Environment Controls LEE Regulation in Enteropathogenic Escherichia coli

Platenkamp, Amy; Mellies, Jay L.

doi:10.3389/fmicb.2018.01694

Cited by 29 publications

(28 citation statements)

References 149 publications

(261 reference statements)

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“…The epidemiology of infectious diarrhea caused by EPEC changed in the last decades. While for many decades typical EPEC strains were strongly associated with diarrhea in children under 1 year old (especially under 6 months) [1,25,27,105], more recent studies failed to identify the same strong association. In Brazil, in a study conducted between 1998-1999, 38% of the EPEC strains were atypical, while between 2001-2002, 92% were atypical [11,90,106].…”

Section: Epidemiologymentioning

confidence: 99%

Enteropathogenic Escherichia coli—A Summary of the Literature

Mare

Ciurea

Man

et al. 2021

Gastroenterology Insights

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Diarrheal disease is still a major public health concern, as it is still considered an important cause of death in children under five years of age. A few decades ago, the detection of enteropathogenic E. coli was made by detecting the O, H, and K antigens, mostly by agglutination. The recent protocols recommend the molecular methods for diagnosing EPEC, as they can distinguish between typical and atypical EPEC by identifying the presence/absence of specific virulence factors. EPEC are defined as diarrheagenic strains of E. coli that can produce attaching and effacing lesions on the intestinal epithelium while being incapable of producing Shiga toxins and heat-labile or heat-stable enterotoxins. The ability of these strains to produce attaching and effacing lesions enable them to cause localized lesions by attaching tightly to the surface of the intestinal epithelial cells, disrupting the surfaces of the cells, thus leading to the effacement of the microvilli. EPEC are classified on typical and atypical isolates, based on the presence or absence of E. coli adherence factor plasmids. All the EPEC strains are eae positive; typical EPEC strains are eae+, bfpA+, while atypical strains are eae+, bfpA−. No vaccines are currently available to prevent EPEC infections.

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Section: Epidemiologymentioning

confidence: 99%

Enteropathogenic Escherichia coli—A Summary of the Literature

Mare

Ciurea

Man

et al. 2021

Gastroenterology Insights

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“…The T3aSS constitutes a major virulence factor that allows the assembly of a cell-surface needle structure, the injectisome which enables the direct transport of virulence effectors into a host cell (Cornelis, 2006;Desvaux et al, 2006;Brutinel and Yahr, 2008;Mueller et al, 2008;Diepold and Wagner, 2014,? ;Platenkamp and Mellies, 2018;Lara-Tejero and Galán, 2019;Ageorges et al, 2020). The regulation and function of the T3aSS has been extensively reviewed and readers are invited to consult the above reviews for further details on this vast field of research.…”

Section: Lee Paimentioning

confidence: 99%

“…As first described in prototypical EPEC strain E2348/69 ( Perna et al, 1998 ; Iguchi et al, 2009 ) and EHEC strain EDL933 (or strain Sakai) ( Hayashi et al, 2001 ; Perna et al, 2001 ; Latif et al, 2014 ), the core region of the PAI consists of 41 CDS, organized into (i) 5 operons named LEE-1 to LEE-5 encoding transcriptional regulators, including the master LEE-encoded regulator (Ler), chaperones and structural components of the T3aSS, as well as some effectors, (ii) one grlAB bicistron encoding transcriptional regulators, and (iii) some monocistrons. The T3aSS constitutes a major virulence factor that allows the assembly of a cell-surface needle structure, the injectisome which enables the direct transport of virulence effectors into a host cell ( Cornelis, 2006 ; Desvaux et al, 2006 ; Brutinel and Yahr, 2008 ; Mueller et al, 2008 ; Diepold and Wagner, 2014 , 2014 ; Platenkamp and Mellies, 2018 ; Lara-Tejero and Galán, 2019 ; Ageorges et al, 2020 ). The regulation and function of the T3aSS has been extensively reviewed and readers are invited to consult the above reviews for further details on this vast field of research.…”

Section: Diarrheagenic Escherichia Colimentioning

confidence: 99%

Pathogenicity Factors of Genomic Islands in Intestinal and Extraintestinal Escherichia coli

Desvaux¹,

Dalmasso²,

Beyrouthy³

et al. 2020

Front. Microbiol.

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Escherichia coli is a versatile bacterial species that includes both harmless commensal strains and pathogenic strains found in the gastrointestinal tract in humans and warmblooded animals. The growing amount of DNA sequence information generated in the era of "genomics" has helped to increase our understanding of the factors and mechanisms involved in the diversification of this bacterial species. The pathogenic side of E. coli that is afforded through horizontal transfers of genes encoding virulence factors enables this bacterium to become a highly diverse and adapted pathogen that is responsible for intestinal or extraintestinal diseases in humans and animals. Many of the accessory genes acquired by horizontal transfers form syntenic blocks and are recognized as genomic islands (GIs). These genomic regions contribute to the rapid evolution, diversification and adaptation of E. coli variants because they are frequently subject to rearrangements, excision and transfer, as well as to further acquisition of additional DNA. Here, we review a subgroup of GIs from E. coli termed pathogenicity islands (PAIs), a concept defined in the late 1980s by Jörg Hacker and colleagues in Werner Goebel's group at the University of Würzburg, Würzburg, Germany. As with other GIs, the PAIs comprise large genomic regions that differ from the rest of the genome by their G + C content, by their typical insertion within transfer RNA genes, and by their harboring of direct repeats (at their ends), integrase determinants, or other mobility loci. The hallmark of PAIs is their contribution to the emergence of virulent bacteria and to the development of intestinal and extraintestinal diseases. This review summarizes the current knowledge on the structure and functional features of PAIs, on PAI-encoded E. coli pathogenicity factors and on the role of PAIs in host-pathogen interactions.

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“…Tryptophanase, encoded by tnaA and decreased in transcription in the STECs (Table 2), catabolizes tryptophan to indole, ammonia, and pyruvate which allows E. coli to utilize tryptophan as a source of carbon and nitrogen in addition to using it in protein synthesis (Yanofsky et al, 1991). Indole facilitates inter-and intracellular signaling among microbiota in the human intestine, and indole concentration affects expression of genes associated with colonization and virulence in pathogenic E. coli including the LEE genes and stx2a (Lee and Lee, 2010;Bommarius et al, 2013;Platenkamp and Mellies, 2018;Kumar and Sperandio, 2019). The pronounced disparity between the STECs and HS in the regulation of genes associated with tryptophan biosynthesis, import, and catabolism when transitioning to an adhered lifestyle will result in differing effects on the interplay between the human host and E. coli cells.…”

Section: Discussionmentioning

confidence: 99%