SdiA, an <i>Escherichia coli</i> homologue of quorum‐sensing regulators, controls the expression of virulence factors in enterohaemorrhagic <i>Escherichia coli</i> O157:H7

Kanamaru, Kyoko; Kanamaru, Kengo; Tatsuno, Ichiro; Tobe, Toru; Sasakawa, Chihiro

doi:10.1046/j.1365-2958.2000.02171.x

Cited by 167 publications

(157 citation statements)

References 33 publications

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“…An insertion was mapped to sdiA, which encodes a quorum sensing regulator thought to sense an acyl homoserine lactone autoinducer (AI-1) owing to its similarity to Vibrio fisheri LuxR. SdiA negatively regulates the expression of EspD and intimin in E. coli O157 : H7 (Kanamaru et al, 2000), and one might have anticipated that upregulation of LEE expression caused by mutation of sdiA would enhance the carriage and virulence of EHEC. Mutation of sdiA has been reported to increase the virulence of Salmonella enterica serovar Typhimurium following oral inoculation of mice (Volf et al, 2002).…”

Section: Resultsmentioning

confidence: 99%

Identification of Escherichia coli O157 : H7 genes influencing colonization of the bovine gastrointestinal tract using signature-tagged mutagenesis

et al. 2004

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Enterohaemorrhagic Escherichia coli (EHEC) cause acute gastroenteritis in humans that may be complicated by life-threatening systemic sequelae. The predominant EHEC serotype affecting humans in the UK and North America is O157 : H7 and infections are frequently associated with contact with ruminant faeces. Strategies to reduce the carriage of EHEC in ruminants are expected to lower the incidence of human EHEC infections; however, the molecular mechanisms underlying persistence of EHEC in ruminants are poorly understood. This paper reports the first comprehensive survey for EHEC factors mediating colonization of the bovine intestines by using signature-tagged transposon mutagenesis. Seventy-nine E. coli O157 : H7 mutants impaired in their ability to colonize calves were isolated and 59 different genes required for intestinal colonization were identified by cloning and sequencing of the transposon insertion sites. Thirteen transposon insertions were clustered in the locus of enterocyte effacement (LEE), which encodes a type III protein secretion system required for the formation of attaching and effacing lesions on intestinal epithelia. A putative structural component of the apparatus (EscN) is essential for intestinal colonization; however, the type III secreted effector protein Map plays only a minor role. Other Type III secretion-associated genes were implicated in colonization of calves by E. coli O157 : H7, including z0990 (ecs0850), which encodes the non-LEE-encoded type III secreted effector NleD and the closely related z3023 (ecs2672) and z3026 (ecs2674) genes which encode homologues of Shigella IpaH proteins. We also identified a novel fimbrial locus required for intestinal colonization in calves by E. coli O157 : H7 (z2199-z2206; ecs2114-ecs2107/locus 8) and demonstrated that a mutant harbouring a deletion of the putative major fimbrial subunit gene is rapidly out-competed by the parent strain in co-infection studies. Our data provide valuable new information for the development of intervention strategies. INTRODUCTIONEnterohaemorrhagic Escherichia coli (EHEC) were first recognized as a cause of human disease in 1983 and are associated with diarrhoea and haemorrhagic colitis, which may be complicated by life-threatening renal and neurological sequelae, including haemolytic uraemic syndrome and thrombocytopaenic purpura (Karmali et al., 1983;Riley et al., 1983). EHEC, and in particular serotype O157 : H7, have since emerged as a major cause of severe diarrhoeal illness worldwide and EHEC infections are the leading antecedent to paediatric acute renal failure in many countries (Ammon, 1997; Mead et al., 1999; WHO, 1997). E. coli O157 : H7 strains are estimated to cause 73 480 cases and 60 deaths per annum in the United States, with serotypes other than O157 : H7 accounting for a further 36 740 illnesses (Mead et al., 1999). Non-O157 EHEC are an emerging problem, and indeed may be more prevalent than serogroup O157 in some countries (Bettelheim, 2000). EHEC are defined by their ability to produce one or mo...

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Section: Resultsmentioning

confidence: 99%

Identification of Escherichia coli O157 : H7 genes influencing colonization of the bovine gastrointestinal tract using signature-tagged mutagenesis

et al. 2004

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“…LEE1 expression is dependent on activation by Integration Host Factor (IHF) (Friedberg et al, 1999). Additional factors, including Fis, Per and quorum sensing, are involved in modulation of LEE1 gene expression (Goldberg et al, 2001 ;Kanamaru et al, 2000 ;Mellies et al, 1999 ;Sperandio et al, 1999).…”

Section: Expression Of Lee2 Lee3 Lee4 Lee5 Espg and Orf19mentioning

confidence: 99%

Thermoregulated expression of virulence genes in enteropathogenic Escherichia coli

2002

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Enteropathogenic Escherichia coli (EPEC) causes severe diarrhoea in young children. The locus of enterocyte effacement (LEE) pathogenicity island comprises a cluster of operons encoding a type III secretion system and related proteins that are associated with EPEC virulence. The LEE1 operon encodes Ler that positively regulates the LEE2, LEE3, LEE4, LEE5 and espG transcriptional units. The LEE operons are repressed at 27 SC and expressed at 37 SC. This paper describes a regulatory cascade of the thermoregulation of LEE operons. LEE1 including ler is repressed by H-NS at 27 SC but not at 37 SC. In contrast, the expression of the LEE2, LEE3, LEE4, LEE5 and espG transcriptional units is repressed by H-NS at both 27 SC and 37 SC. Upon shifting the culture temperature from 27 SC to 37 SC, Ler is synthesized and in turn activates the expression of LEE2, LEE3, LEE4 and espG by releasing the H-NS mediated repression. In the case of LEE5, Ler acts both by alleviating the H-NS mediated repression and by an additional mechanism, as yet to be defined.

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“…In this study, the HDRsEf1 intestine benefit mechanism was explored in vitro by using enterocyte-like HT-29 to mimic IEC. This study focuses on whether HDRsEf1 can regulate TLRs, NF-κB, pro-inflammatory cytokines, and anti-inflammatory cytokines, and EHEC O157:H7 was used as an intestine pathogen representative based on the fact that it is a common human and animal pathogenic bacterium and it can cause severe hemolytic-uremic syndrome (Kanamaru et al 2000).…”

Section: Introductionmentioning

confidence: 99%

The inflammation regulation effects ofEnterococcus faeciumHDRsEf1 on human enterocyte-like HT-29 cells

Tian

Yang

et al. 2016

Animal Cells and Systems

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Enterococcus faecium HDRsEf1 strain used as a probiotic to inhibit intestine inflammation and improve animal growth performance has been proved by our research team; however, it remains unclear how HDRsEf1 was recognized by intestine cells and how it activates the downstream pathway which benefit intestine health. In this study, HDRsEf1 was used to stimulate HT-29 cell line to partially uncover the intestine benefit mechanism of HDRsEf1. The results of cell viability assays showed that HDRsEf1 had no toxicity on HT-29 at concentrations up to 1 × 10 8 CFU/mL, HDRsEf1 could upregulate the TLR1, TLR2, and TLR6 mRNA level, especially TLR2, and significantly downregulate the mRNA level of TLR4, TLR5, TLR7, TLR8, but did not significantly affect the mRNA or protein level of MyD88, which suggests that HDRsEf1 activates the TLR2 pathway in an MyD88-independent pattern. HDRsEf1 could significantly downregulate the mRNA level of pro-inflammatory factors IL-1β, IL-6, IL-8, IL-12p35, IL-17, and TNF-α and did not affect the anti-inflammatory factors IL-10, PPAR-γ, and TSLP; besides HDRsEf1 did not upregulate the degradation of IκB in HT-29 cells. By contrast, enterohemorrhagic E. coli (EHEC) O157:H7 strongly up-regulated the mRNA level of pro-inflammatory factors IL-1β, IL-6, IL-8, IL-23, and TNF-α, downregulated obviously anti-inflammatory factor PPAR-ɣ, and obviously upregulated the degradation of IκB, which suggested that HDRsEf1 may act as an antagonist to regulate intestine inflammation response to intestine pathogen. These findings shed a light on the intestine benefit mechanism of HDRsEf1. ARTICLE HISTORY

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SdiA, an Escherichia coli homologue of quorum‐sensing regulators, controls the expression of virulence factors in enterohaemorrhagic Escherichia coli O157:H7

Cited by 167 publications

References 33 publications

Identification of Escherichia coli O157 : H7 genes influencing colonization of the bovine gastrointestinal tract using signature-tagged mutagenesis

Identification of Escherichia coli O157 : H7 genes influencing colonization of the bovine gastrointestinal tract using signature-tagged mutagenesis

Thermoregulated expression of virulence genes in enteropathogenic Escherichia coli

The inflammation regulation effects ofEnterococcus faeciumHDRsEf1 on human enterocyte-like HT-29 cells

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