Induction of Nitric Oxide Synthase Expression by Vibrio vulnificus Cytolysin

Kang, Mikyung; Jhee, Eun-Chung; Koo, Bon-Sun; Yang, Jeong‐Yeh; Park, Byung‐Hyun; Kim, Jong‐Suk; Rho, Hye-Won; Kim, Hyung-Rho; Park, Jin-Woo

doi:10.1006/bbrc.2001.6311

Cited by 21 publications

(11 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, recent data demonstrated that VVC induce mammalian cell activation through production of intracellular signaling molecules such as hydrogen peroxide (H 2 O 2 ) or nitric oxide (NO) (Kwon et al, 2001;Kang et al, 2002). These reports supported that VVC could act as a ligand which stimulates intracellular signaling systems.…”

Section: Introductionmentioning

confidence: 85%

“…VVC shows a high affinity to mammalian cell membranes, indicating that it has a broad spectrum of cytotoxicity against a variety of cells including erythrocytes, neutrophils, mast cells, endothelial cells, and macrophages (Kreger and Lockwood, 1981;Yamanaka et al, 1990;Kim et al, 1993;Park et al, 1994;Chae et al, 1996;Kim, 1997;Kim et al, 1998;Kwon et al, 2001;Kang et al, 2002). Furthermore, recent data demonstrated that VVC induce mammalian cell activation through production of intracellular signaling molecules such as hydrogen peroxide (H 2 O 2 ) or nitric oxide (NO) (Kwon et al, 2001;Kang et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Cholesterol induce oligomerization of Vibrio vulnificus cytolysin specifically

Kim

Kim²

2002

Exp Mol Med

Self Cite

View full text Add to dashboard Cite

Vibrio vulnificus cytolysin (VVC) has been implicated as one of the important virulence determinants of V. vulnificus that causes serious septicemia and wound infection. An attempt was made to investigate that VVC could act as a ligand which stimulates intracellular signaling systems. Cholesterol dose-dependently blocked VVC hemolytic activity through oligomerization of cytolysin. Among cholesterol derivatives including 7-dehydrocholesterol, cholesteryl esters, deoxycholate, and cholestane tested, only 7-dehydrocholesterol induced oligomerization as well as inactivation of VVC. These results show that oligomerization of VVC is completely dependent on three-dimensional structure of cholesterol where specific interaction of cholesterol at oligomerization sites of VVC is very selective. These findings support the idea that cholesterol which constitute many of cellular plasma membrane could be a receptor of VVC on plasma membrane of target cells.

show abstract

Section: Introductionmentioning

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Cholesterol induce oligomerization of Vibrio vulnificus cytolysin specifically

Kim

Kim²

2002

Exp Mol Med

Self Cite

View full text Add to dashboard Cite

show abstract

“…Additional symptoms resulting from hemolysin exposure include fluid accumulation, intestinal irregularities, partial paralysis, and lethality (37,81). Direct examination of the effects of hemolysin on host cells revealed that toxin exposure increased vascular permeability, apoptosis of endothelial cells, induction of inducible nitric oxide synthase activity, increased nitric oxide production, and possibly increased neutrophil recruitment (55,58,80). Cell death caused by hemolysin occurs through pore formation in the cellular membrane, and it has been suggested that this activity ultimately leads to the vascular permeability and hypotension characteristic of V. vulnificus disease (62).…”

Section: Cellular Damage and Cytotoxicitymentioning

confidence: 99%

Vibrio vulnificus: Disease and Pathogenesis

2009

View full text Add to dashboard Cite

Vibrio vulnificus is an opportunistic human pathogen that is highly lethal and is responsible for the overwhelming majority of reported seafood-related deaths in the United States (30,117). This bacterium is a part of the natural flora of coastal marine environments worldwide and has been isolated from water, sediments, and a variety of seafood, including shrimp, fish, oysters, and clams (4,7,25,26,43,97,109,116,118,149,165). Consumption of seafood (primarily raw oysters) containing V. vulnificus can result in a severe, fulminant systemic infection. Characteristics of this disease include fever, chills, nausea, hypotensive septic shock, and the formation of secondary lesions on the extremities of patients (11,22,41,74,115,146). This primary septicemia is the most lethal infection caused by V. vulnificus, with an average mortality rate exceeding 50% (30, 41). A review of 459 U.S. cases reported by the FDA between 1992 and 2007 (J. D. Oliver, unpublished) revealed that 51.6% of the patients died. Interestingly, 85.6% of the cases were male; this aspect of the infection is discussed later in this review. Of 180 cases in 2002 to 2007 for which FDA data were available, 92.8% of patients had consumed raw oysters prior to the onset of symptoms and 95.3% had some preexisting disease(s). The latter are clearly associated with V. vulnificus infection, with liver diseases, such as cirrhosis or hepatitis, being the most common (116). In addition to septicemia, V. vulnificus can produce serious wound infections that typically result from exposure of open wounds to water harboring the bacterium (114). Wound infections are frequently contracted as a result of recreational swimming, fishing injuries, or seafood handling (7, 46). Like systemic disease, wound infections progress rapidly to cellulitis, ecchymoses, and bullae, which can progress to necrotizing fasciitis at the site of infection; however, the mortality rate for wound infections (ca. 25%) is lower than that for systemic disease (10,13,74). This organism possesses a wide array of virulence factors, including acid neutralization, capsular polysaccharide expression, iron acquisition, cytotoxicity, motility, and expression of proteins involved in attachment and adhesion. These factors likely require concerted expression for pathogenesis to take place and appear to be under the control of global regulators. Overall, V. vulnificus is a complex microorganism with physiological characteristics that contribute to its survival in the marine environment and in the human host.

show abstract

“…VVC is an extremely active exotoxin and is characteristic of the Vibrio vulnificus species. In addition to hemolytic activities (4)(5), VVC destroys various other mammalian cells including mast (6,7), macrophages (8) and endothelial cells (9). Studies have shown that VVC perforates the target cell membrane by binding to cholesterol in the host cell membrane and plays an important role in the dissolution of cells (10,11).…”

Section: Introductionmentioning

confidence: 99%

Apoptotic effect of Vibrio vulnificus cytolysin on A549 human lung adenocarcinoma cells

et al. 2011

View full text Add to dashboard Cite

Abstract. Vibrio vulnificus cytolysin (VVC) has a very strong cytotoxic effect on various types of mammalian cells. However, the inhibitory effect of VVC on the proliferation of human lung cancer cells has scarcely been reported. This study aimed to analyze the effects of recombinant VVC (rVVC) on the A549 human lung adenocarcinoma cell line and to investigate the underlying molecular mechanisms governing these effects. This study showed that rVVC inhibited the proliferation of A549 cells in a concentration-and time-dependent manner (as measured by the MTT assay). rVVC failed to induce the release of intracellular lactate dehydrogenase (LDH) from the target cells suggesting that osmotic lysis may not contribute to its cytolysin-induced cytotoxicity. Treatment of A549 cells with an IC 50 (concentration of drug that inhibits cell growth by 50%) of rVVC resulted in morphological changes and blebbing typical of apoptosis. Annexin-V FITC analysis by FCM indicated that rVVC-induced apoptosis in A549 cells occurs in a dosedependent manner. A DNA fragmentation assay was utilized to investigate the apoptosis induced by rVVC. The pro-apoptotic activity of rVVC was attributed to its ability to modulate, in a concerted manner, the expression of Bcl-2 and Bax proteins, which were down-and up-regulated, respectively. Caspase-9 and -3 were subsequently activated, however caspase-8 was not. These results prove that rVVC effectively induces programmed cell death and suggests that rVVC-induced apoptosis in the A549 cell line is mediated by the regulation of Bcl-2 protein expression and the activation of caspase-9 and -3.

show abstract

Induction of Nitric Oxide Synthase Expression by Vibrio vulnificus Cytolysin

Cited by 21 publications

References 30 publications

Cholesterol induce oligomerization of Vibrio vulnificus cytolysin specifically

Cholesterol induce oligomerization of Vibrio vulnificus cytolysin specifically

Vibrio vulnificus: Disease and Pathogenesis

Apoptotic effect of Vibrio vulnificus cytolysin on A549 human lung adenocarcinoma cells

Contact Info

Product

Resources

About