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

Gobert, Alain P.; Coste, Alix T.; Guzmán, Carlos A.; Vareille, Marjolaine; Hindré, Thomas; Sablet, Thibaut de; Girardeau, J P; Martin, Christine

doi:10.1016/j.micinf.2007.10.018

Cited by 15 publications

(10 citation statements)

References 38 publications

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“…2001) and induction of chemokine response (Rogers et al. 2003; Gobert et al. 2008), respectively, suggests a high virulence potential for those two isolates, especially the one carrying the highly toxic stx2d variant of stx2 .…”

Section: Discussionmentioning

confidence: 99%

“…Both isolates lacked the eae gene, as expected for potential atypical EHEC; only one possessed the activatable stx2d variant. The simultaneous presence of ehxA, saa, and fliC-H21 involved in enterohemolysin production (Schmidt et al 1995), adherence (Paton et al 2001) and induction of chemokine response (Rogers et al 2003;Gobert et al 2008), respectively, suggests a high virulence potential for those two isolates, especially the one carrying the highly toxic stx2d variant of stx2. The three other recovered STEC O91 strains were negative for ehxA, saa, fliC-H21 and eae and might thus be less pathogenic for humans.…”

Section: Discussionmentioning

confidence: 99%

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Screening of food raw materials for the presence of Shiga toxin-producingEscherichia coliO91:H21

Madic

Lécureuil

Dilasser

et al. 2009

Letters in Applied Microbiology

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Aims: To provide information on the prevalence and detection, in foods, of Shiga toxin‐producing Escherichia coli (STEC) O91:H21. Methods and Results: Seven hundred fifteen minced beef meats and 205 raw milk samples were analysed by stx‐specific PCR‐ELISA. Samples positive for stx were subsequently tested for the presence of wzy‐O91, fliC‐H21 and the adhesin‐encoding gene saa. For minced meat, 16 (2·2%) and 11 (1·5%) samples were found positive for (stx, wzy‐O91, fliC‐H21) and (stx, wzy‐O91, fliC‐H21, saa) combinations, respectively. For raw milk, seven (3·4%) samples were found positive for the (stx, wzy‐O91, fliC‐H21) combination but none of these contained saa. Two STEC O91:H21 saa‐positive strains and three STEC O91 H21– and saa‐negative strains were isolated by colony hybridization. Conclusions: A low prevalence of potentially pathogenic STEC O91:H21 in food products was found using a combination of PCR assays targeting stx, wzy‐O91, fliC‐H21 and saa. Significance and Impact of the Study: The PCR‐based approach described here represents a valuable method for rapid screening of food samples contaminated by STEC O91:H21.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Screening of food raw materials for the presence of Shiga toxin-producingEscherichia coliO91:H21

Madic

Lécureuil

Dilasser

et al. 2009

Letters in Applied Microbiology

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“…These genes encode a type 3 secretion system (T3SS; LEE1, LEE2, LEE3), a translocon and a syringe (LEE4) that allows bacteria to inject effectors in epithelial cells, such as the LEE5-encoded intimin receptor Tir; moreover, other proteins not carried by the LEE can be translocated by the T3SS into enterocytes [3], [4]. The injected effectors and/or protein of the translocon itself interact with the host signal transduction, leading to actin polymerization and to microvilli effacement [2], to regulation of the innate immune response [5], [6], and to increased electrolyte transport [7]. Regulation of gene expression within the LEE is known to be complex and governed by a large number of influences, including environmental cues or quorum sensing, and involves several specific or global regulators [8], [9].…”

Section: Introductionmentioning

confidence: 99%

NsrR, GadE, and GadX Interplay in Repressing Expression of the Escherichia coli O157:H7 LEE Pathogenicity Island in Response to Nitric Oxide

Branchu¹,

Matrat²,

Vareille³

et al. 2014

PLoS Pathog

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Expression of genes of the locus of enterocyte effacement (LEE) is essential for adherence of enterohemorrhagic Escherichia coli (EHEC) to intestinal epithelial cells. Gut factors that may modulate LEE gene expression may therefore influence the outcome of the infection. Because nitric oxide (NO) is a critical effector of the intestinal immune response that may induce transcriptional regulation in enterobacteria, we investigated its influence on LEE expression in EHEC O157:H7. We demonstrate that NO inhibits the expression of genes belonging to LEE1, LEE4, and LEE5 operons, and that the NO sensor nitrite-sensitive repressor (NsrR) is a positive regulator of these operons by interacting directly with the RNA polymerase complex. In the presence of NO, NsrR detaches from the LEE1/4/5 promoter regions and does not activate transcription. In parallel, two regulators of the acid resistance pathway, GadE and GadX, are induced by NO through an indirect NsrR-dependent mechanism. In this context, we show that the NO-dependent LEE1 down-regulation is due to absence of NsrR-mediated activation and to the repressor effect of GadX. Moreover, the inhibition of expression of LEE4 and LEE5 by NO is due to loss of NsrR-mediated activation, to LEE1 down-regulation and to GadE up-regulation. Lastly, we establish that chemical or cellular sources of NO inhibit the adherence of EHEC to human intestinal epithelial cells. These results highlight the critical effect of NsrR in the regulation of the LEE pathogenicity island and the potential role of NO in the limitation of colonization by EHEC.

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“…Secondly, flagellins are potent inducers of chemokine expression in vitro, and appear to play a role in host immune responses to STEC. IL-8, a chemokine that promotes neutrophil recruitment and chemotaxis, and CCL20 (MIP3A), a chemokine promoting chemotaxis of lymphocytes and dendritic cells, are both upregulated and secreted by cultured intestinal epithelial cells in response to H flagellin (49). Finally, signaling through TLR5 in colonic epithelial cells in response to H7 flagellin induced chemokine expression (176).…”

Section: Flagellinmentioning

confidence: 99%

Role of Shiga toxin dissemination and inflammation in the pathogenesis of Shiga toxin-producing Escherichia coli infection

Hostetter

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an attempt to further clarify the contribution of Stx2e to the enhanced TNF-α levels observed in livers of clinical pigs, porcine macrophages were stimulated with either Stx2e or erythrocyte-bound Stx2e. Neither Stx2e nor erythrocyte-bound Stx2e were potent stimulators of TNF-α production by porcine macrophages. In conclusion, higher levels of liver IL-1β and TNF-α were detected in clinical pigs than subclinical pigs. This could indicate a greater systemic inflammatory response in STEC inoculated pigs that develop clinical disease. Importantly, clinical pigs had higher levels of plasma TNF-α prior to the onset of clinical disease, making plasma TNF-α a potential candidate for systemic disease risk assessment in STEC infected individuals.

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

Cited by 15 publications

References 38 publications

Screening of food raw materials for the presence of Shiga toxin-producingEscherichia coliO91:H21

Screening of food raw materials for the presence of Shiga toxin-producingEscherichia coliO91:H21

NsrR, GadE, and GadX Interplay in Repressing Expression of the Escherichia coli O157:H7 LEE Pathogenicity Island in Response to Nitric Oxide

Role of Shiga toxin dissemination and inflammation in the pathogenesis of Shiga toxin-producing Escherichia coli infection

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