The StcE Protease Contributes to Intimate Adherence of Enterohemorrhagic<i>Escherichia coli</i>O157:H7 to Host Cells

Grys, Thomas E.; Siegel, Matthew B.; Lathem, Wyndham W.; Welch, Rodney A.

doi:10.1128/iai.73.3.1295-1303.2005

Cited by 124 publications

(135 citation statements)

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“…In this study, two effectors of type II secretion previously suggested to contribute to adherence, StcE (Grys et al, 2005) and AdfO (Ho et al, 2008), were upregulated in TW14359. The StcE metalloprotease, the expression of which is positively influenced by Ler (Lathem et al, 2002), is hypothesized to promote adherence by cleaving proteins in the glycocalyx and mucin layers atop the intestinal epithelium, facilitating close contact with the intestinal mucosa (Grys et al, 2005). The contribution of AdfO to adherence is not clear, as an adfO mutation has been shown to markedly decrease epithelial cell adherence in vitro, but does not attenuate colonization following oral challenge of infant rabbits (Ho et al, 2008).…”

Section: Discussionmentioning

confidence: 58%

“…Mutation of etpC, the first gene in the etp operon, has been shown to result in a significant reduction of O157 : H7 colonization in an infant rabbit model of disease (Ho et al, 2008). In this study, two effectors of type II secretion previously suggested to contribute to adherence, StcE (Grys et al, 2005) and AdfO (Ho et al, 2008), were upregulated in TW14359. The StcE metalloprotease, the expression of which is positively influenced by Ler (Lathem et al, 2002), is hypothesized to promote adherence by cleaving proteins in the glycocalyx and mucin layers atop the intestinal epithelium, facilitating close contact with the intestinal mucosa (Grys et al, 2005).…”

Section: Discussionmentioning

confidence: 59%

“…The type II apparatus secretes several factors that influence colonization (Sandkvist, 2001). The transcription of one such gene, stcE (tagA), which encodes a metalloprotease that contributes to intimate adherence (Grys et al, 2005), was elevated in TW14359. Expression of adfO (ECs1772), which encodes another type II secretion effector that promotes adherence of O157 : H7 to epithelial cells (Ho et al, 2008), was also elevated in TW14359.…”

Section: Differential Expression Of Adherence and Motility Genesmentioning

confidence: 99%

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Differences in adherence and virulence gene expression between two outbreak strains of enterohaemorrhagic Escherichia coli O157 : H7

et al. 2010

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The Escherichia coli O157 : H7 TW14359 strain was implicated in a multi-state outbreak in North America in 2006, which resulted in high rates of severe disease. Similarly, the O157 : H7 RIMD0509952 (Sakai) strain caused the largest O157 : H7 outbreak to date. Both strains were shown to represent divergent phylogenetic lineages. Here we compared global gene expression patterns before and after epithelial cell exposure, as well as the ability to adhere to and invade epithelial cells, between the two outbreak strains. Epithelial cell assays demonstrated a 2.5-fold greater adherence of the TW14359 strain relative to Sakai, while whole-genome microarrays detected significant differential expression of 914 genes, 206 of which had a fold change ≥1.5. Interestingly, most locus of enterocyte effacement (LEE) genes were upregulated in TW14359, whereas flagellar and chemotaxis genes were primarily upregulated in Sakai, suggesting discordant expression of these genes between the two strains. The Shiga toxin 2 genes were also upregulated in the TW14359 strain, as were several pO157-encoded genes that promote adherence, including type II secretion genes and their effectors stcE and adfO. Quantitative RT-PCR confirmed the expression differences detected in the microarray analysis, and expression levels were lower for a subset of LEE genes before versus after exposure to epithelial cells. In all, this study demonstrated the upregulation of major and ancillary virulence genes in TW14359 and of flagellar and chemotaxis genes in Sakai, under conditions that precede intimate bacterial attachment to epithelial cells. Differences in the level of adherence to epithelial cells were also observed, implying that these two phylogenetically divergent O157 : H7 outbreak strains vary in their ability to colonize, or initiate the disease process.

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Section: Discussionmentioning

confidence: 58%

Section: Discussionmentioning

confidence: 59%

Section: Differential Expression Of Adherence and Motility Genesmentioning

confidence: 99%

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Differences in adherence and virulence gene expression between two outbreak strains of enterohaemorrhagic Escherichia coli O157 : H7

et al. 2010

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“…Upon sequencing the E. coli O157:H7 genome of strain EDL933, it was noted that this organism has at least 10 fimbrial gene clusters and 13 regions that encode nonfimbrial adhesins, some of which were not found in nonpathogenic E. coli (86,87). Extracellular structures include the E. coli YcbQ laminin-binding fimbriae (ELF) (88), two long polar fimbriae (LPF) (89,90), the F9 fimbriae (91), a type IV pilus called "hemorrhagic coli pilus" (HCP) (92), curli (93,94), OmpA (95), the EHEC factor for adherence (Efa1) (96), the IgrA homolog adhesin (Iha) (97), the ECP, the autotransporter protein EhaG (98), and the pO157 virulence plasmid-encoded StcE (99,100). Surely these molecules contribute to adherence to surfaces, both biotic and abiotic, but a comprehensive understanding of the role of these adhesins in human disease, carriage in cattle, and survival and propagation in food does not exist.…”

Section: Non-leementioning

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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“…Another recent study identified an association of a DMBT1 variant allele with Crohn's disease and also corre-lation of expression levels of DMBT1 with inflammatory bowel disease severity (44). Additionally, the pathogen Escherichia coli O157:H7 expresses a protease (StcE) that selectively degrades gp340 (19). Degradation of gp340 enhances the attachment of bacteria to epithelial cells, which indicates the importance of this glycoprotein as an innate defense factor.…”

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confidence: 99%