Characterization of a mutant of Vibrio vulnificus for heme utilization

Miyoshi, Shin‐ichi; Inami, Yu; Moriya, Yuko; Kamei, Takehito; Rahman, Md.Monzur; Yamamoto, Satoshi; Tomochika, Ken Ichi; Shinoda, Sumió

doi:10.1111/j.1574-6968.1997.tb10274.x

Cited by 9 publications

(2 citation statements)

References 22 publications

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“…This fact strongly suggests that vvhA transcription may be negatively regulated by iron via Fur. Nevertheless, VvhA has been known to be produced sufficiently under iron-sufficient conditions [44], and we and others also have used iron-sufficient conventional laboratory media, such as Luria-Bertani and HI media, Figure 4. Iron-mediated stimulation of extracellular cytolysin-hemolysin (VvhA) secretion via the PilD-mediated type II general secretion system.…”

Section: Discussionmentioning

confidence: 99%

Iron Differentially Regulates Gene Expression and Extracellular Secretion ofVibrio vulnificusCytolysin‐Hemolysin

Kim¹,

Chung²,

Shin³

2009

J INFECT DIS

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In a previous study, we showed that Vibrio vulnificus is a ferrophilic bacterium that requires high levels of available iron for growth. In the present study, we show that iron stimulates, in an unusual manner, the production of cytolysin-hemolysin (VvhA), the most potent exotoxin produced by V. vulnificus. The vvhA gene possesses a putative ferric uptake regulator (Fur)-binding box in the regulatory region, andvvhA transcription was repressed by iron and de-repressed by fur mutation. However, extracellular secretion of VvhA was conversely increased by iron. Iron increased transcription of pilD, which encodes PilD, a component of the type II general secretion system responsible for extracellular VvhA secretion. These results indicate that iron increases extracellular VvhA secretion via the type II general secretion system, although it can repress vvhA transcription via Fur.

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Section: Discussionmentioning

confidence: 99%

Iron Differentially Regulates Gene Expression and Extracellular Secretion ofVibrio vulnificusCytolysin‐Hemolysin

Kim¹,

Chung²,

Shin³

2009

J INFECT DIS

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“…The outer membrane was collected by treatment with 1% Sarkosyl followed by centrifugation (100000 × g, 60 min), 10) and then, the membrane preparation was mixed with an equal volume of 125 mM Tris-HCl buffer containing 2% sodium dodecyl sulfate (SDS), 20% grycerol and 0.05% bromophenol blue (pH 6.8). Thereafter, the outer membrane proteins were solubilized by heat treatment at 100 • C for 5 min, and to remove SDS, the solubilized proteins were precipitated by the addition of 5% trichloroacetic acid and rinsed with acetone.…”

Section: Methodsmentioning

confidence: 99%

Role of the Enterotoxic Hemolysin in Pathogenicity of Vibrio mimicus

Kobayashi

Takata

et al. 2008

JOURNAL OF HEALTH SCIENCE

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Vibrio mimicus (V. mimicus) is a causative agent of human gastroenteritis and food poisoning. Although several toxic or virulence factors have been isolated from the bacterium, an enterotoxic hemolysin is a sole toxin produced by all clinical isolates. In the present study, we found that the antibody against the hemolysin significantly inhibited the fluidaccumulating action of the living cells inoculated into a rabbit ileal loop, and that the hemolysin gene (vmhA) was probably expressed by the bacterium in the ileal loop. Additionally, in spit of the comparable motility and similar proteome profiles, a vmhA mutant revealed the reduced fluid-accumulating activity. Theses findings suggest that the hemolysin contributes to full virulence of V. mimicus.

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Mechanism of High Susceptibility of Iron‐Overloaded Mouse to Vibrio vulnificus Infection

Hor

Chang

et al. 2000

Microbiology and Immunology

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Vibrio vulnificus produces fulminant septicemia in humans with underlying conditions, particularly those with diseases that elevate the iron level. The effect of a high iron level on the virulence of V vulnificus was therefore investigated in mice treated with iron dextran. The mice loaded with iron became highly susceptible to V vulnificus infection, the LD50 (50% lethal dose) decreased five logs when infected per peritoneum. However, when infected via the oral route, the LD50 was affected little unless the mouse was treated with an additional drug such as cyclophosphamide or D-galactosamine. Mice with or without iron-overloading died when the bacterial concentration in the blood reached 105 cfu/ml or above. Iron increased the growth rate of the bacteria, both inside and outside of the animal, quickly reaching a lethal concentration in the iron-overloaded mouse. V vulnificus, grown with or without the addition of iron, showed strong cytotoxicity on the isolated cells or within the animal at high bacterial concentration. Iron overload stimulated the production of tumor necrosis factor a (TNF-a), a major factor of septic shock, in mice upon infection with the bacteria, probably caused by the endotoxin; however, the neutrophils, whose migration is effected by TNF-a, appeared to be less active. Taken together, the major virulence factor of V vulnificus appeared to be the accelerated growth of bacteria to quickly reach the lethal level and the lower activity of immune cells including neutrophil as a result of iron-overloading. These two effects manifest other virulence factors, the host's as well as bacterial. Such factors, other than TNF-a stimulated by the endotoxin, enhanced cytotoxicity, which kills the host cells including the host's immune cells.

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Characterization of a mutant of Vibrio vulnificus for heme utilization

Cited by 9 publications

References 22 publications

Iron Differentially Regulates Gene Expression and Extracellular Secretion ofVibrio vulnificusCytolysin‐Hemolysin

Iron Differentially Regulates Gene Expression and Extracellular Secretion ofVibrio vulnificusCytolysin‐Hemolysin

Role of the Enterotoxic Hemolysin in Pathogenicity of Vibrio mimicus

Mechanism of High Susceptibility of Iron‐Overloaded Mouse to Vibrio vulnificus Infection

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