Infection strategies of enteric pathogenic Escherichia coli

Clements, Abigail; Young, Joanna C.; Constantinou, Nicholas; Frankel, Gad

doi:10.4161/gmic.19182

Cited by 284 publications

(247 citation statements)

References 197 publications

(179 reference statements)

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“…Para la adherencia de ECET a las células epiteliales, la bacteria expresa la EtpA, exoproteína de adhesión (TPS: two-partner secretion) situada al extremo del flagelo, para permitir que los CFs se adhieran a éstas. Inmediatamente después, el auto-transportador EatA (EatA: autotransporter A) incluida en el grupo de las serin-proteasas (SPATEs: serine protease autotransporter of Enterobacteriaceae) inhiben la actividad de EtpA, lo que da origen a la adhesión de ECET a los enterocitos por el loci toxigénico de invasión A (Tia: toxigenic invasion loci A), una proteína de membrana externa y el loci toxigénico de invasión B (TibA: toxigenic invasion loci B) (Figura 3) [69][70][71][72] . P) 50,51 , que contribuye a la formación de microcolonias y a la adhesión a células epiteliales de colon T84 51 (Figura 2b); b) Transcitosis: mediante vesículas la toxina pasa de un espacio extracelular a otro (Figura 2b) 52 .…”

Section: Artículo Originalunclassified

“…Existen dos tipos de LT (LT-I y LT-II); las LT-I están directamente asociadas a cepas humanas. Cada toxina se divide en dos subunidades A y B 72 . ECET secreta, mediante el sistema de secreción tipo 2, la LT dentro de las vesículas de la membrana externa (OMVs: outer membrane vesicles) 75 y posteriormente con ayuda de la subunidad B de LT se une al gangliósido GM1, que por endocitosis permite que las OMV ingresen al citoplasma.…”

Section: Patogeniaunclassified

“…El segundo mecanismo es mediante la invasión de las células M. Escherichia coli adherente invasora posee una fimbria polar larga (LPF: long polar fimbriae) que permite la aproximación a las células M 113 . Utiliza el mismo proceso de ECEI donde atraviesa la célula por medio de transcitosis 72 . Es fagocitada por los macrófagos, donde se replica dentro de los fagosomas sin estimular la muerte celular 6,116 e induce en el macrófago infectado la secreción de FNT-α, el cual causa la inflamación del íleon y conlleva la formación de granulomas 6,8 .…”

Section: Escherichia Coli Adherente Invasoraunclassified

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Mecanismos de virulencia de Escherichia coli enteropatógena

Farfán-García¹,

Ariza-Rojas²,

Vargas-Cárdenas³

et al. 2016

Rev. chil. infectol.

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Section: Artículo Originalunclassified

Section: Patogeniaunclassified

Section: Escherichia Coli Adherente Invasoraunclassified

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Mecanismos de virulencia de Escherichia coli enteropatógena

Farfán-García¹,

Ariza-Rojas²,

Vargas-Cárdenas³

et al. 2016

Rev. chil. infectol.

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“…Compared with their symbiotic counterparts, pathogenic E. coli strains have acquired virulence factors involved in attachment, invasion, and toxin production (2). Inflammatory bowel disease (IBD), comprising Crohn's disease (CD) and ulcerative colitis (UC), is a relapsing-remitting chronic inflammatory disorder influenced by genetic and environmental factors (3).…”

mentioning

confidence: 99%

QseC inhibition as an antivirulence approach for colitis-associated bacteria

Rooks

Veiga

Reeves

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Hosts and their microbes have established a sophisticated communication system over many millennia. Within mammalian hosts, this dynamic cross-talk is essential for maintaining intestinal homeostasis. In a genetically susceptible host, dysbiosis of the gut microbiome and dysregulated immune responses are central to the development of inflammatory bowel disease (IBD). Previous surveys of stool from the T-bet −/− Rag2 −/− IBD mouse model revealed microbial features that discriminate between health and disease states. Enterobacteriaceae expansion and increased gene abundances for benzoate degradation, two-component systems, and bacterial motility proteins pointed to the potential involvement of a catecholamine-mediated bacterial signaling axis in colitis pathogenesis. Enterobacteriaceae sense and respond to microbiota-generated signals and host-derived catecholamines through the two-component quorum-sensing Escherichia coli regulators B and C (QseBC) system. On signal detection, QseC activates a cascade to induce virulence gene expression. Although a single pathogen has not been identified as a causative agent in IBD, adherent-invasive Escherichia coli (AIEC) have been implicated. Flagellar expression is necessary for the IBD-associated AIEC strain LF82 to establish colonization. Thus, we hypothesized that qseC inactivation could reduce LF82's virulence, and found that an absence of qseC leads to down-regulated flagellar expression and motility in vitro and reduced colonization in vivo. We extend these findings on the potential of QseC-based IBD therapeutics to three preclinical IBD models, wherein we observe that QseC blockade can effectively modulate colitogenic microbiotas to reduce intestinal inflammation. Collectively, our data support a role for QseC-mediated bacterial signaling in IBD pathogenesis and indicate that QseC inhibition may be a useful microbiota-targeted approach for disease management.colitis | Escherichia coli | QseC | antivirulence | gut microbiome

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“…Enteric E. coli have traditionally been divided into six pathotypes: enteropathogenic E. coli (EPEC), enterotoxigenic E. coli (ETEC), enteroinvasive E. coli (EIEC), verocytotoxigenic E. coli (VTEC), enteroaggregative E. coli (EAEC) and diffusely adherent E. coli (DAEC) (European Food Safety Authority [EFSA], 2013). Two further pathotypes have been proposed by Clements et al (2012), including adherent invasive E. coli (AIEC), thought to be associated with Crohn's disease, and the verocytotoxin (Vtx)-producing enteroaggregative E. coli (STEAEC) responsible for the 2011 Germany E. coli outbreak. Verocytotoxigenic E. coli (VTEC), also referred to as Shiga toxin-producing E. coli (STEC), are characterised by the production of Vtxs.…”

Section: Introductionmentioning

confidence: 99%

The effect of antimicrobials on verocytotoxin bacteriophage transduction under bovine rumen fluid and broth conditions

Nyambe

Burgess

Whyte

et al. 2017

Irish Journal of Agricultural and Food Research

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The verocytotoxin genes in verocytotoxigenic Escherichia coli (VTEC) are carried by bacteriophages, incorporated into the bacterial genome (prophage). Antibiotics may promote phage replication and release to infect other cells (transduction), thus leading to the emergence of new VTEC strains. This study investigated transduction of a verocytotoxin2-encoding bacteriophage (3538(vtx2::cat)) under laboratory conditions, including the effect of antibiotic treatments. Luria-Bertani Miller broth and rumen fluid (raw and sterilised by irradiation) were inoculated with the donor (C600φ3538(Δvtx2::cat)) and recipient (E. coli C600::kanamycinR) strains (4 log10 cfu/mL) and incubated at 38°C. Antibiotic treatments (minimal inhibitory and sub-inhibitory concentrations of ampicillin, cefquinome, oxytetracycline and sodium sulfamethazine) were applied after 3 h. Samples were tested for donor, recipient, cell-free phage and transductants at times t = 0, 3, 4, 6, 27 (24 h post-antibiotic treatment) and 51 h. Free phage was detected in the untreated broth and rumen samples, as were the transductants confirmed by polymerase chain reaction. The antibiotic treatments did not significantly (P > 0.01) increase the concentrations of free phage or transductants detected. It was therefore concluded that, under laboratory conditions, the antibiotics tested did not induce bacteriophage lysis, release and infection of new bacterial cells beyond that constitutively found in the phage population.

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Infection strategies of enteric pathogenic Escherichia coli

Cited by 284 publications

References 197 publications

Mecanismos de virulencia de Escherichia coli enteropatógena

Mecanismos de virulencia de Escherichia coli enteropatógena

QseC inhibition as an antivirulence approach for colitis-associated bacteria

The effect of antimicrobials on verocytotoxin bacteriophage transduction under bovine rumen fluid and broth conditions

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