scholarly journals Bile Salts Differentially Enhance Resistance of Enterohemorrhagic Escherichia Coli O157:H7 to Human Cationic Antimicrobial Peptides

2021 ◽  
Author(s):  
Crystal Gadishaw-Lue
Keyword(s):  
Escherichia Coli ◽  
Lipid A ◽  
Enterohemorrhagic Escherichia Coli ◽  
Escherichia Coli O157 ◽  
Salt Mixture ◽  
Two Component System ◽  
Two Component ◽  
Genes Encoding ◽  
Uremic Syndrome ◽  
Bacterial Outer Membrane

Enterohemorrhagic Escherichia coli (EHEC) causes severe food and water-borne illness associated with diarrhea, hemorrhagic colitis (HC), and hemolytic-uremic syndrome (HUS). Previously, we reported that treatment of EHEC with a physiologically relevant bile salt mixture (BSM) upregulates genes encoding a two-component system (TCS) (basRS) and a lipid A modification pathway (arnBCADTEF). The current study examines the effect of BSM treatment on EHEC resistance to human cationic antimicrobials, human defensin, HD-5 and cathelicidin, LL-37. Results show a significant increase in resistance to HD-5 when EHEC are pre-treated with BSM as compared to untreated EHEC. The BS-induced resistance phenotype is lost in each of the arnT and basS mutants. Interestingly, BSM treatment does not affect resistance to LL-37. The results of this study provide evidence that BS serve as an environmental cue by triggering changes via a TCS that result in protective modifications of the bacterial outer membrane, thereby increasing resistance to HD-5.

scholarly journals Bile Salts Differentially Enhance Resistance of Enterohemorrhagic Escherichia Coli O157:H7 to Human Cationic Antimicrobial Peptides

2021 ◽  
Author(s):  
Crystal Gadishaw-Lue
Keyword(s):  
Escherichia Coli ◽  
Lipid A ◽  
Enterohemorrhagic Escherichia Coli ◽  
Escherichia Coli O157 ◽  
Salt Mixture ◽  
Two Component System ◽  
Two Component ◽  
Genes Encoding ◽  
Uremic Syndrome ◽  
Bacterial Outer Membrane

Enterohemorrhagic Escherichia coli (EHEC) causes severe food and water-borne illness associated with diarrhea, hemorrhagic colitis (HC), and hemolytic-uremic syndrome (HUS). Previously, we reported that treatment of EHEC with a physiologically relevant bile salt mixture (BSM) upregulates genes encoding a two-component system (TCS) (basRS) and a lipid A modification pathway (arnBCADTEF). The current study examines the effect of BSM treatment on EHEC resistance to human cationic antimicrobials, human defensin, HD-5 and cathelicidin, LL-37. Results show a significant increase in resistance to HD-5 when EHEC are pre-treated with BSM as compared to untreated EHEC. The BS-induced resistance phenotype is lost in each of the arnT and basS mutants. Interestingly, BSM treatment does not affect resistance to LL-37. The results of this study provide evidence that BS serve as an environmental cue by triggering changes via a TCS that result in protective modifications of the bacterial outer membrane, thereby increasing resistance to HD-5.

scholarly journals Bile salts differentially enhance resistance of enterohemorrhagic escherichia coli 0157:H7 to human cationic antimicrobial peptides

2021 ◽  
Author(s):  
Crystal Gadishaw-Lue
Keyword(s):  
Escherichia Coli ◽  
Bile Salts ◽  
Lipid A ◽  
Enterohemorrhagic Escherichia Coli ◽  
Salt Mixture ◽  
Two Component System ◽  
Two Component ◽  
Genes Encoding ◽  
Uremic Syndrome ◽  
Bacterial Outer Membrane

Enterohemorrhagic Escherichia coli (EHEC) causes severe food and water-borne illness associated with diarrhea, hemorrhagic colitis (HC), and hemolytic-uremic syndrome (HUS). Previously, we reported that treatment of EHEC with a physiologically relevant bile salt mixture (BSM) upregulates genes encoding a two-component system (TCS) (basRS) and a lipid A modification pathway (arnBCADTEF). The current study examines the effect of BSM treatment on EHEC resistance to human cationic antimicrobials, human defensin, HD-5 and cathelicidin, LL-37. Results show a significant increase in resistance to HD-5 when EHEC are pre-treated with BSM as compared to untreated EHEC. The BS-induced resistance phenotype is lost in each of the arnT and basS mutants. Interestingly, BSM treatment does not affect resistance to LL-37. The results of this study provide evidence that BS serve as an environmental cue by triggering changes via a TCS that result in protective modifications of the bacterial outer membrane, thereby increasing resistance to HD-5.

scholarly journals Bile salts differentially enhance resistance of enterohemorrhagic escherichia coli 0157:H7 to human cationic antimicrobial peptides

2021 ◽  
Author(s):  
Crystal Gadishaw-Lue
Keyword(s):  
Escherichia Coli ◽  
Bile Salts ◽  
Lipid A ◽  
Enterohemorrhagic Escherichia Coli ◽  
Salt Mixture ◽  
Two Component System ◽  
Two Component ◽  
Genes Encoding ◽  
Uremic Syndrome ◽  
Bacterial Outer Membrane

Enterohemorrhagic Escherichia coli (EHEC) causes severe food and water-borne illness associated with diarrhea, hemorrhagic colitis (HC), and hemolytic-uremic syndrome (HUS). Previously, we reported that treatment of EHEC with a physiologically relevant bile salt mixture (BSM) upregulates genes encoding a two-component system (TCS) (basRS) and a lipid A modification pathway (arnBCADTEF). The current study examines the effect of BSM treatment on EHEC resistance to human cationic antimicrobials, human defensin, HD-5 and cathelicidin, LL-37. Results show a significant increase in resistance to HD-5 when EHEC are pre-treated with BSM as compared to untreated EHEC. The BS-induced resistance phenotype is lost in each of the arnT and basS mutants. Interestingly, BSM treatment does not affect resistance to LL-37. The results of this study provide evidence that BS serve as an environmental cue by triggering changes via a TCS that result in protective modifications of the bacterial outer membrane, thereby increasing resistance to HD-5.

scholarly journals Novel Type of Fimbriae Encoded by the Large Plasmid of Sorbitol-Fermenting Enterohemorrhagic Escherichia coli O157:H−

2001 ◽  
Vol 69 (7) ◽  
pp. 4447-4457 ◽  
Author(s):  
Werner Brunder ◽  
A. Salam Khan ◽  
Jörg Hacker ◽  
Helge Karch
Keyword(s):  
Escherichia Coli ◽  
Gene Cluster ◽  
Enterohemorrhagic Escherichia Coli ◽  
Plasmid Replication ◽  
Escherichia Coli O157 ◽  
E Coli ◽  
Significant Homology ◽  
Genes Encoding ◽  
Uremic Syndrome ◽  
Six Genes

ABSTRACT Sorbitol-fermenting (SF) enterohemorrhagic Escherichia coli (EHEC) O157:H− have emerged as important causes of diarrheal diseases and the hemolytic-uremic syndrome in Germany. In this study, we characterized a 32-kb fragment of the plasmid of SF EHEC O157:H−, pSFO157, which differs markedly from plasmid pO157 of classical non-sorbitol-fermenting EHEC O157:H7. We found a cluster of six genes, termed sfpA,sfpH, sfpC, sfpD,sfpJ, and sfpG, which mediate mannose-resistant hemagglutination and the expression of fimbriae.sfp genes are similar to the pap genes, encoding P-fimbriae of uropathogenic E. coli, but thesfp cluster lacks homologues of genes encoding subunits of a tip fibrillum as well as regulatory genes. The major pilin, SfpA, despite its similarity to PapA, does not cluster together with known PapA alleles in a phylogenetic tree but is structurally related to the PmpA pilin of Proteus mirabilis. The putative adhesin gene sfpG, responsible for the hemagglutination phenotype, shows significant homology neither to papGnor to other known sequences. Sfp fimbriae are 3 to 5 nm in diameter, in contrast to P-fimbriae, which are 7 nm in diameter. PCR analyses showed that the sfp gene cluster is a characteristic of SF EHEC O157:H− strains and is not present in other EHEC isolates, diarrheagenic E. coli, or otherEnterobacteriaceae. The sfp gene cluster is flanked by two blocks of insertion sequences and an origin of plasmid replication, indicating that horizontal gene transfer may have contributed to the presence of Sfp fimbriae in SF EHEC O157:H−.

scholarly journals Regulation of tartrate metabolism by TtdR and relation to the DcuS–DcuR-regulated C4-dicarboxylate metabolism of Escherichia coli

Microbiology ◽  
2009 ◽  
Vol 155 (11) ◽  
pp. 3632-3640 ◽  
Author(s):  
Ok Bin Kim ◽  
Julia Reimann ◽  
Hanna Lukas ◽  
Uwe Schumacher ◽  
Jan Grimpo ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Promoter Region ◽  
Anaerobic Conditions ◽  
Two Component System ◽  
Two Component ◽  
Fumarate Respiration ◽  
Mutual Regulation ◽  
Genes Encoding ◽  
Type Gene ◽  
Tartrate Dehydratase

Escherichia coli catabolizes l-tartrate under anaerobic conditions to oxaloacetate by the use of l-tartrate/succinate antiporter TtdT and l-tartrate dehydratase TtdAB. Subsequently, l-malate is channelled into fumarate respiration and degraded to succinate by the use of fumarase FumB and fumarate reductase FrdABCD. The genes encoding the latter pathway (dcuB, fumB and frdABCD) are transcriptionally activated by the DcuS–DcuR two-component system. Expression of the l-tartrate-specific ttdABT operon encoding TtdAB and TtdT was stimulated by the LysR-type gene regulator TtdR in the presence of l- and meso-tartrate, and repressed by O2 and nitrate. Anaerobic expression required a functional fnr gene, and nitrate repression depended on NarL and NarP. Expression of ttdR, encoding TtdR, was repressed by O2, nitrate and glucose, and positively regulated by TtdR and DcuS. Purified TtdR specifically bound to the ttdR–ttdA promoter region. TtdR was also required for full expression of the DcuS–DcuR-dependent dcuB gene in the presence of tartrate. Overall, expression of the ttdABT genes is subject to l-/meso-tartrate-dependent induction, and to aerobic and nitrate repression. The control is exerted directly at ttdA and in addition indirectly by regulating TtdR levels. TtdR recognizes a subgroup (l- and meso-tartrate) of the stimuli perceived by the sensor DcuS, which responds to all C4-dicarboxylates; both systems apparently communicate by mutual regulation of the regulatory genes.

scholarly journals Phylogenetic Clades 6 and 8 of Enterohemorrhagic Escherichia coli O157:H7 With Particular stx Subtypes are More Frequently Found in Isolates From Hemolytic Uremic Syndrome Patients Than From Asymptomatic Carriers

2014 ◽  
Vol 1 (2) ◽  
Author(s):  
Sunao Iyoda ◽  
Shannon D. Manning ◽  
Kazuko Seto ◽  
Keiko Kimata ◽  
Junko Isobe ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Hemolytic Uremic Syndrome ◽  
Clinical Presentation ◽  
Pulsed Field Gel Electrophoresis ◽  
Enterohemorrhagic Escherichia Coli ◽  
Escherichia Coli O157 ◽  
Nitric Oxide Reductase ◽  
Asymptomatic Carriers ◽  
Uremic Syndrome ◽  
Risk Of Disease

Abstract Background.  Enterohemorrhagic Escherichia coli (EHEC) O157:H7 infection causes severe diseases such as bloody diarrhea and hemolytic uremic syndrome (HUS). Although EHEC O157:H7 strains have exhibited high genetic variability, their abilities to cause human diseases have not been fully examined. Methods.  Clade typing and stx subtyping of EHEC O157:H7 strains, which were isolated in Japan during 1999–2011 from 269 HUS patients and 387 asymptomatic carriers (ACs) and showed distinct pulsed-field gel electrophoresis patterns, were performed to determine relationships between specific lineages and clinical presentation. Results.  Clades 6 and 8 strains were more frequently found among the isolates from HUS cases than those from ACs (P = .00062 for clade 6, P < .0001 for clade 8). All clade 6 strains isolated from HUS patients harbored stx2a and/or stx2c, whereas all clade 8 strains harbored either stx2a or stx2a/stx2c. However, clade 7 strains were predominantly found among the AC isolates but less frequently found among the HUS isolates, suggesting a significant association between clade 7 and AC (P < .0001). Logistic regression analysis revealed that 0–9 year old age is a significant predictor of the association between clade 8 and HUS. We also found an intact norV gene, which encodes for a nitric oxide reductase that inhibits Shiga toxin activity under anaerobic condition, in all clades 1–3 isolates but not in clades 4–8 isolates. Conclusions.  Early detection of EHEC O157:H7 strains that belonged to clades 6/8 and harbored specific stx subtypes may be important for defining the risk of disease progression in EHEC-infected 0- to 9-year-old children.

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