Enteroaggregative Escherichia coli expresses a novel flagellin that causes IL-8 release from intestinal epithelial cells

Steiner, Theodore S.; Nataro, James P.; Poteet‐Smith, Celeste E.; Smith, Jeffrey A.; Guerrant, Richard L.

doi:10.1172/jci8892

Cited by 229 publications

(194 citation statements)

References 29 publications

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“…Since the discovery that flagellin from enteroaggregative E. coli induces IL-8 release from IEC (40), flagellins from many bacterial pathogens, including EPEC flagellin, have been assessed for their proinflammatory roles. These earlier studies found that purified EPEC flagellin induces IL-8 expression in IEC (47), while similar findings were made with EHEC flagellin (4).…”

Section: Discussionmentioning

confidence: 99%

Flagellin-Dependent and -Independent Inflammatory Responses following Infection by EnteropathogenicEscherichia coliandCitrobacter rodentium

Khan

Bouzari

et al. 2008

Infect Immun

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Enteropathogenic Escherichia coli (EPEC) and the murine pathogen Citrobacter rodentium belong to the attaching and effacing (A/E) family of bacterial pathogens. These noninvasive bacteria infect intestinal enterocytes using a type 3 secretion system (T3SS), leading to diarrheal disease and intestinal inflammation. While flagellin, the secreted product of the EPEC fliC gene, causes the release of interleukin 8 (IL-8) from epithelial cells, it is unclear whether A/E bacteria also trigger epithelial inflammatory responses that are FliC independent. The aims of this study were to characterize the FliC dependence or independence of epithelial inflammatory responses to direct infection by EPEC or C. rodentium. Following infection of Caco-2 intestinal epithelial cells by wild-type and ⌬fliC EPEC, a rapid activation of several proinflammatory genes, including those encoding IL-8, monocyte chemoattractant protein 1, macrophage inflammatory protein 3␣ (MIP3␣), and ␤-defensin 2, occurred in a FliC-dependent manner. These responses were accompanied by mitogen-activated protein kinase activation, as well as the Toll-like receptor 5 (TLR5)-dependent activation of NF-B. At later infection time points, a subset of these proinflammatory genes (IL-8 and MIP3␣) was also induced in cells infected with ⌬fliC EPEC. The nonmotile A/E pathogen C. rodentium also triggered similar innate responses through a TLR5-independent but partially NF-B-dependent mechanism. Moreover, the EPEC FliC-independent responses were increased in the absence of the locus of enterocyte effacement-encoded T3SS, suggesting that translocated bacterial effectors suppress rather than cause the FliC-independent inflammatory response. Thus, we demonstrate that infection of intestinal epithelial cells by A/E pathogens can trigger an array of proinflammatory responses from epithelial cells through both FliC-dependent and -independent pathways, expanding our understanding of the innate epithelial response to infection by these pathogens.

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Section: Discussionmentioning

confidence: 99%

Flagellin-Dependent and -Independent Inflammatory Responses following Infection by EnteropathogenicEscherichia coliandCitrobacter rodentium

Khan

Bouzari

et al. 2008

Infect Immun

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“…EAggEC infections are usually associated with watery diarrhoea, which is often persistent [20]. Illness results from a complex interaction between pathogen and host, which implicates the initial adherence of the bacteria to the epithelium of terminal ileum and colon, by virtue of the aggregative adherence fimbriae (characteristic aggregative pattern), followed by a damage/secretion stage manifested by cytokine release, mucosal toxicity, intestinal secretion and induction of mucosal inflammation [22][23][24][25][26]. EAggEC is best known for its role in persistent diarrhoea (>14 days) in infants and children in developing countries.…”

Section: General Characteristics Of Eaggecmentioning

confidence: 99%

Characteristics of the enteroaggregative Shiga toxin/verotoxin-producing Escherichia coli O104:H4 strain causing the outbreak of haemolytic uraemic syndrome in Germany, May to June 2011

et al. 2011

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The Escherichia coli strain causing a large outbreak of haemolytic uraemic syndrome and bloody diarrhoea in Germany in May and June 2011 possesses an unusual combination of pathogenic features typical of enteroaggregative E. coli together with the capacity to produce Shiga toxin. Through rapid national and international exchange of information and strains the known occurrence in humans was quickly assessed. We describe simple diagnostic screening tools to detect the outbreak strain in clinical specimens and a novel real-time PCR for its detection in foods.

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“…Poly(I:C) was obtained from Amersham Biosciences (Amersham, U.K.). Flagellin, from Salmonella typhimurium, and trypsin-inactivated flagellin (flagellin-control) were a kind gift from Dr. J.-C. Sirard (Institut Suisse de Recherches Experimentales sur le Cancer, Epalinges, Switzerland) (28). CpG oligodeoxynucleotide motif GTCGTT (2006) was provided by Invitrogen Life Technologies (Rockville, MD).…”

Section: Cell Culture Media and Reagentsmentioning

confidence: 99%

Toll Receptor-Mediated Regulation of NADPH Oxidase in Human Dendritic Cells

Vulcano

Dusi

Lissandrini

et al. 2004

The Journal of Immunology

122

108

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Activation of NADPH oxidase represents an essential mechanism of defense against pathogens. Dendritic cells (DC) are phagocytic cells specialized in Ag presentation rather than in bacteria killing. Human monocyte-derived DC were found to express the NADPH oxidase components and to release superoxide anions in response to phorbol esters and phagocytic agonists. The NADPH oxidase components p47phox and gp91phox were down-regulated during monocyte differentiation to DC, and maturation of DC with pathogen-derived molecules, known to activate TLRs, increased p47phox and gp91phox expression and enhanced superoxide anions release. Similar results were obtained with plasmacytoid DC following maturation with influenza virus. In contrast, activation of DC by immune stimuli (CD40 ligand) did not regulate NADPH oxidase components or respiratory burst. NADPH oxidase-derived oxygen radicals did not play any role in DC differentiation, maturation, cytokine production, and induction of T cell proliferation, as based on the normal function of DC generated from chronic granulomatous disease patients and the use of an oxygen radical scavenger. However, NADPH oxidase activation was required for DC killing of intracellular Escherichia coli. It is likely that the selective regulation of oxygen radicals production by pathogen-activated DC may function to limit pathogen dissemination during DC trafficking to secondary lymphoid tissues.

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Enteroaggregative Escherichia coli expresses a novel flagellin that causes IL-8 release from intestinal epithelial cells

Cited by 229 publications

References 29 publications

Flagellin-Dependent and -Independent Inflammatory Responses following Infection by EnteropathogenicEscherichia coliandCitrobacter rodentium

Flagellin-Dependent and -Independent Inflammatory Responses following Infection by EnteropathogenicEscherichia coliandCitrobacter rodentium

Characteristics of the enteroaggregative Shiga toxin/verotoxin-producing Escherichia coli O104:H4 strain causing the outbreak of haemolytic uraemic syndrome in Germany, May to June 2011

Toll Receptor-Mediated Regulation of NADPH Oxidase in Human Dendritic Cells

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