Nitric oxide‐enhanced Shiga toxin production was regulated by Fur and RecA in enterohemorrhagic <i>Escherichia coli</i> O157

Ichimura, Kimitoshi; Shimizu, Takeshi; Matsumoto, Akio; Hirai, Shinichiro; Yokoyama, Eiji; Takeuchi, Hiroki; Yahiro, Kinnosuke; Noda, Masatoshi

doi:10.1002/mbo3.461

Cited by 16 publications

(20 citation statements)

References 71 publications

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“…The gene for Stx is encoded on lambdoid bacteriophages integrated into the STEC genome, and phage induction is connected with the bacterial SOS response 60 . Thus, production of Stx2 in O157:H7 strain was stimulated by treatment with DNA-damaging agents, such as antibiotics 61 – 63 , H 2 O 2 64 or nitric oxide 65 , which is consistent with our result as shown in Supplementary Figure S6 B. Thus, antimicrobial activity by LCN2 for STEC did not stimulate bacteriophage-mediated Stx2 production in STEC O157:H7 and O113:H21.…”

Section: Discussionsupporting

confidence: 90%

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Subtilase cytotoxin induces a novel form of Lipocalin 2, which promotes Shiga-toxigenic Escherichia coli survival

Yahiro¹,

Ogura²,

Goto³

et al. 2020

Sci Rep

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Shiga-toxigenic Escherichia coli (STEC) infection causes severe bloody diarrhea, renal failure, and hemolytic uremic syndrome. Recent studies showed global increases in Locus for Enterocyte Effacement (LEE)-negative STEC infection. Some LEE-negative STEC produce Subtilase cytotoxin (SubAB), which cleaves endoplasmic reticulum (ER) chaperone protein BiP, inducing ER stress and apoptotic cell death. In this study, we report that SubAB induces expression of a novel form of Lipocalin-2 (LCN2), and describe its biological activity and effects on apoptotic cell death. SubAB induced expression of a novel LCN2, which was regulated by PRKR-like endoplasmic reticulum kinase via the C/EBP homologous protein pathway. SubAB-induced novel-sized LCN2 was not secreted into the culture supernatant. Increased intracellular iron level by addition of holo-transferrin or FeCl3 suppressed SubAB-induced PARP cleavage. Normal-sized FLAG-tagged LCN2 suppressed STEC growth, but this effect was not seen in the presence of SubAB- or tunicamycin-induced unglycosylated FLAG-tagged LCN2. Our study demonstrates that SubAB-induced novel-sized LCN2 does not have anti-STEC activity, suggesting that SubAB plays a crucial role in the survival of LEE-negative STEC as well as inducing apoptosis of the host cells.

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Section: Discussionsupporting

confidence: 90%

“…Primers used for PCR are shown in Supplementary Table S1 . Relative expression was normalized to gapdh or etuA and calibrated to the respective controls 73 .…”

Section: Methodsmentioning

confidence: 99%

Subtilase cytotoxin induces a novel form of Lipocalin 2, which promotes Shiga-toxigenic Escherichia coli survival

Yahiro¹,

Ogura²,

Goto³

et al. 2020

Sci Rep

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“…Authors of these works proposed norV as a direct virulence determinant for the pathogenesis of EHEC. We and others have also demonstrated that NO strongly affects the expression of both stx and LEE genes in EHEC, and therefore modulates the expression of key virulence factors [46][47][48]. Altogether, these data argue that establishment of an adapted response to nitrosative stress is a key component of both the adaptation of EHEC to the GIT and the control of its virulence program.…”

Section: Discussionsupporting

confidence: 64%

Identification and prevalence of in vivo-induced genes in enterohaemorrhagic Escherichia coli

et al. 2019

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Enterohaemorrhagic Escherichia coli (EHEC) are food-borne pathogens responsible for bloody diarrhoea and renal failure in humans. While Shiga toxin (Stx) is the cardinal virulence factor of EHEC, its production by E. coli is not sufficient to cause disease and many Shiga-toxin producing E. coli (STEC) strains have never been implicated in human infection. So far, the pathophysiology of EHEC infection is not fully understood and more knowledge is needed to characterize the "auxiliary" factors that enable a STEC strain to cause disease in humans. In this study, we applied a recombinase-based in vivo expression technology (RIVET) to the EHEC reference strain EDL933 in order to identify genes specifically induced during the infectious process, using mouse as an infection model. We identified 31 in vivo-induced (ivi) genes having functions related to metabolism, stress adaptive response and bacterial virulence or fitness. Eight of the 31 ivi genes were found to be heterogeneously distributed in EHEC strains circulating in France these last years. In addition, they are more prevalent in strains from the TOP seven priority serotypes and particularly strains carrying significant virulence determinants such as Stx2 and intimin adhesin. This work sheds further light on bacterial determinants over-expressed in vivo during infection that may contribute to the potential of STEC strains to cause disease in humans.

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“…Recent studies reported that some genetic factors, other than the Stx2a phage subtype, enhanced the level of Stx2 production in O157 strains. Stx2 production in O157 strains was reported to be enhanced by deletion of anaerobic nitric oxide reductase genes ( norV ) [ 37 , 38 ]. A recent study suggested that the level of Stx2 production in O157 strains was affected by insertion of IS 629 into the Stx2a phage genome and by the presence of SNPs in the phage genome [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Enterohemorrhagic Escherichia coli O157 subclade 8b strains in Chiba Prefecture, Japan, produced larger amounts of Shiga toxin 2 than strains in subclade 8a and other clades

et al. 2018

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Enterohemorrhagic Escherichia coli O157 (O157) strains can be classified into clades (one of several phylogenetic groups) by single nucleotide polymorphisms (SNPs): these are clade 1, clade 2, clade 3, descendant and ancestral clades 4/5, clade 6, clade 7, clade 8, clade 9, and clade 12. Some recent studies showed that some O157 strains in clade 8 produced a larger amount of Shiga toxin (Stx) 2 than other strains. In this study, 1121 epidemiologically unlinked strains of O157 isolated in Chiba Prefecture, Japan were classified into clades during 1996–2014. Clade 8 strains were further classified into subclade 8a (67 strains) and subclade 8b (48 strains) using SNP analysis. In the absence of mitomycin C (MMC), subclade 8a strains in this study produced significantly greater amounts of Stx2 than subclade 8b strains. However, in the presence of MMC, the levels of Stx2 production in subclade 8b strains were significantly greater than subclade 8a strains. On the other hand, a recent study reported that the Stx2 production level in O157 strains was determined mainly by the subtypes of Stx2a phage (ϕStx2_α, β, γ, δ, ε, and ζ). Using O157 strains in this study, the Stx2a phages were classified into these subtypes. In this study, all strains of subclades 8a and 8b carried ϕStx2a_γ and ϕStx2a_δ, respectively. Some strains in clade 6 also carried ϕStx2a_δ. In the presence of MMC, subclade 8b strains produced significantly greater amounts of Stx2 than clade 6 strains carrying ϕStx2_δ. In this study, we propose that Stx2 production in subclade 8b strains in the presence of MMC might be enhanced due to genetic factors other than ϕStx2_δ.

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Nitric oxide‐enhanced Shiga toxin production was regulated by Fur and RecA in enterohemorrhagic Escherichia coli O157

Cited by 16 publications

References 71 publications

Subtilase cytotoxin induces a novel form of Lipocalin 2, which promotes Shiga-toxigenic Escherichia coli survival

Subtilase cytotoxin induces a novel form of Lipocalin 2, which promotes Shiga-toxigenic Escherichia coli survival

Identification and prevalence of in vivo-induced genes in enterohaemorrhagic Escherichia coli

Enterohemorrhagic Escherichia coli O157 subclade 8b strains in Chiba Prefecture, Japan, produced larger amounts of Shiga toxin 2 than strains in subclade 8a and other clades

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