The extracellular cytolysin of Vibrio vulnificus: inactivation and relationship to virulence in mice

Wright, Anita C.; Morris, J. Glenn

doi:10.1128/iai.59.1.192-197.1991

Cited by 126 publications

(46 citation statements)

References 44 publications

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“…In animal models, locally and systemically administered VvhA reproduces the same clinical and pathological manifestations of septicemia that are caused by the administration of live bacteria (Rhee et al, 1984;Gray & Kreger, 1985, 1986Park et al, 1996). Doubts have been raised, however, concerning the pathological significance of VvhA, since it has been demonstrated that the null mutation of vvhA had no effect on the virulence of V. vulnificus (Wright & Morris, 1991). Uncertainty also exists as to whether or not VvhA is produced in vivo.…”

Section: Introductionmentioning

confidence: 99%

Suppression and inactivation ofVibrio vulnificushemolysin in cirrhotic ascites, a humanex vivoexperimental system

Choi¹,

Park²,

Sun³

et al. 2006

FEMS Immunology &Amp; Medical Microbiology

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To elucidate the mechanisms underlying the in vivo suppression and inactivation of Vibrio vulnificus hemolysin (VvhA), we used cirrhotic ascites fluid as a human ex vivo experimental system. VvhA expression was suppressed in proportion to the amount of cirrhotic ascites. The expression of vvhA in undiluted cirrhotic ascites could be suppressed further by the addition of glucose, a constituent of cirrhotic ascites. VvhA was readily inactivated in the presence of cirrhotic ascites by a cholesterol-mediated oligomerization and interaction with an undefined constituent(s) of cirrhotic ascites. These results indicate that the expression of vvhA can be suppressed and that any VvhA produced is inactivated by the constituents of cirrhotic ascites. Our results suggest that only a very small portion of the VvhA that is produced in human body fluids may actually contribute to the pathogenesis of V. vulnificus septicemia. It is suggested that cirrhotic ascites could be used as a human ex vivo experimental system for the studies on the in vivo expression and the significance of V. vulnificus virulence factors.

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Section: Introductionmentioning

confidence: 99%

Suppression and inactivation ofVibrio vulnificushemolysin in cirrhotic ascites, a humanex vivoexperimental system

Choi¹,

Park²,

Sun³

et al. 2006

FEMS Immunology &Amp; Medical Microbiology

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“…RtxA1 is a crucial cytotoxin involved in cellular damage and necrosis of infected tissues (20-24). We previously reported that host cell contact is required for RtxA1 production and cytotoxicity (20).…”

Section: Resultsmentioning

confidence: 99%

A stealth adhesion factor contributes toVibrio vulnificuspathogenicity: Flp pili play roles in host invasion, survival in the blood stream and resistance to complement activation

Duong-Nu

Jeong

Kim

et al. 2019

Preprint

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30The tad operons encode the machinery required for adhesive Flp (fimbrial low-31 molecular-weight protein) pili biogenesis. Vibrio vulnificus, an opportunistic pathogen, harbors 32 three distinct tad loci. Among them, only tad1 locus was highly upregulated in in vivo growing 33 bacteria compared to in vitro culture condition. To understand the pathogenic roles of the three 34 tad loci during infection, we constructed single, double and triple tad loci deletion mutants. 35 Interestingly, only the Δtad123 triple mutant cells exhibited significantly decreased lethality in 36 mice. Ultrastructural observations revealed short, thin filamentous projections disappeared on the 37 Δtad123 mutant cells. Since the pilin was paradoxically non-immunogenic, a V5 tag was fused to 38 Flp to visualize the pilin protein by using immunogold EM and immunofluorescence 39 microscopy. The Δtad123 mutant cells showed attenuated host cell adhesion, delayed RtxA1 40 exotoxin secretion and subsequently impaired translocation across the intestinal epithelium 41 compared to wild type, which could be partially complemented with each wild type operon. The 42Δtad123 mutant was susceptible to complement-mediated bacteriolysis, predominantly via the 43 alternative pathway, suggesting stealth hiding role of the Tad pili. Taken together, all three tad 44 loci cooperate to confer successful invasion of V. vulnificus into deeper tissue and evasion from 45 host defense mechanisms, ultimately resulting in septicemia. 47To understand the roles of the three Tad operons in the pathogenesis of V. vulnificus 53 infection, we constructed mutant strain with single, double and triple Tad loci deletions. 54Employing a variety of mouse infection models coupled with molecular genetic analyses, we 55 demonstrate here that all three Tad operons are required for V. vulnificus pathogenicity as the 56 cryptic pili contribute to host cell and tissue invasion, survival in the blood, and resistance to 57 complement activation. 58 4 59 60Vibrio vulnificus is an opportunistic marine pathogen that causes fatal septicemia and 61 necrotizing wound infections in susceptible individuals with underlying hepatic diseases and 62 other immunocompromised conditions. In humans, this pathogen frequently causes rapidly 63 progressing fatal sepsis with a mortality rate of greater than 50% within a few days post-64 infection (1-4). During the infectious process, V. vulnificus must cope with dramatic 65 environmental changes by sensing changes in the host milieu (5). To establish successful 66 infections in vivo, V. vulnificus must manage spatiotemporally coordinated changes in the 67 expression levels of various virulence genes. 68 To understand the genome-wide gene expression changes in V. vulnificus after infection, 69 we recently performed a transcriptomic analysis of cells grown in vivo using a rat peritoneal 70 infection model. Notably, among the newly identified in vivo-expressed genes, a Flp/Tad pilus-71 encoding gene cluster (the tad1 locus) was found to be highly upregula...

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“…From studies on the encapsulated organism, the production of cytotoxin-hemolysin and iron availability in body fluid have been correlated to the human pathogenicity of V. vulnificus infections. [18][19][20][21] Recently, Park et al studied the systemic effects of V. vulnificus cytolysin in an animal model and discovered that the lungs are major target organs and that neutrophils might be involved in causing pulmonary damage. 22 Although cytolysin is highly cytotoxic to pulmonary endothelial cells and neutrophils, certain factors other than the cytolysin may play a crucial role in the pathogenesis of pulmonary involvement.…”

Section: Discussionmentioning

confidence: 99%

Vibrio vulnificus infection complicated by acute respiratory distress syndrome in a child with nephrotic syndrome

et al. 2000

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A 9‐year‐old girl with nephrotic syndrome visited a local hospital after developing fever, chills, and edematous changes and multiple hemorrhagic bullae on both legs over 2 days. Cultures of blood and an aspirate from the bullae yielded Vibrio vulnificus. The patient was transferred to our hospital because of persistent fever, generalized edema, acute renal failure, and disseminated intravascular coagulopathy. We treated this patient as a V. vulnificus infection complicated with necrotizing fasciitis. With minocycline and ceftazidime combination therapy was instituted. Emergency fasciotomy and continuous peritoneal dialysis were performed. The patient developed acute respiratory distress syndrome (ARDS) during the hospitalization, requiring intubation and mechanical ventilation. She eventually died. The histopathological findings showed diffuse alveolar damage with lobular pneumonitis. Hyaline membranes, composed of proteinaceous exudate and cellular debris, covered the alveolar surfaces. Microscopic examinations of lung could not distinguish the effects of cytolysin from other insults to lungs that occur in ARDS. This report highlights the postmortem pathological findings in V. vulnificus infection in a child with nephrotic syndrome complicated by ARDS. Pediatr Pulmonol. 2000; 29:400–403. © 2000 Wiley‐Liss, Inc.

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The extracellular cytolysin of Vibrio vulnificus: inactivation and relationship to virulence in mice

Cited by 126 publications

References 44 publications

Suppression and inactivation ofVibrio vulnificushemolysin in cirrhotic ascites, a humanex vivoexperimental system

Suppression and inactivation ofVibrio vulnificushemolysin in cirrhotic ascites, a humanex vivoexperimental system

A stealth adhesion factor contributes toVibrio vulnificuspathogenicity: Flp pili play roles in host invasion, survival in the blood stream and resistance to complement activation

Vibrio vulnificus infection complicated by acute respiratory distress syndrome in a child with nephrotic syndrome

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