Adhesion of enteropathogenic Escherichia coli to host cells

Nougayrède, Jean-Philippe; Fernandes, P.J.L.; Donnenberg, Michael S.

doi:10.1046/j.1462-5822.2003.00281.x

Cited by 157 publications

(115 citation statements)

References 132 publications

(194 reference statements)

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“…If so, it is possible that host proteins are not necessary for formation of the moving junction and this would help to explain how Toxoplasma can invade any nucleated cell. This scenario shares intriguing similarities with the TIR proteins from enteropathogenic E. coli, in which the bacterium inserts its own receptors into the host cell for attachment [27]. Alternatively, the RON2/4/5/AMA1 protein complex could interact with host proteins at the moving junction, but such host receptors would need to be nearly universal to account for the broad host cell range infected by this parasite.…”

Section: Defining the Moving Junctionmentioning

confidence: 99%

Rhoptries: an arsenal of secreted virulence factors

Bradley

Sibley

2007

Current Opinion in Microbiology

179

142

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Apicomplexan parasites use actin-based motility coupled with regulated protein secretion from apical organelles to actively invade host cells. Critical in this process are rhoptries, club-shaped secretory organelles that discharge their contents during parasite invasion into host cells. A proteomic analysis of the rhoptries in Toxoplasma gondii demonstrated that this organelle contains a number of novel rhoptry proteins (ROP) including serine-threonine kinases and protein phosphatases. A subset of ROP proteins have been shown to target to the moving junction, which plays a key role in invasion and parasitophorous vacuole formation. Other ROP proteins have various destinations in the host cell including the host cell nucleus and the parasitophorous vacuole, likely reflecting their distinct targets and roles. Forward genetic analysis recently revealed that secretory ROP kinases dramatically influence host gene expression and are the major parasite virulence factors. Thus, ROP proteins are functionally analogous (although not homologous) to effectors released by type III and IV secretion systems, which are factors that play an important role in bacterial virulence. Deciphering the role of ROP effectors may allow specific disruption of these factors, thus offering new options for preventing disease.

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Section: Defining the Moving Junctionmentioning

confidence: 99%

Rhoptries: an arsenal of secreted virulence factors

Bradley

Sibley

2007

Current Opinion in Microbiology

179

142

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“…Propidium iodide counter-staining of specimens confirmed co-localization of actin pedestals and bacteria. Both strains demonstrated the ability to form densely packed microcolonies, or 'localized adherence' (Dibb-Fuller et al, 2001;Matthews et al, 1997;Naylor et al, 2005;Nougayrede et al, 2003), on the surface of MAC-T cells. A/E lesions were not observed following infection with E. coli K-12 (Fig.…”

Section: Interaction Of O157 : H7 With Mac-t Bovine Epithelial Cellsmentioning

confidence: 99%

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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“…Belonging to a family of related gram-negative pathogenic bacteria that includes enterohemorrhagic E. coli (EHEC) and the mouse pathogen Citrobacter rodentium (28), EPEC strains are noninvasive, infecting their hosts by attaching to intestinal epithelial cells (IEC), effacing the epithelial microvilli, and producing pedestal-like structures (2,29). The formation of attaching and effacing (A/E) lesions is required for these microbes to cause diarrheal disease (8,34,42); thus, many studies have characterized the virulence factors used by A/E bacteria to infect their hosts.…”

mentioning

confidence: 99%

Flagellin-Dependent and -Independent Inflammatory Responses following Infection by EnteropathogenicEscherichia coliandCitrobacter rodentium

Khan

Bouzari

et al. 2008

Infect Immun

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Enteropathogenic Escherichia coli (EPEC) and the murine pathogen Citrobacter rodentium belong to the attaching and effacing (A/E) family of bacterial pathogens. These noninvasive bacteria infect intestinal enterocytes using a type 3 secretion system (T3SS), leading to diarrheal disease and intestinal inflammation. While flagellin, the secreted product of the EPEC fliC gene, causes the release of interleukin 8 (IL-8) from epithelial cells, it is unclear whether A/E bacteria also trigger epithelial inflammatory responses that are FliC independent. The aims of this study were to characterize the FliC dependence or independence of epithelial inflammatory responses to direct infection by EPEC or C. rodentium. Following infection of Caco-2 intestinal epithelial cells by wild-type and ⌬fliC EPEC, a rapid activation of several proinflammatory genes, including those encoding IL-8, monocyte chemoattractant protein 1, macrophage inflammatory protein 3␣ (MIP3␣), and ␤-defensin 2, occurred in a FliC-dependent manner. These responses were accompanied by mitogen-activated protein kinase activation, as well as the Toll-like receptor 5 (TLR5)-dependent activation of NF-B. At later infection time points, a subset of these proinflammatory genes (IL-8 and MIP3␣) was also induced in cells infected with ⌬fliC EPEC. The nonmotile A/E pathogen C. rodentium also triggered similar innate responses through a TLR5-independent but partially NF-B-dependent mechanism. Moreover, the EPEC FliC-independent responses were increased in the absence of the locus of enterocyte effacement-encoded T3SS, suggesting that translocated bacterial effectors suppress rather than cause the FliC-independent inflammatory response. Thus, we demonstrate that infection of intestinal epithelial cells by A/E pathogens can trigger an array of proinflammatory responses from epithelial cells through both FliC-dependent and -independent pathways, expanding our understanding of the innate epithelial response to infection by these pathogens.

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Adhesion of enteropathogenic Escherichia coli to host cells

Cited by 157 publications

References 132 publications

Rhoptries: an arsenal of secreted virulence factors

Rhoptries: an arsenal of secreted virulence factors

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

Flagellin-Dependent and -Independent Inflammatory Responses following Infection by EnteropathogenicEscherichia coliandCitrobacter rodentium

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