The
            <i>pyrH</i>
            Gene of
            <i>Vibrio vulnificus</i>
            Is an Essential In Vivo Survival Factor

Lee, Shee Eun; Kim, Soo Young; Kim, Choon Mee; Kim, Mi-Kwang; Kim, Young Ran; Jeong, Kwangjoon; Ryu, Hwa-Ja; Lee, Youn Suhk; Chung, Sun Sik; Choy, Hyon E.; Rhee, Joon Haeng

doi:10.1128/iai.01499-06

Cited by 40 publications

(33 citation statements)

References 37 publications

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“…Previous studies have shown that some ivi genes are related to bacterial pathogenesis (Deb et al 2002;Kim et al 2003;Fernández et al 2004;Akhtar et al 2006;Lee et al 2007). To confirm these findings, three ivi genes identified in this study were evaluated for their roles in virulence of V. anguillarum.…”

Section: Discussionmentioning

confidence: 99%

“…Among these technologies, IVIAT is significantly superior to other reported in vivo expression technologies because it avoids the use of animal model (Handfield et al 2005). It has been applied in several important pathogenic bacteria for the identification of new virulent factors (Deb et al 2002;Kim et al 2003;Fernández et al 2004;Akhtar et al 2006;Lee et al 2007).…”

Section: Introductionmentioning

confidence: 99%

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Screening of genes expressed in vivo after infection by Vibrio anguillarum M3

Zou

Hao

et al. 2010

Letters in Applied Microbiology

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Aims: Genes uniquely expressed in vivo may contribute to the overall pathogenicity of an organism and are likely to serve as potential targets for the development of new vaccine. This study aims to screen the genes expressed in vivo after Vibrio anguillarum infection by in vivo‐induced antigen technology (IVIAT). Methods and Results: The convalescent‐phase sera were obtained from turbot (Scophthalmus maximus) survived after infection by the virulent V. anguillarum M3. The pooled sera were thoroughly adsorbed with M3 cells and Escherichia coli BL21 (DE3) cells. A genomic expression library of M3 was constructed and screened for the identification of immunogenic proteins by colony immunoblot analysis with the adsorbed sera. After three rounds of screening, 19 putative in vivo‐induced (ivi) genes were obtained. These ivi genes were catalogued into four functional groups: regulator/signalling, metabolism, biological process and hypothetical proteins. Three ivi genes were insertion‐mutated, and the growth and 50% lethal dose (LD50) of these mutants were evaluated. Conclusions: The identification of ivi genes in V. anguillarum M3 sheds light on understanding the bacterial pathogenesis and provides novel targets for the development of new vaccines and diagnostic reagents. Significance and Impact of the Study: To the best of our knowledge, this is the first report describing in vivo‐expressed genes of V. anguillarum using IVIAT. The screened ivi genes in this study could be new virulent factors and targets for the development of vaccine, which may have implications for the development of diagnostic regents.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Screening of genes expressed in vivo after infection by Vibrio anguillarum M3

Zou

Hao

et al. 2010

Letters in Applied Microbiology

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“…For iron overload experiments in mice, 8-week-old female CD1 mice were pretreated i.p. with 450 g of ferric ammonium citrate (approximately 80 g of elemental iron) (Sigma-Aldrich) 50 min before the bacterial infection (25).…”

Section: Methodsmentioning

confidence: 99%

Monoclonal Antibodies against Vibrio vulnificus RtxA1 Elicit Protective Immunity through Distinct Mechanisms

et al. 2014

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g Vibrio vulnificus causes rapidly progressing septicemia with an extremely high mortality rate (>50%), even with aggressive antibiotic treatment. The bacteria secrete multifunctional autoprocessing repeats-in-toxin (MARTX) toxins, which are involved in the pathogenesis of Gram-negative Vibrio species. Recently, we reported that immunization with the C-terminal region of V. vulnificus RtxA1/MARTX Vv , RtxA1-C, elicits a protective immune response against V. vulnificus through a poorly defined mechanism. In this study, we generated a panel of new monoclonal antibodies (MAbs) against V. vulnificus RtxA1-C and investigated their protective efficacies and mechanisms in a mouse model of infection. Prophylactic administration of seven MAbs strongly protected mice against lethal V. vulnificus infection (more than 90% survival). Moreover, three of these MAbs (21RA, 24RA, and 47RA) demonstrated marked efficacy as postexposure therapy. Notably, 21RA was therapeutically effective against lethal V. vulnificus infection by a variety of routes. Using Fab fragments and a neutropenic mouse model, we showed that 21RA and 24RA mediate protection from V. vulnificus infection through an Fc-independent and/or neutrophil-independent pathway. In contrast, 47RA-mediated protection was dependent on its Fc region and was reduced to 50% in neutropenic mice compared with 21RA-mediated and 24RA-mediated protection. Bacteriological study indicated that 21RA appears to enhance the clearance of V. vulnificus from the blood. Overall, these studies suggest that humoral immunity controls V. vulnificus infection through at least two different mechanisms. Furthermore, our panel of MAbs could provide attractive candidates for the further development of immunoprophylaxis/therapeutics and other therapies against V. vulnificus that target the MARTX toxin.V ibrio vulnificus, a member of the normal marine microbiota, is an important human pathogen associated with the consumption of seafood and wound infection following exposure to water containing this pathogen (1-4). The bacterial infection frequently progresses to severe skin lesions and septicemia in people with hepatic disorders or immunocompromised conditions (5). Despite support care and aggressive antibiotic therapy, V. vulnificus septicemia has a greater than 50% mortality rate; this rate increases to more than 90% for patients with septic shock (5-8). During the past decade, the incidence of V. vulnificus infection has increased worldwide, probably due to the warming of coastal waters (9, 10).V. vulnificus produces a wide range of potential virulence factors required for survival and growth, including capsular polysaccharide (VvPS), iron assimilation systems, flagella, pili, VvhA, VvpE, and the multifunctional autoprocessing repeats-in-toxin (MARTX) toxin (MARTX Vv , or RtxA1) (8, 11). Among them, V. vulnificus RtxA1/MARTX Vv , a large secreted protein, belongs to the repeats-in-toxin (RTX) toxin family, which has been identified in a number of Gram-negative bacterial pathogens (12, 13). V. vuln...

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“…Bacterial translocation from the upper chamber to the lower chamber was measured by twofold serial dilution and subsequent bacterial viable cell counting on 2.5% NaCl HI agar plates as previously described (20).…”

Section: Epithelial Translocation (Invasion) Of the V Vulnificus In mentioning

confidence: 99%

“…Logarithmicphase V. vulnificus strains were inoculated in 75% NPS in PBS at an initial concentration of 1 × 10 8 CFU/ml and incubated at 37℃. Viable V. vulnificus cells were counted on 2.5% NaCl HI agar plates after 30 and 60 min of incubation as previously described (20,21). …”

Section: Serum Bactericidal Activitymentioning

confidence: 99%

Destructive Intestinal Translocation ofVibrio vulnificusDetermines Successful Oral Infection

et al. 2013

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Vibrio vulnificus causes primary septicemia as a result of the consumption of contaminated seafood. The intestinal epithelial layer is the first host barrier encountered by V. vulnificus upon oral intake; however, epithelial translocation (invasion) of V.vulnificus has not been extensively studied. In this study, we investigated in vivo translocation of V. vulnificus using clinical (CMCP6) and environmental isolates (96-11-17M). And we analyzed physiological changes of intestinal epithelium concurrent with bacterial translocation by using polarized HCA-7 transwell culture system. The efficiency of epithelial translocation of 97-11-17M strains was significantly lower than that of pathogenic clinical isolate CMCP6 in a murine ligated ileal loop model. In an oral infection model, the survival rate was reciprocally related with efficacy of in vivo epithelial translocation. These results indicate that efficient translocation of V. vulnificus through intestinal epithelium is highly correlated with successful oral infection. We determined translocation of the bacteria from upper to lower chamber, changes of transepithelial electric resistance (TER) and cytotoxicity of the polarized HCA-7 cells to understand general features of V. vulnificus invasion. Bacterial translocation was accompanied by big decrease of TER (about 90%) and about 50% cytotoxicity of the epithelial cells. Taken together, these results indicate that V. vulnificus actively translocates the epithelium by destruction of epithelium and the efficiency of intestinal invasion by V. vulnificus is critical for successful oral infection. From this result, it is suggested that integrity of intestinal barrier is an important factor for susceptibility to oral infection of V. vulnificus.

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The pyrH Gene of Vibrio vulnificus Is an Essential In Vivo Survival Factor

Cited by 40 publications

References 37 publications

Screening of genes expressed in vivo after infection by Vibrio anguillarum M3

Screening of genes expressed in vivo after infection by Vibrio anguillarum M3

Monoclonal Antibodies against Vibrio vulnificus RtxA1 Elicit Protective Immunity through Distinct Mechanisms

Destructive Intestinal Translocation ofVibrio vulnificusDetermines Successful Oral Infection

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