Relevant bibliographies by topics / Enterohemorrhagic Escherichia coli

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Enterohemorrhagic Escherichia coli'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 July 2024

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Journal articles on the topic "Enterohemorrhagic Escherichia coli"

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Kaper, James B. "Enterohemorrhagic Escherichia coli." Current Opinion in Microbiology 1, no. 1 (February 1998): 103–8. http://dx.doi.org/10.1016/s1369-5274(98)80149-5.

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Kilic, Abdullah. "Enterohemorrhagic Escherichia coli (EHEC)." TAF Preventive Medicine Bulletin 10, no. 4 (2011): 387. http://dx.doi.org/10.5455/pmb.20110823054010.

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Fan, K. T., G. J. Whitman, and F. S. Chew. "Enterohemorrhagic Escherichia coli colitis." American Journal of Roentgenology 166, no. 4 (April 1996): 788. http://dx.doi.org/10.2214/ajr.166.4.8610550.

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Welinder-Olsson, Christina, and Bertil Kaijser. "Enterohemorrhagic Escherichia coli (EHEC)." Scandinavian Journal of Infectious Diseases 37, no. 6-7 (January 2005): 405–16. http://dx.doi.org/10.1080/00365540510038523.

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Schnabel, Uta. "Inactivation of Escherichia coliK-12 and enterohemorrhagic Escherichia coli (EHEC) by atmospheric pressure plasma." Journal of Agricultural Science and Applications 03, no. 03 (September 4, 2014): 81–91. http://dx.doi.org/10.14511/jasa.2014.030305.

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Oishi, Kazunori, Yuichiro Yahata, and Yukihiro Akeda. "8. Enterohemorrhagic Escherichia Coli Infection." Nihon Naika Gakkai Zasshi 102, no. 11 (2013): 2854–59. http://dx.doi.org/10.2169/naika.102.2854.

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Petras, Robert E. "Enterohemorrhagic Escherichia coli-Associated Colitis." Pathology Case Reviews 2, no. 2 (March 1997): 66–70. http://dx.doi.org/10.1097/00132583-199702020-00002.

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DESMARCHELIER, PATRICIA M. "Enterohemorrhagic Escherichia coli—The Australian Perspective†." Journal of Food Protection 60, no. 11 (November 1, 1997): 1447–50. http://dx.doi.org/10.4315/0362-028x-60.11.1447.

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Food borne transmission of hemolytic uremic syndrome (HUS) was first reported in Australia in 1995 when an outbreak of HUS due to Escherichia coli O111 occurred following the consumption of locally produced mettwurst. Federal and state health and food authorities responded rapidly to bring the outbreak under control. Longer-term responses include the introduction by regulatory authorities of a code of practice for uncooked fermented comminuted meat products, the provision of government and industry funds to support the implementation of this code, and research into the ecology and epidemiology of enterohemorrhagic Escherichia coli and the safe production of meat. In addition, general awareness has increased, and activities in food safety control among all sectors has been stimulated. The pattern of EHEC serotypes in the Australian human and animal populations appears different from that in countries in the Northern Hemisphere. Serotype O157:H7 is not the predominant serotype isolated. Other serotypes, including O111, are more common and possess a variety of virulence-associated determinants. Research into food safety and EHEC is therefore aimed at the development of detection methods more appropriate for the Australian situation. Additional research objectives include determining both the prevalence of EHEC in meat and the meat animal population and farming and handling practices that influence EHEC carriage and transmission. These activities will contribute to an assessment of the hazards presented by EHEC in Australia and recommendations for their control.
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Orth, D., and R. Wurzner. "What Makes an Enterohemorrhagic Escherichia coli?" Clinical Infectious Diseases 43, no. 9 (November 1, 2006): 1168–69. http://dx.doi.org/10.1086/508207.

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Benjamin, M. M., and A. R. Datta. "Acid tolerance of enterohemorrhagic Escherichia coli." Applied and environmental microbiology 61, no. 4 (1995): 1669–72. http://dx.doi.org/10.1128/aem.61.4.1669-1672.1995.

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Dissertations / Theses on the topic "Enterohemorrhagic Escherichia coli"

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Dadgar, Ashraf. "Detection of enterohemorrhagic Escherichia coli (EHEC)." Thesis, Uppsala University, Department of Medical Biochemistry and Microbiology, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6011.

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Escherichia coli is a natural inhabitant of the intestines of both humans and animals, but there are also several pathogenic types of E. coli which cause disease in humans.

Strains of enterohemorrhagic E. coli (EHEC) have been associated with outbreaks of diarrhea, hemorrhagic colitis and hemolytic uremic syndrome in humans. Most clinical signs of disease arise as a consequence of the production of shigatoxin 1 and 2 or combination of these toxins. Other major virulence factors include EHEC hemolysin and intimin, the product of the eae gene that is involved in attaching and effacing adherence phenotype. EHEC has also been associated with uncomplicated diarrhea.

The capacity to control EHEC disease and to limit the scale of outbreaks is dependent upon prompt diagnosis and identification of the source of infection.

The principal reservoirs of EHEC are cattle and food products, which presumably have come into contact with domestic animal manure and/or are inadequately pasteurised, these are important vehicles of infection.

In the present study, the PCR technique with primers detecting the verocytotoxin genes was shown to be a possible method to screen for and identify EHEC.

In summary stx genes were detected in 16 samples of 228 sampels and the eae gene was detected in 2 samples using PCR.

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Yu, Angel Chia-yu. "Structural analysis of an enterohemorrhagic Escherichia coli metalloprotease effector." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/42821.

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Mucins are proteins that contain dense clusters of α-O-GalNAc-linked carbohydrate chains and are the major component of the mucosal barrier that lines the mammalian gastrointestinal tract from mouth to gut. A critical biological function of mucins is to protect the underlying epithelial cells from infection. Enterohemorrhagic Escherichia. coli O157:H7 (EHEC), a bacterial pathogen that causes severe food and water borne disease, is capable of breaching this barrier and adhering to intestinal epithelial cells during infection. StcE (secreted protease of C1-esterase inhibitor) is a ~100 kDa zinc metalloprotease virulence factor secreted by EHEC and plays a pivotal role in remodelling the mucosal lining during EHEC pathogenesis. StcE also dampens the host immune response by targeting the mucinlike region of C1-INH, a key complement regulator of innate immunity. To obtain further mechanistic insight into StcE function, I have determined the crystal structure of the fulllength protease to 2.5Å resolution. This structure shows that StcE adopts a dynamic, multidomain architecture featuring an unusually large substrate binding cleft. Electrostatic surface analysis reveals a prominent polarized charge distribution highly suggestive of an electrostatic role in substrate targeting. The observation of key conserved motifs in the active site allows us to propose the structural basis for the specific recognition of α-O-glycan containing substrates, which have been confirmed by glycan array screening to be Oglycosylation of the mucin-type. Complementary biochemical analysis employing domain variants of StcE further extends our understanding of the substrate binding stoichiometry and distinct substrate specificity of this important virulence-associated metalloprotease.
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Treptow, Andrea Lauren. "Investigation of a Thermoregulated Gene in Pathogen Enterohemorrhagic Escherichia coli." Thesis, The University of Arizona, 2014. http://hdl.handle.net/10150/323222.

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MacDonald, Leslie Anne. "Antigenic relationship of enterohemorrhagic Escherichia coli hemolysin to other RTX toxins." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ56344.pdf.

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Thomassin, Jenny-Lee. "Antimicrobial peptide resistance mechanisms used by Enteropathogenic and Enterohemorrhagic «Escherichia coli»." Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=121462.

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Enteropathogenic and enterohemorrhagic Escherichia coli (EPEC and EHEC) are Gram-negative pathogens that cause diarrheal disease in the developed and developing world. To cause infection, these pathogens must overcome innate host defenses, such as secreted cationic antimicrobial peptides (AMPs). There are two groups of human AMPs: cathelicidins (LL-37) and defensins (α-defensin 5). AMPs are expressed in specific locations of the human body. In the small intestine, the infectious niche for EPEC, human α-defensins 5 and 6 (HD-5 and HD-6) are abundant and there are low levels of LL-37. Conversely in the colon, the infectious niche for EHEC, HD-5 and HD-6 are not expressed and LL-37 is abundant. Pathogens can overcome AMP-killing using several mechanisms, including proteolytic inactivation, producing shielding structures and modifying their lipopolysaccharide (LPS). We hypothesized that EPEC and EHEC use AMP-resistance mechanisms to resist killing by secreted AMPs during infection. Previously, CroP the omptin protease in Citrobacter rodentium, a murine pathogen used to model EPEC and EHEC infections, was shown to degrade murine cathelicidin. Both EPEC and EHEC have a CroP-homologue: OmpT. The contribution of OmpT to LL-37 resistance was analyzed in both pathogens. Peptide cleavage assays showed that EHEC OmpT cleaves and inactivates LL-37 more rapidly than EPEC OmpT. Higher ompT-expression and protein levels in EHEC than EPEC are responsible for the differences observed in LL-37 inactivation rates. Additional studies showed that OmpT was unable to cleave folded α-defensins. These data suggest that EPEC uses other mechanisms to resist killing by the AMPs in its infectious niche. To assess this possibility, surface structures that may shield the bacterial membrane from AMPs were identified. High transcript levels of gfcA, a gene required for group 4 capsule (G4C) secretion, were observed in EPEC but not EHEC. The unencapsulated EPEC ΔgfcA and EHEC wild-type strains were more susceptible to HD-5 killing than EPEC wild-type. Since the G4C is composed of the same sugar repeats as the LPS O-antigen, an O-antigen ligase (waaL) deletion mutant was generated to assess the role of the O-antigen in HD-5 resistance. The EPEC ΔwaaL strain was more susceptible to HD-5 than both the wild-type and ΔgfcA strains. Addition of exogenous polysaccharide increased survival of the ΔgfcAΔwaaL strain in the presence of HD-5, suggesting that HD-5 binds the polysaccharides present on the surface of EPEC. These data show that EPEC relies on both the G4C and O-antigen to resist the bactericidal activity of HD-5. Altogether, these data indicate that EHEC and EPEC differentially regulate AMP-specific resistance mechanisms as an adaptation to their specific infectious niches.
Les Escherichia coli entéropathogènes et entérohémorrhagiques (EPEC et EHEC) sont des bactéries à coloration Gram-négative qui causent des diarrhées dans les pays développés et en développement. Pour causer une infection, ces pathogènes doivent surmonter les défenses de l'immunité innée de l'hôte, tel que les peptides antimicrobiens sécrétés (PAMs). Chez l'humain, les PAMs sont divisés en deux groupes, les cathélicidines (ex. LL-37) et les défensines (ex. α-défensine humaine 5). L'expression des PAMs varie selon les tissus. Dans l'intestin grêle, la niche infectieuse des EPEC, les α-défensines humaines 5 et 6 (HD-5 et HD-6) sont abondantes et le niveau de LL-37 est bas. Inversement, HD-5 et HD-6 ne sont pas exprimées dans le côlon, la niche infectieuse des EHEC, et LL-37 est très abondant. Les pathogènes peuvent résister aux PAMs en utilisant différent mécanismes comme l'inactivation protéolytique, la production de structures recouvrant la cellule bactérienne et la modification du lipopolysaccharide (LPS). Notre hypothèse est que les EPEC et EHEC utilisent des mécanismes de résistance aux PAMs pour établir une infection. Précédemment, il a été démontré que la protéase de type omptin, CroP, de Citrobacter rodentium, un pathogène murin utilisé comme modèle pour les infections des EPEC et EHEC, dégrade la cathélicidine murine. Les EPEC et EHEC possèdent un homologue de CroP, OmpT. La contribution de OmpT à la résistance au LL-37 a été examinée chez ces deux pathogènes. Nos tests de clivage de peptide ont démontré que EHEC OmpT clive et inactive LL-37 plus rapidement que EPEC OmpT. La différence observée a été associée à une plus forte expression et production de OmpT chez les EHEC que chez les EPEC. Des tests supplémentaires ont démontré que OmpT ne peut pas cliver les α-défensines repliées. Ces données suggèrent qu'EPEC utilise d'autres mécanismes de résistance pour surmonter l'activité des PAMs présents dans sa niche infectieuse. Pour tester cette possibilité, les structures recouvrant la cellule ont été identifiées. Un haut niveau de transcription de gfcA, un gène requit pour la sécrétion de la capsule du groupe 4 (G4C), a été observé chez EPEC mais pas chez EHEC. Le mutant EPEC non-encapsulé ΔgfcA et la souche sauvage EHEC sont plus susceptible à l'effet du HD-5 que la souche sauvage EPEC. Étant donné que la G4C est composée des mêmes sucres que l'antigène O, la ligase de l'antigène O, waaL, a été délétée pour déterminer le rôle de l'antigène O dans la résistance au HD-5. La souche EPEC ΔwaaL est plus susceptible au HD-5 que la souche sauvage EPEC et le mutant EPEC ΔgfcA. L'addition de polysaccharide exogène augmente la survie du mutant ΔwaaLΔgfcA en présence de HD-5. Ceci indique que HD-5 se lie aux polysaccharides présents à la surface des EPEC. Ces données démontrent que la résistance à HD-5 chez EPEC repose sur la présence de la G4C et de l'antigène O. Toutes ces données indiquent que EHEC et EPEC utilisent des mécanismes de résistance différents aux PAMs, ce qui démontre une adaptation à leurs niches infectieuses respectives.
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Morgan, Jason Kyle. "Genetic basis for the virulence of enterohemorrhagic Escherichia coli strain TW14359." Scholar Commons, 2014. https://scholarcommons.usf.edu/etd/5277.

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Enterohemorrhagic Escherichia coli (EHEC) is a virulent pathotype of E. coli that is associated with major outbreaks of hemorrhagic colitis and the life-threatening kidney disease hemolytic uremic syndrome. For successful host colonization and attachment to the intestinal mucosa, EHEC requires the locus of enterocyte effacement (LEE) pathogenicity island, which encodes a type III secretion system (TTSS) responsible for secreting and translocating effector proteins into host colonocytes. Regulation of the LEE is primarily directed through the first operon, LEE1, encoding the locus encoded regulator (Ler), and occurs through the direct and indirect action of several regulators. The 2006 U.S. spinach outbreak of E. coli O157:H7, characterized by unusually severe disease, has been attributed to a strain (TW14359) with enhanced pathogenic potential including elevated virulence gene expression, robust adherence, and the presence of novel virulence factors. Aim 1 of this dissertation proposes a mechanism for the unique virulence expression and adherence phenotype of this strain, and further expands the role for regulator RcsB in control of the E. coli locus of enterocyte effacement (LEE) pathogenicity island. Proteomic analysis of TW14359 revealed a virulence proteome consistent with previous transcriptome studies that included elevated levels of the LEE regulatory protein Ler and type III secretion system (T3SS) proteins, secreted T3SS effectors, and Shiga toxin 2. Basal levels of the LEE activator and Rcs phosphorelay response regulator, RcsB, were increased in strain TW14359 relative to O157:H7 strain Sakai. Deletion of rcsB eliminated inherent differences between these strains in ler expression, and in T3SS-dependent adherence. A reciprocating regulatory pathway involving RcsB and LEE-encoded activator GrlA was identified and predicted to coordinate LEE activation with repression of the flhDC flagellar regulator and motility. Overexpression of grlA was shown to increase RcsB levels, but did not alter expression from promoters driving rcsB transcription. Expression of rcsDB and RcsB was determined to increase in response to physiologic levels of bicarbonate, and bicarbonate-dependent stimulation of the LEE was shown to be dependent on an intact Rcs system and ler activator grvA. The results of this aim significantly broaden the role for RcsB in EHEC virulence regulation. The bicarbonate ion (HCO3-) has been shown to stimulate LEE gene transcription through the LEE1 promoter, and is predicted to serve as a physiologic signal for EHEC colonization. Results from the previous aim demonstrated that bicarbonate induction of the LEE is mediated through the Rcs phosphorelay, and is dependent upon an intact global regulator of virulence grvA gene. However, the direct mechanism through which RcsB-GrvA regulates ler, and the contribution of GrvA to the virulence of EHEC is unknown. In Aim 2, the RcsB-GrvA regulon of EHEC was determined by RNA sequencing, and the contributions of each to virulence and stress fitness was explored. A significant increase in transcription of the gad genes for extreme acid resistance was observed for both EHEC strains TW14359grvA and TW14359rcsBgrvA compared to TW14359, and corresponded with a significant increase in acid survival for TW14359grvA during exponential growth. Therefore, a model by which RcsB-GrvA coordinate LEE expression with acid resistance through GadE was proposed. Finally, the temporal regulation of both rcsDB and grvAB operons in response to bicarbonate was defined using single copy luxE chromosomal reporter fusions. Taken together, these results demonstrate the role of RcsB and GrvA to EHEC virulence, and reveal a novel role for GrvA in of extreme acid resistance and LEE gene expression and in EHEC. Finally, production of the ECP pilus has been demonstrated in enterohemorrhagic Escherichia coli O157:H7 (EHEC), and has been shown to be required for efficient adherence to epithelial cells during colonization. The first gene of the ecpRABCDE operon encodes a transcriptional regulator (EcpR) that positively regulates its own transcription, and promotes transcription and production of the downstream gene, ecpA, encoding the major ECP subunit EcpA. However, the distance between the ecpR and ecpA genes suggests the presence of regulatory elements that control ecpA directly. Therefore, it was hypothesized that an additional promoter was able to direct transcription of ecpA, independent of the promoter upstream of ecpR. To test this, promoter-lacZ transcriptional reporter fusions were created using the regions upstream of ecpR and ecpA to test for promoter activity, coupled with western blot analysis to detect EcpA in both wild-type and ecpR promoter mutant strains. In Aim 3, we showed that an additional promotable element, downstream of the EHEC O157:H7 strain TW14359 ecpR translational start site, is capable of driving transcription of ecpA, and that its activity is independent of an intact ecpR promoter. In addition, site-directed mutagenesis was used to characterize a TW14359 specific single nucleotide polymorphism within the predicted ecpA promoter region. Overproduction of EcpR was observed to increase cytosolic RcsB and Tir, indicating that ecp production is able to stimulate the LEE, and that the ecpA promoter polymorphism may contribute to intrinsically increased rcsB transcription in TW14359. Taken together, the results, and those obtained in Aims 1 and 2, expand the model for regulation of the ecp operon in EHEC O157:H7 strain TW14359, and broaden the model for EcpR and RcsB in the coordinate regulation of E. coli common pilus and type III secretion.
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Tsai, Wan-Ling. "Investigation of Systems For Detection of Enterohemorrhagic Escherichia Coli Contamination In Foods /." The Ohio State University, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487933245536054.

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Eichhorn, Inga [Verfasser]. "Microevolution of epidemiological highly relevant non-O157 enterohemorrhagic Escherichia coli (EHEC) / Inga Eichhorn." Berlin : Freie Universität Berlin, 2016. http://d-nb.info/1115722530/34.

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Chong, Yuwen. "Intimate interactions between enteropathogenic and enterohemorrhagic Escherichia coli and intestinal epithelium in vitro." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445194/.

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Enteropathogenic Escherichia coli (EPEC) and enterohaemorrhagic E. coli (EHEC) are diarrhoeagenic human pathogens that colonize intestinal epithelial cells via an attaching and effacing (A/E) lesion. Intimate adherence is mediated through binding of the intimin adhesin to the bacterial translocated intimin receptor, Tir. EPEC adheres to all regions of the human intestine in the in vitro organ culture (IVOC) system. In contrast, although EHEC is associated with colonic pathology in human infections, a prototypical strain of EHEC has shown a restricted tropism towards follicle-associated epithelium (FAE) of the terminal ileum without evidence of colonic adhesion. This thesis used the human IVOC system to further examine the intestinal interaction of EHEC 0157:H7 and related EPEC serotypes. To address the apparent paradox of non-adherence of EHEC to colonic tissue in the IVOC experimental system, the role of environmental, host and bacterial factors in modulating EHEC colonisation and tissue tropism were studied. No environmental factor (modulation of IVOC system, bicarbonate, serum, and mannose) was found to induce colonic adhesion. The investigation of the hypothesis that prior host-bacterial interactions might enhance subsequent EHEC colonic adhesion found that exposure to FAE promoted subsequent colonic adhesion, but in a non-intimate manner, demonstrating a novel form of interaction with human intestine. Great diversity was found in EPEC and EHEC in relation to the presence and sequence of tir, tccP and espJ fccP-negative strains expressing TireHEc were identified indicating that novel Nck-like molecules may be awaiting discovery. Tir was essential for EPEC and EHEC adhesion in IVOC but its phosphorylation (EPEC) and its interaction with TccP (EHEC) were not necessary for colonisation and A/E lesion formation on IVOC, questioning the role of pedestal formation in enterocyte infection. This is in direct contrast to cell culture findings and demonstrates the importance of IVOC in establishing 0157:H7 human pathogenesis.
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Lai, YuShuan (Cindy). "EspFU, an Enterohemorrhagic E. Coli Secreted Effector, Hijacks Mammalian Actin Assembly Proteins by Molecular Mimicry and Repetition: A Dissertation." eScholarship@UMMS, 2014. https://escholarship.umassmed.edu/gsbs_diss/715.

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Enterohemorrhagic E. coli (EHEC) is a major cause of food borne diarrheal illness worldwide. While disease symptoms are usually self-resolving and limited to severe gastroenteritis with bloody diarrhea, EHEC infection can lead to a life threatening complication known as Hemolytic Uremic Syndrome (HUS), which strikes children disproportionately and is the leading cause of kidney failure in children. Upon infection of gut epithelia, EHEC produces characteristic lesions called actin pedestals. These striking formations involve dramatic rearrangement of host cytoskeletal proteins. EHEC hijacks mammalian signaling pathways to cause destruction of microvilli and rebuilds the actin cytoskeleton underneath sites of bacterial attachment. Here, we present a brief study on a host factor, Calpain, involved in microvilli effacement, and an in depth investigation on a bacterial factor, EspFU, required for actin pedestal formation in intestinal cell models. Calpain is activated by both EHEC and the related pathogen, enteropathogenic E. coli (EPEC), during infection and facilitates microvilli disassembly by cleavage of a key membrane-cytoskeleton anchoring substrate, Ezrin. Actin pedestal formation is facilitated by the injection of two bacterial effectors, Tir and EspFU, into host cells, which work in concert to manipulate the host actin nucleators N-WASP and Arp2/3. EspFU hijacks key host signaling proteins N-WASP and IRTKS by mimetic displacement and has evolved to outcompete mammalian host ligands. Multiple repeats of key functional domains of EspFU are essential for actin pedestal activity through proper localization and competition against the an abundant host factor Eps8 for binding to IRTKS.
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Books on the topic "Enterohemorrhagic Escherichia coli"

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Sperandio, Vanessa, and Carolyn J. Hovde, eds. Enterohemorrhagic Escherichia coli and Other Shiga Toxin-Producing E. coli. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555818791.

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Enterohemorrhagic Escherichia coli and Other Shiga Toxin-Producing E. coli. ASM Press, 2015.

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Sperandia, Vanessa, and Carolyn J. Hovde. Enterohemorrhagic Escherichia Coli and Other Shiga Toxin-Producing E. Coli. Wiley & Sons, Limited, John, 2015.

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Book chapters on the topic "Enterohemorrhagic Escherichia coli"

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Meng, Jianghong, Jeffrey T. LeJeune, Tong Zhao, and Michael P. Doyle. "Enterohemorrhagic Escherichia coli." In Food Microbiology, 287–309. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555818463.ch12.

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McWilliams, Brian D., and Alfredo G. Torres. "Enterohemorrhagic Escherichia coli Adhesins." In Enterohemorrhagic Escherichia coli and Other Shiga Toxin-Producing E. coli, 131–55. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555818791.ch7.

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Gooch, Jan W. "Enterohemorrhagic Strain of Escherichia Coli." In Encyclopedic Dictionary of Polymers, 890. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13664.

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Tsch�pe, H., and A. Fruth. "Enterohemorrhagic Escherichia coli." In Contributions to Microbiology, 1–11. Basel: KARGER, 2001. http://dx.doi.org/10.1159/000060396.

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Rivas, Marta, Isabel Chinen, and Beatriz E. C. Guth. "Enterohemorrhagic (Shiga Toxin-Producing) Escherichia coli." In Escherichia coli in the Americas, 97–123. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-45092-6_5.

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Mellies, Jay L., and Emily Lorenzen. "Enterohemorrhagic Escherichia coli Virulence Gene Regulation." In Enterohemorrhagic Escherichia coli and Other Shiga Toxin-Producing E. coli, 175–95. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555818791.ch9.

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Harmon, Barry G., Cathy A. Brown, Michael P. Doyle, and Tong Zhao. "Enterohemorrhagic Escherichia coli in Ruminant Hosts." In Emerging Diseases of Animals, 201–15. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555818050.ch10.

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Ritchie, Jennifer M. "Animal Models of Enterohemorrhagic Escherichia coli Infection." In Enterohemorrhagic Escherichia coli and Other Shiga Toxin-Producing E. coli, 157–74. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555818791.ch8.

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Pearson, Jaclyn S., and Elizabeth L. Hartland. "The Inflammatory Response during Enterohemorrhagic Escherichia coli Infection." In Enterohemorrhagic Escherichia coli and Other Shiga Toxin-Producing E. coli, 321–39. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555818791.ch16.

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Karpman, Diana, and Anne-lie Ståhl. "Enterohemorrhagic Escherichia coli Pathogenesis and the Host Response." In Enterohemorrhagic Escherichia coli and Other Shiga Toxin-Producing E. coli, 381–402. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555818791.ch19.

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Conference papers on the topic "Enterohemorrhagic Escherichia coli"

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Feng, Jian, Yan-hong Bai, Yun-long Wang, and Jian-zhou Jing. "Detection and Identification of Enterohemorrhagic Escherichia coli O157:H7 Using Agilent 2100 Bioanalyzer." In 2010 4th International Conference on Bioinformatics and Biomedical Engineering (iCBBE 2010). IEEE, 2010. http://dx.doi.org/10.1109/icbbe.2010.5515776.

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Nihayati, Khoirun, Yuanita Rachmawati, Saiku Rokhim, and Linda Prasetyaning Widayanti. "Detection of Enterohemorrhagic Escherichia coli (EHEC) in Consumption Water Source using Multiplex PCR Method." In Built Environment, Science and Technology International Conference 2018. SCITEPRESS - Science and Technology Publications, 2018. http://dx.doi.org/10.5220/0008907001080112.

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Oyong, Glenn, and James Christopher Chua. "High resolution melting (HRM)-coupled multiplex real-time PCR for rapid identification and virulence gene profiling of enterohemorrhagic Escherichia coli (EHEC) O157:H7 from slaughterhouse pigs." In INTERNATIONAL CONFERENCE ON BIOMEDICAL ENGINEERING (ICoBE 2021). AIP Publishing, 2023. http://dx.doi.org/10.1063/5.0111198.

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Reports on the topic "Enterohemorrhagic Escherichia coli"

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McKee, Marian L. Adherence of Enterohemorrhagic Escherichia coli to Human Epithelial Cells: The Role of Intimin. Fort Belvoir, VA: Defense Technical Information Center, March 1995. http://dx.doi.org/10.21236/ad1011453.

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