well adapted to their hosts. Therefore, GI genes can be regulated by some environmental signals, such as pH (115), osmolarity (116), temperature (117), cell density (118), or the concentration of specific elements (116,(119)(120)(121).…”

Section: Mobile Elementsmentioning

confidence: 99%

Bacterial Genome Instability

Darmon

Leach

2014

Microbiol Mol Biol Rev

348

289

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SUMMARY Bacterial genomes are remarkably stable from one generation to the next but are plastic on an evolutionary time scale, substantially shaped by horizontal gene transfer, genome rearrangement, and the activities of mobile DNA elements. This implies the existence of a delicate balance between the maintenance of genome stability and the tolerance of genome instability. In this review, we describe the specialized genetic elements and the endogenous processes that contribute to genome instability. We then discuss the consequences of genome instability at the physiological level, where cells have harnessed instability to mediate phase and antigenic variation, and at the evolutionary level, where horizontal gene transfer has played an important role. Indeed, this ability to share DNA sequences has played a major part in the evolution of life on Earth. The evolutionary plasticity of bacterial genomes, coupled with the vast numbers of bacteria on the planet, substantially limits our ability to control disease.

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The Interacting Cra and KdpE Regulators Are Involved in the Expression of Multiple Virulence Factors in Enterohemorrhagic Escherichia coli

Cited by 42 publications

References 66 publications

Escherichia coli EDL933 Requires Gluconeogenic Nutrients To Successfully Colonize the Intestines of Streptomycin-Treated Mice Precolonized with E. coli Nissle 1917

Escherichia coli EDL933 Requires Gluconeogenic Nutrients To Successfully Colonize the Intestines of Streptomycin-Treated Mice Precolonized with E. coli Nissle 1917

Enterohemorrhagic Escherichia coli Virulence Gene Regulation

Bacterial Genome Instability

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