Recognition of enteroinvasive Escherichia coli and Shigella flexneri by dendritic cells: distinct dendritic cell activation states

Moreno, Ana Carolina Ramos; Ferreira, Karen Spadari; Ferreira, Lucas Gonçalves; Almeida, Sandro Rogério de; Martinez, Marina Baquerizo

doi:10.1590/s0074-02762012000100020

Cited by 14 publications

(12 citation statements)

References 20 publications

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“…To this end, use has been made of experimental models that mimick the intestinal microenvironment of the host, such as cultures of intestinal epithelial cells, macrophages and dendritic cells 411, 415, 416. Our results showed that the initial ability to invade the intestinal cell is similar between EIEC and Shigella , but that the expression of virulence genes ( ipaABCD , icsA , icsB , virF , virB ), capacity to escape from the phagosome, intracellular proliferation and dissemination of EIEC, as well as the ability to cause cell damage during the infection, are much lower than with S. flexneri 411 .…”

Section: Enteroinvasive E Colimentioning

confidence: 99%

Diarrheagenic Escherichia coli

Gomes

Elias

Scaletsky

et al. 2016

Brazilian Journal of Microbiology

384

353

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Most Escherichia coli strains live harmlessly in the intestines and rarely cause disease in healthy individuals. Nonetheless, a number of pathogenic strains can cause diarrhea or extraintestinal diseases both in healthy and immunocompromised individuals. Diarrheal illnesses are a severe public health problem and a major cause of morbidity and mortality in infants and young children, especially in developing countries. E. coli strains that cause diarrhea have evolved by acquiring, through horizontal gene transfer, a particular set of characteristics that have successfully persisted in the host. According to the group of virulence determinants acquired, specific combinations were formed determining the currently known E. coli pathotypes, which are collectively known as diarrheagenic E. coli. In this review, we have gathered information on current definitions, serotypes, lineages, virulence mechanisms, epidemiology, and diagnosis of the major diarrheagenic E. coli pathotypes.

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Section: Enteroinvasive E Colimentioning

confidence: 99%

Diarrheagenic Escherichia coli

Gomes

Elias

Scaletsky

et al. 2016

Brazilian Journal of Microbiology

384

353

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“…The illness caused by Shigella or EIEC is characterized by the destruction of the colonic epithelium caused by the inflammatory response induced upon invasion of the mucosa by bacteria ( Parsot, 2005 ). It is well established that the disease induced by EIEC is generally less severe than Shigella does ( DuPont et al , 1989 ; Moreno et al , 2009 ; Bando et al , 2010 ; Moreno et al , 2012 ). Recombination techniques and the sequencing of the invasion plasmid and chromosomal genes associated with virulence, gave insight of the precise mechanism of infection by Shigella .…”

Section: Pathogenesis Processmentioning

confidence: 99%

“…EIEC produce less severe disease than S. flexneri ( Moreno et al , 2009 ; Bando et al , 2010 ; Moreno et al , 2012 ). An inoculum of 10 6 EIEC cells is sufficient for infection, whereas as low as 10 2 Shigella cells can cause successful infection ( DuPont et al , 1971 ).…”

Section: Difference In Pathogenecity and Virulence Genes Expressionmentioning

confidence: 99%

Relationship among Shigella spp. and enteroinvasive Escherichia coli (EIEC) and their differentiation

Ud-Din¹,

Wahid²

2014

Braz. J. Microbiol.

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Shigellosis produces inflammatory reactions and ulceration on the intestinal epithelium followed by bloody or mucoid diarrhea. It is caused by enteroinvasive E. coli (EIEC) as well as any species of the genus Shigella, namely, S. dysenteriae, S. flexneri, S. boydii, and S. sonnei. This current species designation of Shigella does not specify genetic similarity. Shigella spp. could be easily differentiated from E. coli, but difficulties observed for the EIEC-Shigella differentiation as both show similar biochemical traits and can cause dysentery using the same mode of invasion. Sequencing of multiple housekeeping genes indicates that Shigella has derived on several different occasions via acquisition of the transferable forms of ancestral virulence plasmids within commensal E. coli and form a Shigella-EIEC pathovar. EIEC showed lower expression of virulence genes compared to Shigella, hence EIEC produce less severe disease than Shigella spp. Conventional microbiological techniques often lead to confusing results concerning the discrimination between EIEC and Shigella spp. The lactose permease gene (lacY) is present in all E. coli strains but absent in Shigella spp., whereas β-glucuronidase gene (uidA) is present in both E. coli and Shigella spp. Thus uidA gene and lacY gene based duplex real-time PCR assay could be used for easy identification and differentiation of Shigella spp. from E. coli and in particular EIEC.

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“…Reduction of endogenous MUC17 in undifferentiated Caco-2 cells is associated with enhanced bacterial invasion in response to exposure to EIEC infection (765). Moreno et al (766) compared the innate and adaptive immune responses to EIEC and S. flexneri infection. EIEC triggered DC activation to produce IL-10, IL-12, and TNF-␣, whereas S. flexneri induced only the production of TNF-␣.…”

Section: Host Cellular Defense Responsesmentioning

confidence: 99%

Pathogenesis of Human Enterovirulent Bacteria: Lessons from Cultured, Fully Differentiated Human Colon Cancer Cell Lines

Moal

Servin

2013

Microbiol Mol Biol Rev

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SUMMARY Hosts are protected from attack by potentially harmful enteric microorganisms, viruses, and parasites by the polarized fully differentiated epithelial cells that make up the epithelium, providing a physical and functional barrier. Enterovirulent bacteria interact with the epithelial polarized cells lining the intestinal barrier, and some invade the cells. A better understanding of the cross talk between enterovirulent bacteria and the polarized intestinal cells has resulted in the identification of essential enterovirulent bacterial structures and virulence gene products playing pivotal roles in pathogenesis. Cultured animal cell lines and cultured human nonintestinal, undifferentiated epithelial cells have been extensively used for understanding the mechanisms by which some human enterovirulent bacteria induce intestinal disorders. Human colon carcinoma cell lines which are able to express in culture the functional and structural characteristics of mature enterocytes and goblet cells have been established, mimicking structurally and functionally an intestinal epithelial barrier. Moreover, Caco-2-derived M-like cells have been established, mimicking the bacterial capture property of M cells of Peyer's patches. This review intends to analyze the cellular and molecular mechanisms of pathogenesis of human enterovirulent bacteria observed in infected cultured human colon carcinoma enterocyte-like HT-29 subpopulations, enterocyte-like Caco-2 and clone cells, the colonic T84 cell line, HT-29 mucus-secreting cell subpopulations, and Caco-2-derived M-like cells, including cell association, cell entry, intracellular lifestyle, structural lesions at the brush border, functional lesions in enterocytes and goblet cells, functional and structural lesions at the junctional domain, and host cellular defense responses.

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Recognition of enteroinvasive Escherichia coli and Shigella flexneri by dendritic cells: distinct dendritic cell activation states

Abstract: The innate and adaptive immune responses of dendritic cells (DCs)

Cited by 14 publications

References 20 publications

Diarrheagenic Escherichia coli

Diarrheagenic Escherichia coli

Relationship among Shigella spp. and enteroinvasive Escherichia coli (EIEC) and their differentiation

Pathogenesis of Human Enterovirulent Bacteria: Lessons from Cultured, Fully Differentiated Human Colon Cancer Cell Lines

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