Inhibitory Effect of Capsular Antigen of <i>Vibrio vulnificus</i> on Bactericidal Activity of Human Serum

Shinoda, Sumió; Kobayashi, Masakazu; Yamada, Hiroyuki; Yoshida, Shin Ichi; Ogawa, Midori; Mizuguchi, Yasuo

doi:10.1111/j.1348-0421.1987.tb03102.x

Cited by 22 publications

(6 citation statements)

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“…V. vulnificus strains with encapsulated phenotypes (opaque colonies) have a much higher lethality in mice than those with unencapsulated phenotypes (translucent colonies). This is considered to be due to CPS providing a protective barrier against phagocytosis by neutrophils and macrophages and against bacteriolysis by complement (24,29,31,32). Many reports have focused on the interaction between phagocytes and CPS (17,25,28,33); however, there is little in the literature on host immune responses to V. vulnificus.…”

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confidence: 97%

Vibrio vulnificus Damages Macrophages during the Early Phase of Infection

et al. 2007

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Vibrio vulnificus is an estuarine bacterium that can cause primary septicemia as well as serious wound infections. Generally, clinical isolates have a high lethal effect compared with environmental isolates. However, little is known about the mechanisms by which V. vulnificus causes disease. In this study, we compared the pathogenicity of a clinical isolate, strain M2799, with that of an environmental isolate, strain JCM3731. The clinical isolate showed 100 times higher lethality in mice than the environmental isolate. In strain M2799-inoculated mice, the number of macrophages decreased significantly, whereas there was no appreciable change in the number of macrophages in strain JCM3731-inoculated mice. The clinical isolate showed high cytotoxic activity, especially to macrophages, compared with the environmental isolate in vitro. The growth of the clinical isolate was almost completely inhibited in the presence of macrophages. Moreover, the survival rate of the clinical isolate-inoculated mice increased by recruitment of macrophages. These results indicate that V. vulnificus infection progresses by damage to macrophages during the early phase of infection.Vibrio vulnificus is a gram-negative halophilic marine bacterium that is found in estuarine waters and contaminates oysters and other seafood. Consumption of raw contaminated seafood or contamination of wounds with V. vulnificus can lead to septicemia or wound infection, respectively. Infection with V. vulnificus is associated with predisposing conditions such as hepatitis, cirrhosis, diabetes, hemochromatosis, and immune compromise (1,2,15,22). V. vulnificus causes a rapid and severe disease process resulting in extensive tissue damage. Mortality was up to 50% in septic patients, with most of them dying within 48 h with a fulminate course after infection (8). In addition, clinical isolates have generally high lethality in mice and high cytotoxicity to various cultured cells compared with environmental isolates (11,26,27).Several putative virulence factors of V. vulnificus, such as metalloprotease (14, 19), hemolysin-cytolysin (7, 23), capsular polysaccharide (CPS) (25,32), and means of iron acquisition (e.g., siderophore) (18), have been reported in vivo and in vitro. Lethality in animal models is clearly related to CPS expression. Both CPS expression and virulence are associated with an opaque colony morphology (25, 33). V. vulnificus strains with encapsulated phenotypes (opaque colonies) have a much higher lethality in mice than those with unencapsulated phenotypes (translucent colonies). This is considered to be due to CPS providing a protective barrier against phagocytosis by neutrophils and macrophages and against bacteriolysis by complement (24, 29, 31, 32). Many reports have focused on the interaction between phagocytes and CPS (17,25,28,33); however, there is little in the literature on host immune responses to V. vulnificus. Despite considerable published research on the virulence factors of V. vulnificus, very little definitive information has been ...

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confidence: 97%

Vibrio vulnificus Damages Macrophages during the Early Phase of Infection

et al. 2007

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“…Currently, the capsule which may interfere with complement-dependent host defence system (1,8,15,17,21), siderophores which may facilitate in vivo growth of the bacteria through uptake of iron, an in vivo growth factor (16,20), and cytolysin which may be responsible for tissue damage (6) are reported to be putative virulence factors of V. vulnzficus. In addition to these factors, the protease which enhances vascular permeability also seems to be an important virulence factor of V.…”

Section: Vascular Permeability-enhancing Activity Of Protease-deficiementioning

confidence: 99%

Role of the Protease in the Permeability Enhancement by Vibrio vulnificus

Miyoshi

Shinoda

1988

Microbiology and Immunology

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The protease produced by Vibrio vulnificus enhances vascular permeability through histamine release from mast cells and activation of the plasma kallikreinkinin system which generates bradykinin when injected into the dorsal skin. V. vulnificus living cells also enhanced vascular permeability within a few hours after the injection into the dorsal skin. The permeability-enhancing activity of living cells was greatly reduced by addition of soybean trypsin inhibitor, a specific inhibitor for plasma kallikrein-kinin system, or anti-protease IgG. Two protease-deficient mutants induced by nitrosoguanidine treatment had only one-tenth permeability- Vibrio vulnificus infections are characterized by edema and ulcer formation on the skin of limbs (2, 3, 18). Extreme hemoconcentration due to edema fluid accumulation and death have been observed experimentally in mice injected with living V. vulnificus cells. (4). Thus, the permeability-enhancing factor which forms edema appears to be important in the pathogenesis of V. vulnificus.V. vulnificus produces many toxic or pathogenic factors, including cytolysin (5, 7, 14), protease (7, 12), and siderophores (16, 20). Of these factors, cytolysin have been found to possess vascular permeability-enhancing activity (5,7,14). We recently noted that V. vulnificus protease also enhanced hypodermic permeability through release of chemical mediators such as histamine and bradykinin (10, 11, 13). However, contribution of these factors to permeability enhancement followed by edema formation during V. vulnificus infection is not clear.The protease of V. vulnificus is a metalloprotease containing zinc atom (unpublished observation). No specific protease inhibitor for bacterial metalloprotease is present in plasma (19), although the V. vulnificus cytolysin is inactivated by cholesterol, a normal constituent of plasma (5,9,14). Therefore, if the protease is elabolated during V. vulnificus infection, the protease might enhance vascular permeability and form edema and ulcer more effectively than the cytolysin.In the present paper, we report that permeability enhancement by protease-1025

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“…In V. vulnificus, CPS production is clearly a prerequisite for virulence and correlates with lethality in mice (7~9), complement-mediated lysis (10), cytokine induction (11), 26 and resistance to phagocytosis (12). CPS is a protective antigen in mice (13,14).…”

Section: Introductionmentioning

confidence: 99%

Cyclic AMP and Cyclic AMP-Receptor Protein are Required for Optimal Capsular Polysaccharide Expression

Cho

Shin

2015

J Bacteriol Virol

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Vibrio vulnificus causes fatal infections in susceptible individuals. Group 1 capsular polysaccharide (CPS) operon is responsible for CPS expression, which plays an essential role in the pathogenesis of this pathogen. Cyclic AMP (cAMP) and cAMP receptor protein (Crp) complex, which responds to glucose availability and functions as a global regulator, has been known to affect CPS production in this pathogen. This study was undertaken to experimentally verify whether cAMP-Crp directly or indirectly affects CPS production. A mutation in cyaA encoding adenylate cyclase, which is required for cAMP biosynthesis, inhibited V. vulnificus growth and changed opaque colonies to translucent colonies, and these changes were recovered by complementing cyaA or by adding exogenous cAMP. A mutation in crp encoding Crp also inhibited V. vulnificus growth and changed opaque colonies to translucent colonies, and these changes were recovered by complementing crp. Moreover, the crp or cyaA mutation decreased the susceptibility of V. vulnificus against NaOCl. The crp mutation reduced the transcription levels of group 1 CPS operon on a per cell basis. Glucose addition in the absence of Crp stimulated V. vulnificus growth, changed translucent colonies to opaque colonies, and increased the transcription levels of group 1 CPS operon. These results indicate that cAMP or Crp is indirectly involved in optimal CPS production by positively affecting metabolism or V. vulnificus growth rather than by directly controlling the expression of group 1 CPS operon.

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Inhibitory Effect of Capsular Antigen of Vibrio vulnificus on Bactericidal Activity of Human Serum

Cited by 22 publications

References 24 publications

Vibrio vulnificus Damages Macrophages during the Early Phase of Infection

Vibrio vulnificus Damages Macrophages during the Early Phase of Infection

Role of the Protease in the Permeability Enhancement by Vibrio vulnificus

Cyclic AMP and Cyclic AMP-Receptor Protein are Required for Optimal Capsular Polysaccharide Expression

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