Enterohemorrhagic<i>Escherichia coli</i>Infection Induces Interleukin-8 Production via Activation of Mitogen-Activated Protein Kinases and the Transcription Factors NF-κB and AP-1 in T84 Cells

Dahan, Stéphanie; Busuttil, V.; Imbert, Véronique; Peyron, Jean François; Rampal, Patrick; Czerucka, Dorota

doi:10.1128/iai.70.5.2304-2310.2002

Cited by 89 publications

(96 citation statements)

References 56 publications

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“…The MAPK p38, ERK1/2, and JNK are stimulated by EHEC in Caco-2 (12) and T84 cells (13). Nonetheless, although these transduction factors play a significant role in regulating intestinal epithelial cell IL-8 production, they are not involved in NF-B activation (12,13).…”

Section: Discussionmentioning

confidence: 99%

“…The activation of NF-B in T84 cells in response to the EHEC strain EDL931 was previously established by Dahan et al (13). Moreover, it has been also described that NF-B is poorly and transiently activated in HeLa cells infected for 3 h with EDL933 or with an O26:H Ϫ STEC strain (27); in this report, the authors also show that cells stimulated with a mutant lacking EspB exhibit increased DNA-binding activity of NF-B, suggesting an inhibition of the cellular response by this translocator and effector protein encoded by the locus of enterocyte effacement.…”

Section: Discussionmentioning

confidence: 99%

“…This inflammatory response may alter the integrity of the epithelial barrier and facilitate the translocation of Stx across the mucosa. As for intracellular pathogens from the Shigella, Salmonella, or Escherichia genus (10,11), numerous in vitro studies have evidenced that NF-B plays a key role in the induction of proinflammatory factors by EHEC-infected human intestinal epithelial cell lines (12,13). EHEC factors, e.g., flagellin or proteins encoded by the locus of enterocyte effacement, have been shown to modulate NF-B activation (14).…”

Section: S Higa Toxin Producing Escherichia Coli (Stec)mentioning

confidence: 99%

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Shiga Toxin Produced by Enterohemorrhagic Escherichia coli Inhibits PI3K/NF-κB Signaling Pathway in Globotriaosylceramide-3-Negative Human Intestinal Epithelial Cells

Gobert

Vareille

Glasser³

et al. 2007

The Journal of Immunology

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Shiga toxin (Stx) produced by enterohemorrhagic Escherichia coli (EHEC) binds to endothelial cells expressing globotriaosylceramide-3 (Gb-3) and induces cell death by inhibiting translation. Nonetheless, the effects of Stx on human enterocytes, which lacks receptor Gb-3, remain less known. In this study, we questioned whether EHEC-derived Stx may modulate cellular signalization in the Gb-3-negative human epithelial cell line T84. Stx produced by EHEC was fixed and internalized by the cells. A weak activation of NF-κB was observed in T84 cells after EHEC infection. Cells infected with an isogenic mutant lacking stx1 and stx2, the genes encoding Stx, displayed an increased NF-κB DNA-binding activity. Consequently, the NF-κB-dependent CCL20 and IL-8 gene transcription and chemokine production were enhanced in T84 cells infected with the Stx mutant in comparison to the wild-type strain. Investigating the mechanism by which Stx modulates NF-κB activation, we showed that the PI3K/Akt signaling pathway was not induced by EHEC but was enhanced by the strain lacking Stx. Pharmacological inhibition of the PI3K/Akt signalization in EHEC ΔStx-infected T84 cells yielded to a complete decrease of NF-κB activation and CCL20 and IL-8 mRNA expression. This demonstrates that the induction of the PI3K/Akt/NF-κB pathway is potentially induced by EHEC, but is inhibited by Stx in Gb-3-negative epithelial cells. Thus, Stx is an unrecognized modulator of the innate immune response of human enterocytes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: S Higa Toxin Producing Escherichia Coli (Stec)mentioning

confidence: 99%

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Shiga Toxin Produced by Enterohemorrhagic Escherichia coli Inhibits PI3K/NF-κB Signaling Pathway in Globotriaosylceramide-3-Negative Human Intestinal Epithelial Cells

Gobert

Vareille

Glasser³

et al. 2007

The Journal of Immunology

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“…It has been proposed that the colonic mucosa damaged by the inflammation represents a way for Stx to cross the epithelial barrier. In vitro studies have shown that STEC strains induce the expression in intestinal epithelial cells of IL-8 and CCL20 [13,18], which can recruit neutrophils and dendritic cells, respectively. In this context, the ability of STEC strains to induce the host innate immune response could be a reliable marker of bacterial virulence.…”

Section: Introductionmentioning

confidence: 99%

Modulation of chemokine gene expression by Shiga-toxin producing Escherichia coli belonging to various origins and serotypes

Gobert¹,

Coste²,

Guzmán

et al. 2008

Microbes and Infection

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“…35 The phosphorylation of multiple MAPKs, including ERK1/2, p38 and JNK, is induced upon EHEC infection, followed by AP-1 activation at later stages of infection. 62 Moreover, the phosphorylation of the T42 residue of RPS3 by ERK facilitates its nuclear entry. 63 The precise role of NleH2 in ERK/MAPK pathways, whether via the ERK substrate RPS3 or independent of RPS3, requires more investigation.…”

Section: Mapk Inflammatory Signaling Pathwaysmentioning

confidence: 99%

Modulation of host signaling in the inflammatory response by enteropathogenic Escherichia coli virulence proteins

Zhuang

Chen

et al. 2016

Cell Mol Immunol

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To successfully infect host cells and evade the host immune response, a type III secretion system (T3SS) is commonly used by enteric bacterial pathogens such as enteropathogenic Escherichia coli (EPEC). Recent findings have revealed that various effectors are injected into host cells through the T3SS and exert an inhibitory effect on inflammatory signaling pathways, subverting the immune responses to these pathogens. Here we review recent studies aimed at addressing the modulation of several important inflammatory signaling pathways modulated by EPEC effector proteins, such as the nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) pathways, which provides insight into the unfinished work in this unexplored field and helps to identify novel positions in inflammatory signaling networks for EPEC effectors.

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EnterohemorrhagicEscherichia coliInfection Induces Interleukin-8 Production via Activation of Mitogen-Activated Protein Kinases and the Transcription Factors NF-κB and AP-1 in T84 Cells

Cited by 89 publications

References 56 publications

Shiga Toxin Produced by Enterohemorrhagic Escherichia coli Inhibits PI3K/NF-κB Signaling Pathway in Globotriaosylceramide-3-Negative Human Intestinal Epithelial Cells

Shiga Toxin Produced by Enterohemorrhagic Escherichia coli Inhibits PI3K/NF-κB Signaling Pathway in Globotriaosylceramide-3-Negative Human Intestinal Epithelial Cells

Modulation of chemokine gene expression by Shiga-toxin producing Escherichia coli belonging to various origins and serotypes

Modulation of host signaling in the inflammatory response by enteropathogenic Escherichia coli virulence proteins

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