Adherence of Diarrheagenic<i>Escherichia coli</i>Strains to Epithelial Cells

Torres, Alfredo G.; Zhou, Xin; Kaper, James B.

doi:10.1128/iai.73.1.18-29.2005

Cited by 202 publications

(187 citation statements)

References 152 publications

(128 reference statements)

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“…EHEC O157 : H7 virulence factors include many fimbrial and non-fimbrial adhesins, flagella, toxins including Shiga toxins, and a type III secretion system (TTSS). Non-fimbrial adhesins include intimin, considered to play a major role in bacterial-host adhesion, as well as the plasmid-encoded toxB, the chromosomal genetic locus efa1 (EHEC factor for adherence), and the chromosomally encoded adhesins Iha (Vibrio cholerae IrgA homologue), Cah (calcium-binding antigen 43 homologue) and OmpA (outer-membrane protein A) (Johnson et al, 2005;McKee et al, 1995;Tatsuno et al, 2001Tatsuno et al, , 2001Torres et al, 2005). Fimbrial structures that have been identified include two long polar fimbriae, F9 (a type 1 pilus homologue), two type IV pili (HCP in EHEC O157 and TFP in a non-O157 EHEC), the sorbitol-fermenting EHEC O157 : H-plasmid-encoded fimbriae, SFP and ECP (E. coli common pilus) produced by both pathogenic and non-pathogenic E. coli (Blackburn et al, 2009;Brunder et al, 2001;Low et al, 2006;Xicohtencatl-Cortes et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Acid-stress-induced changes in enterohaemorrhagic Escherichia coli O157 : H7 virulence

et al. 2009

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Enterohaemorrhagic Escherichia coli (EHEC) O157 : H7 is naturally exposed to a wide variety of stresses including gastric acid shock, and yet little is known about how this stress influences virulence. This study investigated the impact of acid stress on several critical virulence properties including survival, host adhesion, Shiga toxin production, motility and induction of host-cell apoptosis. Several acid-stress protocols with relevance for gastric passage as well as external environmental exposure were included. Acute acid stress at pH 3 preceded by acid adaptation at pH 5 significantly enhanced the adhesion of surviving organisms to epithelial cells and bacterial induction of host-cell apoptosis. Motility was also significantly increased after acute acid stress. Interestingly, neither secreted nor periplasmic levels of Shiga toxin were affected by acid shock. Pretreatment of bacteria with erythromycin eliminated the acid-induced adhesion enhancement, suggesting that de novo protein synthesis was required for the enhanced adhesion of acidshocked organisms. DNA microarray was used to analyse the transcriptome of an EHEC O157 : H7 strain exposed to three different acid-stress treatments. Expression profiles of acidstressed EHEC revealed significant changes in virulence factors associated with adhesion, motility and type III secretion. These results document profound changes in the virulence properties of EHEC O157 : H7 after acid stress, provide a comprehensive genetic analysis to substantiate these changes and suggest strategies that this pathogen may use during gastric passage and colonization in the human gastrointestinal tract.

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Section: Introductionmentioning

confidence: 99%

Acid-stress-induced changes in enterohaemorrhagic Escherichia coli O157 : H7 virulence

et al. 2009

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“…La expresión de algunos alelos de la intimina se ha asociado con el tropismo tisular de cepas de E. coli causantes de diarrea (38)(39)(40)(41). Sin embargo, la frecuencia de los alelos de intimina evaluados en el presente estudio concordó con otros reportes previos, en los cuales no se encontraron diferencias significativas en la distribución de estos alelos en las cepas ECEP típicas y atípicas, o en la condición clínica de los pacientes (33,35).…”

Section: Discussionunclassified

Identificación de Escherichia coli enteropatógena en niños con síndrome diarreico agudo del Estado Sucre, Venezuela

et al. 2016

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: concepción y diseño del estudio Adriana Millán, Mirian Michelli, Jesús Luiggi y Numirin Carreño: recolección y procesamiento de muestras Elvia Michelli: redacción del manuscrito Todos los autores participaron en el análisis y la interpretación de los datos. Materiales y métodos. Previo consentimiento informado, se recolectaron muestras fecales y se identificó E. coli mediante coprocultivo estándar y serología con antisueros polivalentes y monovalentes. Se aisló el ADN y se amplificaron los genes eae (intimina) y bfpA (bundlina) mediante dos pruebas de reacción en cadena de la polimerasa (PCR) múltiples. Identificación deResultados. En 39,6 % de los coprocultivos se determinó la presencia de infección bacteriana. La prevalencia de E. coli fue de 54,7 %; 82,9 % de estas cepas fue positivo por serología para los serogrupos y el serotipo evaluados, principalmente en niños entre los 0 y los 2 años (37,9 %). El 48,6 % de las cepas de E. coli amplificaron para el gen eae y, de estas, 58,8 % se clasificó como cepas de E. coli enteropatógena típica (eae+ y bfp+). El ECEP II fue el serogrupo más frecuente (38,7 %), con predominio de bacterias E. coli enteropatógenas típicas (60 %). El alelo β de la intimina fue el más identificado (74,5 %) en las cepas positivas para el gen eae. Solo se identificaron cuatro cepas con el serotipo O157:H7 utilizando antisueros, las cuales no amplificaron mediante PCR para los genes eae y bfpA. Conclusiones. Este estudio demostró la importancia de aplicar pruebas moleculares en la identificación de las cepas de E. coli causantes de diarrea de diversa gravedad. Materials and methods:After obtaining the informed consent, stool samples were collected. Escherichia coli was identified using standard coproculture methods and serology with polyvalent and monovalent antisera. DNA was isolated, and eae (intimin) and bfpA (bundlin) genes were amplified through two multiplex polymerase chain reactions (PCR). Results:The presence of bacterial infection was determined in 39.6% of coprocultures. The prevalence of E. coli was 54.7%; 82.9% of these isolates were positive by serology for the evaluated serogroups and serotypes, which were mostly identified in children between 0 and 2 years (37.9%); 48.6% of E. coli strains amplified the eae gene; of these, 58.8% were classified as typical EPEC (eae+ y bfp+). EPEC II was the most common serogroup (38.7%), with predominance of typical EPEC

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“…The ability to adhere to host surfaces by microbial pathogens is the most critical step in a successful colonization and a key property to block by secreted antibodies. 17,18 Higher the probability of adherence of a given protein along with other high-scored parameters provides an extra edge to that protein compared to others with similar scores but low adherence property. These parameters help in refining the selection of fewer candidates to be validated in our in vivo model of infection.…”

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confidence: 99%

“…15 In support of our analysis, the HP group includes several proteins that we and others have previously identified as important virulence factors of EHEC O157:H7 as well as other proteins not previously identified in virulence but which were consider important immunogens. [18][19][20][21][22][23] Several studies in murine models of EHEC infection have emphasized the importance of mucosal delivery routes as a promising way to induce immune responses offering a combination of protection and blockage of EHEC intestinal colonization, mainly through expression of secretory IgA (sIgA) 24 (Fig. 1).…”

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confidence: 99%