scholarly journals Capsular Polysaccharide Phase Variation in Vibrio vulnificus

2006 ◽  
Vol 72 (11) ◽  
pp. 6986-6993 ◽  
Author(s):  
Tamara Hilton ◽  
Tom Rosche ◽  
Brett Froelich ◽  
Benjamin Smith ◽  
James Oliver
Keyword(s):  
Oxidative Stress ◽  
Quorum Sensing ◽  
Cell Surface ◽  
Serum Iron ◽  
Capsular Polysaccharide ◽  
Vibrio Vulnificus ◽  
Phase Variation ◽  
Fatality Rate ◽  
Single Colony ◽  
And Oxidative Stress

ABSTRACT Commonly found in raw oysters, Vibrio vulnificus poses a serious health threat to immunocompromised individuals and those with serum iron overload, with a fatality rate of approximately 50%. An essential virulence factor is its capsular polysaccharide (CPS), which is responsible for a significant increase in virulence compared to nonencapsulated strains. However, this bacterium is known to vary the amount of CPS expressed on the cell surface, converting from an opaque (Op) colony phenotype to a translucent (Tr) colony phenotype. In this study, the consistency of CPS conversion was determined for four strains of V. vulnificus. Environmental conditions including variations in aeration, temperature, incubation time, oxidative stress, and media (heart infusion or modified maintenance medium agar) were investigated to determine their influence on CPS conversion. All conditions, with the exception of variations in media and oxidative stress, significantly affected the conversion of the population, with high ranges of CPS expression found even within cells from a single colony. The global quorum-sensing regulators RpoS and AI-2 were also examined. While RpoS was found to significantly mediate phenotypic conversion, quorum sensing was not. Finally, 12 strains that comprise the recently found clinical (C) and environmental (E) genotypes of V. vulnificus were examined to determine their rates of population conversion. C-genotype strains, which are most often associated with infection, had a significantly lower rate of population conversion from Op to Tr phenotypes than did E-genotype strains (ca. 38% versus ca. 14%, respectively). Biofilm capabilities of these strains, however, were not correlated with increased population conversion.

scholarly journals Structure, Function, and Regulation of the Essential Virulence Factor Capsular Polysaccharide of Vibrio vulnificus

2020 ◽  
Vol 21 (9) ◽  
pp. 3259 ◽  
Author(s):  
Gregg S. Pettis ◽  
Aheli S. Mukerji
Keyword(s):  
Coastal Waters ◽  
Capsular Polysaccharide ◽  
Vibrio Vulnificus ◽  
Critical Role ◽  
Phase Variation ◽  
Innate Immune ◽  
Repeat Sequences ◽  
Life Threatening ◽  
Inflammatory Cytokine Response ◽  
Group 1

Vibrio vulnificus populates coastal waters around the world, where it exists freely or becomes concentrated in filter feeding mollusks. It also causes rapid and life-threatening sepsis and wound infections in humans. Of its many virulence factors, it is the V. vulnificus capsule, composed of capsular polysaccharide (CPS), that plays a critical role in evasion of the host innate immune system by conferring antiphagocytic ability and resistance to complement-mediated killing. CPS may also provoke a portion of the host inflammatory cytokine response to this bacterium. CPS production is biochemically and genetically diverse among strains of V. vulnificus, and the carbohydrate diversity of CPS is likely affected by horizontal gene transfer events that result in new combinations of biosynthetic genes. Phase variation between virulent encapsulated opaque colonial variants and attenuated translucent colonial variants, which have little or no CPS, is a common phenotype among strains of this species. One mechanism for generating acapsular variants likely involves homologous recombination between repeat sequences flanking the wzb phosphatase gene within the Group 1 CPS biosynthetic and transport operon. A considerable number of environmental, genetic, and regulatory factors have now been identified that affect CPS gene expression and CPS production in this pathogen.

scholarly journals Inflammatory and oxidative status in European captive black rhinoceroses: a link with Iron Overload Disorder?

2020 ◽  
Author(s):  
Hanae Pouillevet ◽  
Nicolas Soetart ◽  
Delphine Boucher ◽  
Rudy Wedlarski ◽  
Laetitia Jaillardon
Keyword(s):  
Oxidative Stress ◽  
Iron Overload ◽  
Serum Iron ◽  
Iron Status ◽  
The Body ◽  
Stress Markers ◽  
Oxidative Markers ◽  
Inflammatory Status ◽  
The Impact ◽  
And Oxidative Stress

AbstractIron Overload Disorder (IOD) is a syndrome developed by captive browsing rhinoceroses like black rhinoceroses (Diceros bicornis) in which hemosiderosis settles in vital organs while free iron accumulates in the body, potentially predisposing to various secondary diseases. Captive grazing species like white rhinoceroses (Ceratotherium simum) do not seem to be affected. The pro-oxidant and pro-inflammatory properties of iron, associated with the poor antioxidant capacities of black rhinoceroses, could enhance high levels of inflammation and oxidative stress leading to rapid ageing and promoting diseases. In this prospective study, 15 black (BR) and 29 white rhinoceroses (WR) originating from 22 European zoos were blood-sampled and compared for their iron status (serum iron), liver/muscle biochemical parameters (AST, GGT, cholesterol), inflammatory status (total proteins, protein electrophoresis) and oxidative stress markers (SOD, GPX, dROMs). Results showed higher serum iron and liver enzyme levels in black rhinoceroses (P<0.01), as well as higher GPX (P<0.05) and dROM (P<0.01) levels. The albumin/globulin ratio was lower in black rhinoceroses (P<0.05) due to higher α2-globulin levels (P<0.001). The present study suggests a higher inflammatory and oxidative profile in captive BR than in WR, possibly in relation to iron status. This could be either a consequence or a cause of iron accumulation, potentially explaining rapid ageing and various diseases. Further investigations are needed to assess the prognostic value of the inflammatory and oxidative markers in captive black rhinoceroses, particularly for evaluating the impact of reduced-iron and antioxidant-supplemented diets.

scholarly journals Identification of a Group 1-Like Capsular Polysaccharide Operon for Vibrio vulnificus

2001 ◽  
Vol 69 (11) ◽  
pp. 6893-6901 ◽  
Author(s):  
Anita C. Wright ◽  
Jan L. Powell ◽  
James B. Kaper ◽  
J. Glenn Morris
Keyword(s):  
Capsular Polysaccharide ◽  
Vibrio Vulnificus ◽  
Phase Variation ◽  
Surface Expression ◽  
Open Reading Frames ◽  
Biosynthetic Genes ◽  
Virulent Phenotype ◽  
Phase Variants ◽  
Group 1

ABSTRACT Virulence of Vibrio vulnificus correlates with changes in colony morphology that are indicative of a reversible phase variation for expression of capsular polysaccharide (CPS). Encapsulated variants are virulent with opaque colonies, whereas phase variants with reduced CPS expression are attenuated and are translucent. Using TnphoA mutagenesis, we identified a V.vulnificus CPS locus, which included an upstreamops element, a wza gene (wza Vv), and several open reading frames with homology to CPS biosynthetic genes. This genetic organization is characteristic of group 1 CPS operons. The wzagene product is required for transport of CPS to the cell surface inEscherichia coli. Polar transposon mutations inwza Vv eliminated expression of downstream biosynthetic genes, confirming operon structure. On the other hand, nonpolar inactivation of wza Vv was specific for CPS transport, did not alter CPS biosynthesis, and could be complemented in trans. Southern analysis of CPS phase variants revealed deletions or rearrangements at this locus. A survey of environmental isolates indicated a correlation between deletions inwza Vv and loss of virulent phenotype, suggesting a genetic mechanism for CPS phase variation. Full virulence in mice required surface expression of CPS and supported the essential role of capsule in the pathogenesis of V.vulnificus.

scholarly journals Inhibition of Erythrocyte Cell Membrane Scrambling by ASP3026

2017 ◽  
Vol 43 (2) ◽  
pp. 507-517 ◽  
Author(s):  
Abdulla Al Mamun Bhuyan ◽  
Rosi Bissinger ◽  
Hang Cao ◽  
Florian Lang
Keyword(s):  
Oxidative Stress ◽  
Cell Membrane ◽  
Cell Surface ◽  
Small Cell Lung Carcinoma ◽  
Annexin V ◽  
Forward Scatter ◽  
Energy Depletion ◽  
Cell Lung Carcinoma ◽  
Anaplastic Lymphoma ◽  
And Oxidative Stress

Background/Aims: The anaplastic lymphoma kinase (ALK) inhibitor ASP3026 is in clinical development for the treatment of ALK expressing non-small cell lung carcinoma (NSCLC). ASP3026 is in part effective by inducing apoptosis of tumor cells. Erythrocytes lack mitochondria and nuclei, key organelles in the execution of apoptosis, but are nevertheless able to enter suicidal death or eryptosis, which is characterized by cell membrane scrambling with phosphatidylserine translocation to the cell surface and by cell shrinkage. Eryptosis is triggered by cell stress, such as energy depletion, hyperosmotic shock, oxidative stress and excessive increase of cytosolic Ca2+ activity ([Ca2+]i). The present study explored, whether ASP3026 impacts on eryptosis. Methods: Human erythrocytes have been exposed to energy depletion (glucose withdrawal for 48 hours), oxidative stress (addition of 0.3 mM tert-butylhydroperoxide [tBOOH] for 50 min) or Ca2+ loading with Ca2+ ionophore ionomycin (1 µM for 60 min) in absence and presence of ASP3026 (1-4 µg/ml). Flow cytometry was employed to quantify phosphatidylserine exposure at the cell surface from annexin-V-binding, and cell volume from forward scatter. Results: Treatment with ASP3026 alone did not significantly modify annexin-V-binding or forward scatter. Energy depletion, oxidative stress and ionomycin, all markedly and significantly increased the percentage of annexin-V-binding erythrocytes, and decreased the forward scatter. ASP3026 significantly blunted the effect of energy depletion and oxidative stress, but not of ionomycin on annexin-V-binding. ASP3026 did not significantly influence the effect of any maneuver on forward scatter. Conclusions: ASP3026 is a novel inhibitor of erythrocyte cell membrane scrambling following energy depletion and oxidative stress.

scholarly journals Inactivation of Transcriptional Regulator FabT Influences Colony Phase Variation of Streptococcus pneumoniae

mBio ◽  
2021 ◽  
Author(s):  
Jinghui Zhang ◽  
Weijie Ye ◽  
Kaifeng Wu ◽  
Shengnan Xiao ◽  
Yuqiang Zheng ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Cell Surface ◽  
Virulence Factors ◽  
Capsular Polysaccharide ◽  
Phase Variation ◽  
Transcriptional Regulator ◽  
Human Pathogen ◽  
Content Type ◽  
Reversible Phase

Streptococcus pneumoniae is a major human pathogen, and its virulence factors and especially the capsular polysaccharide have been extensively studied. In addition to virulence components that are present on its cell surface that directly interact with the host, S. pneumoniae undergoes a spontaneous and reversible phase variation that allows survival in different host environments.

scholarly journals Genetic Variation in the Vibrio vulnificus Group 1 Capsular Polysaccharide Operon

2006 ◽  
Vol 188 (5) ◽  
pp. 1987-1998 ◽  
Author(s):  
Maria Chatzidaki-Livanis ◽  
Melissa K. Jones ◽  
Anita C. Wright
Keyword(s):  
Capsular Polysaccharide ◽  
Vibrio Vulnificus ◽  
Allelic Variation ◽  
Phase Variation ◽  
Phase Variable ◽  
Deletion Mutations ◽  
Underlying Illness ◽  
Dna Elements ◽  
Repetitive Dna Elements ◽  
Group 1

ABSTRACT Vibrio vulnificus produces human disease associated with raw-oyster consumption or wound infections, but fatalities are limited to persons with chronic underlying illness. Capsular polysaccharide (CPS) is required for virulence, and CPS expression correlates with opaque (Op) colonies that show “phase variation” to avirulent translucent (Tr) phenotypes with reduced CPS. The results discussed here confirmed homology of a V. vulnificus CPS locus to the group 1 CPS operon in Escherichia coli. However, two distinct V. vulnificus genotypes or alleles were associated with the operon, and they diverged at sequences encoding hypothetical proteins and also at unique, intergenic repetitive DNA elements. Phase variation was examined under conditions that promoted high-frequency transition of Op to Tr forms. Recovery of Tr isolates in these experiments showed multiple genotypes, which were designated TR1, TR2, and TR3: CPS operons of TR1 isolates were identical to the Op parent, and cells remained phase variable but expressed reduced CPS. TR2 and TR3 showed deletion mutations in one (wzb) or multiple genes, respectively, and deletion mutants were acapsular and locked in the Tr phase. Complementation in trans restored the Op phenotype in strains with the wzb deletion mutation. Allelic variation in repetitive elements determined the locations, rates, and extents of deletion mutations. Thus, different mechanisms are responsible for reversible phase variation in CPS expression versus genetic deletions in the CPS operon of V. vulnificus. Repetitive-element-mediated deletion mutations were highly conserved within the species and are likely to promote survival in estuarine environments.

Role of GacA in virulence of Vibrio vulnificus

Microbiology ◽  
2010 ◽  
Vol 156 (12) ◽  
pp. 3722-3733 ◽  
Author(s):  
Julie D. Gauthier ◽  
Melissa K. Jones ◽  
Patrick Thiaville ◽  
Jennifer L. Joseph ◽  
Rick A. Swain ◽  
...  
Keyword(s):  
Capsular Polysaccharide ◽  
Vibrio Vulnificus ◽  
Phase Variation ◽  
Dependent Manner ◽  
Wild Type ◽  
Significant Impairment ◽  
Life Threatening ◽  
Two Component Signal Transduction ◽  
Systemic Infections

The GacS/GacA two-component signal transduction system regulates virulence, biofilm formation and symbiosis in Vibrio species. The present study investigated this regulatory pathway in Vibrio vulnificus, a human pathogen that causes life-threatening disease associated with the consumption of raw oysters and wound infections. Small non-coding RNAs (csrB1, csrB2, csrB3 and csrC) commonly regulated by the GacS/GacA pathway were decreased (P<0.0003) in a V. vulnificus CMCP6 ΔgacA : : aph mutant compared with the wild-type parent, and expression was restored by complementation of the gacA deletion mutation in trans. Of the 20 genes examined by RT-PCR, significant reductions in the transcript levels of the mutant in comparison with the wild-type strain were observed only for genes related to motility (flaA), stationary phase (rpoS) and protease (vvpE) (P=0.04, 0.01 and 0.002, respectively). Swimming motility, flagellation and opaque colony morphology indicative of capsular polysaccharide (CPS) were unchanged in the mutant, while cytotoxicity, protease activity, CPS phase variation and the ability to acquire iron were decreased compared with the wild-type (P<0.01). The role of gacA in virulence of V. vulnificus was also demonstrated by significant impairment in the ability of the mutant strain to cause either skin (P<0.0005) or systemic infections (P<0.02) in subcutaneously inoculated, non-iron-treated mice. However, the virulence of the mutant was equivalent to that of the wild-type in iron-treated mice, demonstrating that the GacA pathway in V. vulnificus regulates the virulence of this organism in an iron-dependent manner.

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