Genome Sequence of the Human-Pathogenetic Bacterium Vibrio vulnificus B2

Wang, Zhigang; Wu, Zhan He; Xu, Shuiling; Zha, Jia Wei

doi:10.1128/jb.01955-12

Cited by 5 publications

(6 citation statements)

References 15 publications

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“…The evolutionary scenario of vuuA and hupA was evaluated from the whole sequence of each gene and was compared with an MLSA reconstruction (51) from the partial sequences (254 nucleotides [nt] by gene) of four virulence-associated genes (vvha, rtxA1, wzz, and pilF) and four housekeeping genes (glp, mdh, pyrC, and pntA) taken from GenBank (17,(52)(53)(54)(55)(56). Phylogenetic trees for each single gene and for the concatenated MLSA were obtained by using the maximum likelihood (ML) method with PhyML software (57).…”

Section: Rna Isolation and Quantitative Reverse Transcription-pcr (Qrmentioning

confidence: 99%

Host-Nonspecific Iron Acquisition Systems and Virulence in the Zoonotic Serovar of Vibrio vulnificus

et al. 2014

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dThe zoonotic serovar of Vibrio vulnificus (known as biotype 2 serovar E) is the etiological agent of human and fish vibriosis. The aim of the present work was to discover the role of the vulnibactin-and hemin-dependent iron acquisition systems in the pathogenicity of this zoonotic serovar under the hypothesis that both are host-nonspecific virulence factors. To this end, we selected three genes for three outer membrane receptors (vuuA, a receptor for ferric vulnibactin, and hupA and hutR, two hemin receptors), obtained single and multiple mutants as well as complemented strains, and tested them in a series of in vitro and in vivo assays, using eels and mice as animal models. The overall results confirm that hupA and vuuA, but not hutR, are host-nonspecific virulence genes and suggest that a third undescribed host-specific plasmid-encoded system could also be used by the zoonotic serovar in fish. hupA and vuuA were expressed in the internal organs of the animals in the first 24 h of infection, suggesting that they may be needed to achieve the population size required to trigger fatal septicemia. vuuA and hupA were sequenced in strains representative of the genetic diversity of this species, and their phylogenies were reconstructed by multilocus sequence analysis of selected housekeeping and virulence genes as a reference. Given the overall results, we suggest that both genes might form part of the core genes essential not only for disease development but also for the survival of this species in its natural reservoir, the aquatic environment.

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Section: Rna Isolation and Quantitative Reverse Transcription-pcr (Qrmentioning

confidence: 99%

Host-Nonspecific Iron Acquisition Systems and Virulence in the Zoonotic Serovar of Vibrio vulnificus

et al. 2014

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“…vulnificus is highly invasive, causing rapidly damage to the inherent immunity following apoptosis of lymphocyte, macrophagocyte and DCs [13,[22][23][24][25]. These cells are critical parts of the barrier in the immune system, and also closely associated with adaptive immunity [3,[26][27][28].…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies demonstrated that STAT3, a key target of many anticancer drugs, was constitutively activated in the anti-apoptotic possesses [17][18][19], and STAT3 molecular was involved in the apoptosis induced by environmental isolation of V. vulnificus [13], we, therefore, hypothesized that STAT3 molecular may also be involved in V. vulnificus -induced DC2.4 cell apoptosis. We detected the expression of phosphorylation of STAT3 at Ser727 (p-STAT3-727) which regulated the transcriptional activation and found that the expression of p-STAT3-727 was significantly decreased during V. vulnificus B2 contagion.…”

Section: Stat3 Was Involved In V Vulnificus B2-induced Dc24 Cell Apmentioning

confidence: 99%

“…V. vulnificus strain B2 was cultured in Columbia blood agar base medium at 37°C for 24 h until the late logarithmic growth phase. Bacteria were collected, washed with phosphate buffer saline (PBS), and then suspended with RPMI 1640 medium (2.5×10 7 colony-forming units/mL [CFU/mL]) [13]. V. vulnificus B2 and DC 2.4 cells (80:1) were co-cultured at 37°C for 4h.…”

Section: Cell and V Vulnificus Culturementioning

confidence: 99%

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Ethylenediaminetetraacetic Acid Inhibits Vibrio Vulnificus-Induced Dendritic Cell Apoptosis by Lowering [Ca2+]i

Qian

Zhu

et al. 2018

Neurosignals

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Background/Aims: Vibrio vulnificus (V. vulnificus) is a Gram-negative marine bacterium that can cause life-threatening primary septicemia, especially in the innate immune system. But how V. vulnificus affects and acts on dendritic cells (DC) is not well understood. The aim of the present study is to investigate [Ca²⁺]_i change and the expression of the mTor-STAT3-Bcl-2 signaling pathway in V. vulnificus B2-induced DC apoptosis, and explore the protective effect of ethylenediaminetetraacetic acid (EDTA) against DC apoptosis in a V. vulnificus B2 and DC2.4 cell coculture infection model, using EDTA as an intervenient. Methods: The apoptosis rate, [Ca²⁺]_i, and the expression of STAT3, m-Tor and Bcl-2 were detected by cytometry, Fluo-8-AM and Western blotting respectively. Results: The results demonstrated that EDTA inhibited the increase of [Ca²⁺]_i, upregulated the expression of m-Tor-STAT3-Bcl-2 signaling pathway, and protected DC against V. vulnificus B2-induced apoptosis. Conclusions: EDTA inhibits V. Vulnificus-induced DC apoptosis by lowering [Ca²⁺]_i via m-Tor-STAT3-Bcl-2 signaling pathway.

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“…Both recombination events resulted in rtxA1 genes that encode for MARTX toxins with only four effectors and missing the DUF5 effector domain (35). This variant is termed MARTX/M (35) or type II (34) and is encoded by many clinical isolates including sequenced strains MO6–24/O, ATCC 27562, and B2 (34, 35, 78, 79, 80). …”

Section: Martx Toxins Of V Vulnificusmentioning

confidence: 99%

Multifunctional-autoprocessing repeats-in-toxin (MARTX) Toxins of Vibrios

Satchell

2015

Microbiol Spectr

105

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Multifunctional-autoprocessing repeats-in-toxin (MARTX) toxins are a heterogeneous group of toxins found in a number of Vibrio species and other Gram-negative bacteria. The toxins are composed of conserved repeat regions and an autoprocessing protease domain that together function as a delivery platform for transfer of cytotoxic and cytopathic domains into target eukaryotic cell cytosol. Within the cells, the effectors can alter biological processes such as signaling or cytoskeletal structure, presumably to the benefit of the bacterium. Ten effector domains are found in the various Vibrio MARTX toxins, although any one toxin carries only two to five effector domains. The specific toxin variant expressed by a species can be modified by homologous recombination to acquire or lose effector domains, such that different strains within the same species can express distinct variants of the toxins. This review examines the conserved structural elements of the MARTX toxins and details the different toxin arrangements carried by Vibrio species and strains. The catalytic function of domains and how the toxins are linked to pathogenesis of human and animals is described.

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Genome Sequence of the Human-Pathogenetic Bacterium Vibrio vulnificus B2

Abstract: bVibrio vulnificus, which can lead to rapidly expanding cellulitis or septicemia, is present in the marine environment. Here, we present the draft genome sequence of strain B2, which was isolated from a septicemia patient in 2010.

Cited by 5 publications

References 15 publications

Host-Nonspecific Iron Acquisition Systems and Virulence in the Zoonotic Serovar of Vibrio vulnificus

Host-Nonspecific Iron Acquisition Systems and Virulence in the Zoonotic Serovar of Vibrio vulnificus

Ethylenediaminetetraacetic Acid Inhibits <b><i>Vibrio Vulnificus</i></b>-Induced Dendritic Cell Apoptosis by Lowering [Ca<sup>2+</sup>]<sub>i</sub>

Multifunctional-autoprocessing repeats-in-toxin (MARTX) Toxins of Vibrios

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