scholarly journals A Point Mutation in carR Is Involved in the Emergence of Polymyxin B-Sensitive Vibrio cholerae O1 El Tor Biotype by Influencing Gene Transcription

2020 ◽  
Vol 88 (5) ◽  
Author(s):  
Prosenjit Samanta ◽  
Rahul Shubhra Mandal ◽  
Rudra Narayan Saha ◽  
Sreeja Shaw ◽  
Priyanka Ghosh ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Lipid A ◽  
Polymyxin B ◽  
Sensitive Strain ◽  
Two Component System ◽  
Content Type ◽  
Vibrio Cholerae O1 ◽  
Binding Cleft ◽  
Culturing Conditions ◽  
El Tor

ABSTRACT Antimicrobial peptides play an important role in host defense against Vibrio cholerae. Generally, the V. cholerae O1 classical biotype is polymyxin B (PB) sensitive and El Tor is relatively resistant. Detection of classical biotype traits like the production of classical cholera toxin and PB sensitivity in El Tor strains has been reported in recent years, including in the devastating Yemen cholera outbreak during 2016-2018. To investigate the factor(s) responsible for the shift in the trend of sensitivity to PB, we studied the two-component system encoded by carRS, regulating the lipid A modification of El Tor vibrios, and found that only carR contains a single nucleotide polymorphism (SNP) in recently emerged PB-sensitive strains. We designated the two alleles present in PB-resistant and -sensitive strains carRr and carRs alleles, respectively, and replaced the carRs allele of a sensitive strain with the carRr allele, using an allelic-exchange approach. The sensitive strain then became resistant. The PB-resistant strain N16961 was made susceptible to PB in a similar fashion. Our in silico CarR protein models suggested that the D89N substitution in the more stable CarRs protein brings the two structural domains of CarR closer, constricting the DNA binding cleft. This probably reduces the expression of the carR-regulated almEFG operon, inducing PB susceptibility. Expression of almEFG in PB-sensitive strains was found to be downregulated under natural culturing conditions. In addition, the expression of carR and almEG decreased in all strains with increased concentrations of extracellular Ca2+ but increased with a rise in pH. The downregulation of almEFG in CarRs strains confirmed that the G265A mutation is responsible for the emergence of PB-sensitive El Tor strains.

scholarly journals Polymyxin B Resistance in El Tor Vibrio cholerae Requires Lipid Acylation Catalyzed by MsbB

2010 ◽  
Vol 192 (8) ◽  
pp. 2044-2052 ◽  
Author(s):  
Jyl S. Matson ◽  
Hyun Ju Yoo ◽  
Kristina Hakansson ◽  
Victor J. DiRita
Keyword(s):  
Antimicrobial Peptides ◽  
Vibrio Cholerae ◽  
Lipid A ◽  
Polymyxin B ◽  
Mass Spectrometry Analysis ◽  
Peptide Antibiotic ◽  
Wild Type ◽  
Spectrometry Analysis ◽  
Antimicrobial Peptide Resistance ◽  
El Tor

ABSTRACTAntimicrobial peptides are critical for innate antibacterial defense. Both Gram-negative and Gram-positive microbes have mechanisms to alter their surfaces and resist killing by antimicrobial peptides. InVibrio cholerae, two natural epidemic biotypes, classical and El Tor, exhibit distinct phenotypes with respect to sensitivity to the peptide antibiotic polymyxin B: classical strains are sensitive and El Tor strains are relatively resistant. We carried out mutant screens of both biotypes, aiming to identify classicalV. choleraemutants resistant to polymyxin B and El TorV. choleraemutants sensitive to polymyxin B. Insertions in a gene annotatedmsbB(encoding a predicted lipid A secondary acyltransferase) answered both screens, implicating its activity in antimicrobial peptide resistance ofV. cholerae. Analysis of a defined mutation in the El Tor biotype demonstrated thatmsbBis required for resistance to all antimicrobial peptides tested. Mutation ofmsbBin a classical strain resulted in reduced resistance to several antimicrobial peptides but in no significant change in resistance to polymyxin B.msbBmutants of both biotypes showed decreased colonization of infant mice, with a more pronounced defect observed for the El Tor mutant. Mass spectrometry analysis showed that lipid A of themsbBmutant for both biotypes was underacylated compared to lipid A of the wild-type isolates, confirming that MsbB is a functional acyltransferase inV. cholerae.

scholarly journals Polymyxin B Resistance and Biofilm Formation in Vibrio cholerae Are Controlled by the Response Regulator CarR

2015 ◽  
Vol 83 (3) ◽  
pp. 1199-1209 ◽  
Author(s):  
Kivanc Bilecen ◽  
Jiunn C. N. Fong ◽  
Andrew Cheng ◽  
Christopher J. Jones ◽  
David Zamorano-Sánchez ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Biofilm Formation ◽  
Lipid A ◽  
Response Regulator ◽  
Regulatory Region ◽  
Regulatory System ◽  
Polymyxin B ◽  
Content Type ◽  
Two Component ◽  
Antimicrobial Peptide Resistance

Two-component systems play important roles in the physiology of many bacterial pathogens.Vibrio cholerae's CarRS two-component regulatory system negatively regulates expression ofvps(Vibriopolysaccharide) genes and biofilm formation. In this study, we report that CarR confers polymyxin B resistance by positively regulating expression of thealmEFGgenes, whose products are required for glycine and diglycine modification of lipid A. We determined that CarR directly binds to the regulatory region of thealmEFGoperon. Similarly to acarRmutant, strains lackingalmE,almF, andalmGexhibited enhanced polymyxin B sensitivity. We also observed that strains lackingalmEor thealmEFGoperon have enhanced biofilm formation. Our results reveal that CarR regulates biofilm formation and antimicrobial peptide resistance inV. cholerae.

scholarly journals Complete Genome Sequence of Vibrio cholerae O1 El Tor Strain C6706

2021 ◽  
Vol 10 (3) ◽  
Author(s):  
Yuding Weng ◽  
X. Renee Bina ◽  
James E. Bina
Keyword(s):  
Global Health ◽  
Vibrio Cholerae ◽  
Genome Sequence ◽  
Complete Genome Sequence ◽  
Human Disease ◽  
Complete Genome ◽  
Content Type ◽  
Health Threat ◽  
Vibrio Cholerae O1 ◽  
El Tor

ABSTRACT Vibrio cholerae is a global health threat and a model enteric pathogen that causes the human disease cholera. Here, we report the complete genome sequence of the seventh-pandemic V. cholerae O1 El Tor strain C6706.

scholarly journals Whole-Genome Sequencing of Vibrio cholerae O1 El Tor Strains Isolated in Ukraine (2011) and Russia (2014)

2017 ◽  
Vol 5 (8) ◽  
Author(s):  
Nina I. Smirnova ◽  
Yaroslav M. Krasnov ◽  
Elena Y. Agafonova ◽  
Elena Y. Shchelkanova ◽  
Zhanna V. Alkhova ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Genome Sequencing ◽  
Genetic Similarity ◽  
Whole Genome Sequence ◽  
Whole Genome ◽  
Content Type ◽  
Vibrio Cholerae O1 ◽  
El Tor ◽  
Highly Virulent ◽  
High Genetic Similarity

ABSTRACT Here, we present the draft whole-genome sequence of Vibrio cholerae O1 El Tor strains 76 and M3265/80, isolated in Mariupol, Ukraine, and Moscow, Russia. The presence of various mutations detected in virulence-associated mobile elements indicates high genetic similarity of the strains reported here with new highly virulent variants of the cholera agent V. cholerae.

scholarly journals Vibrio cholerae O1 clinical strains isolated in 1992 in Kolkata with progenitor traits of the 2004 Mozambique variant

2009 ◽  
Vol 58 (2) ◽  
pp. 239-247 ◽  
Author(s):  
Souvik Chatterjee ◽  
Tapas Patra ◽  
Kausik Ghosh ◽  
Amit Raychoudhuri ◽  
Gururaja P. Pazhani ◽  
...  
Keyword(s):  
Retrospective Analysis ◽  
Vibrio Cholerae ◽  
Polymyxin B ◽  
Small Chromosome ◽  
Phenotypic Traits ◽  
Clinical Strains ◽  
Vibrio Cholerae O1 ◽  
Ctx Prophage ◽  
El Tor ◽  
Clinical Cases

Retrospective analysis led to the detection of two Vibrio cholerae variant O1 strains (VC51 and VC53), which were isolated in 1992 in Kolkata from clinical cases, with identical traits to 2004 Mozambique variant O1 strains. The Mozambique O1 strains that caused a huge outbreak in 2004 have been shown to have phenotypic traits of both classical and El Tor biotypes, and thereby have been reported as variant. Our study demonstrated that two O1 strains isolated in Kolkata during 1992 were of the El Tor background as evidenced by polymyxin B (50 U ml−1) resistance, positivity in Voges–Proskauer reactions and sensitivity to biotype-specific vibrio phages. With the features of classical CTX prophage, localization in the small chromosome, and an absence of RS1 and pTLC, both Mozambique and Kolkata strains appeared to be identical. Furthermore, two Kolkata strains exhibited an identical ribotype to that of the Mozambique variant, displaying ribotype pattern RI that had been assigned to Kolkata V. cholerae O1 strains isolated on or before 1992. NotI pulsotype analysis indicated that these 1992 Kolkata strains along with the Mozambique variant O1 belonged to very closely related clones. Considering the chronological events, and the typical identity at the phenotypic and the genotypic level between the two O1 strains isolated during 1992 from Kolkata and during 2004 from Mozambique, we propose that some of the 1992 Kolkata O1 strains might have acted as progenitors for Mozambique variant O1 strains.

scholarly journals Single Circular Chromosome Identified from the Genome Sequence of the Vibrio cholerae O1 bv. El Tor Ogawa Strain V060002

2018 ◽  
Vol 6 (25) ◽  
Author(s):  
Shouji Yamamoto ◽  
Ken-ichi Lee ◽  
Masatomo Morita ◽  
Eiji Arakawa ◽  
Hidemasa Izumiya ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Genome Sequence ◽  
Complete Genome Sequence ◽  
Clinical Strain ◽  
Circular Chromosome ◽  
Single Chromosome ◽  
Content Type ◽  
Vibrio Cholerae O1 ◽  
El Tor ◽  
Single Circular Chromosome

ABSTRACT We report here the complete genome sequence of the Vibrio cholerae O1 bv. El Tor Ogawa strain V060002, isolated in 1997. The data demonstrate that this clinical strain has a single chromosome resulting from recombination of two prototypical chromosomes.

scholarly journals Recent Vibrio cholerae O1 Epidemic Strains Are Unable To Replicate CTXΦ Prophage Genome

mSphere ◽  
2021 ◽  
Author(s):  
Kaoru Ochi ◽  
Tamaki Mizuno ◽  
Prosenjit Samanta ◽  
Asish K. Mukhopadhyay ◽  
Shin-ichi Miyoshi ◽  
...  
Keyword(s):  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Diarrheal Disease ◽  
Content Type ◽  
Ctxφ Prophage ◽  
Vibrio Cholerae O1 ◽  
El Tor

Cholera is an acute diarrheal disease caused by pathogenic strains of V. cholerae generated by lysogenization of the filamentous cholera toxin phage CTXΦ. The analysis revealed that recent isolates possessed altered CTXΦ prophage array of prototype El Tor strain and were defective in replicating the CTXΦ genome.

scholarly journals Transcriptional profiling of Vibrio cholerae O1 following exposure to human anti- lipopolysaccharide monoclonal antibodies

2020 ◽  
Vol 78 (4) ◽  
Author(s):  
Danielle E Baranova ◽  
Graham G Willsey ◽  
Kara J Levinson ◽  
Carol Smith ◽  
Joseph Wade ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Lipid A ◽  
Transcriptional Profiling ◽  
Watery Diarrhea ◽  
Rna Seq ◽  
Intestinal Epithelia ◽  
Vibrio Cholerae O1 ◽  
El Tor ◽  
Upregulated Genes ◽  
Late Stages

ABSTRACT Following an episode of cholera, a rapidly dehydrating, watery diarrhea caused by the Gram-negative bacterium, Vibrio cholerae O1, humans mount a robust anti-lipopolysaccharide (LPS) antibody response that is associated with immunity to subsequent re-infection. In neonatal mouse and rabbit models of cholera, passively administered anti-LPS polyclonal and monoclonal (MAb) antibodies reduce V. cholerae colonization of the intestinal epithelia by inhibiting bacterial motility and promoting vibrio agglutination. Here we demonstrate that human anti-LPS IgG MAbs also arrest V. cholerae motility and induce bacterial paralysis. A subset of those MAbs also triggered V. cholerae to secrete an extracellular matrix (ECM). To identify changes in gene expression that accompany antibody exposure and that may account for motility arrest and ECM production, we subjected V. cholerae O1 El Tor to RNA-seq analysis after treatment with ZAC-3 IgG, a high affinity MAb directed against the core/lipid A region of LPS. We identified > 160 genes whose expression was altered following ZAC-3 IgG treatment, although canonical outer membrane stress regulons were not among them. ompS (VCA1028), a porin associated with virulence and indirectly regulated by ToxT, and norR (VCA0182), a σ54-dependent transcription factor involved in late stages of infection, were two upregulated genes worth noting.

scholarly journals The Vibrio cholerae VprA-VprB Two-Component System Controls Virulence through Endotoxin Modification

mBio ◽  
2014 ◽  
Vol 5 (6) ◽  
Author(s):  
Carmen M. Herrera ◽  
Alexander A. Crofts ◽  
Jeremy C. Henderson ◽  
S. Cassandra Pingali ◽  
Bryan W. Davies ◽  
...  
Keyword(s):  
Immune System ◽  
Antimicrobial Peptides ◽  
Vibrio Cholerae ◽  
Lipid A ◽  
Host Immune System ◽  
Two Component System ◽  
Cationic Antimicrobial Peptides ◽  
Component System ◽  
Content Type ◽  
Two Component

ABSTRACTThe bacterial cell surface is the first structure the host immune system targets to prevent infection. Cationic antimicrobial peptides of the innate immune system bind to the membrane of Gram-negative pathogens via conserved, surface-exposed lipopolysaccharide (LPS) molecules. We recently reported that modern strains of the global intestinal pathogenVibrio choleraemodify the anionic lipid A domain of LPS with a novel moiety, amino acids. Remarkably, glycine or diglycine addition to lipid A alters the surface charge of the bacteria to help evade the cationic antimicrobial peptide polymyxin. However, the regulatory mechanisms of lipid A modification inV. choleraeare unknown. Here, we identify a novel two-component system that regulates lipid A glycine modification by responding to important biological cues associated with pathogenesis, including bile, mildly acidic pH, and cationic antimicrobial peptides. The histidine kinase Vc1319 (VprB) and the response regulator Vc1320 (VprA) respond to these signals and are required for the expression of thealmEFGoperon that encodes the genes essential for glycine modification of lipid A. Importantly, both the newly identified two-component system and the lipid A modification machinery are required for colonization of the mammalian host. This study demonstrates howV. choleraeuses a previously unknown regulatory network, independent of well-studiedV. choleraevirulence factors and regulators, to respond to the host environment and cause infection.IMPORTANCEVibrio cholerae, the etiological agent of cholera disease, infects millions of people every year.V. choleraeEl Tor and classical biotypes have been responsible for all cholera pandemics. The El Tor biotype responsible for the current seventh pandemic has displaced the classical biotype worldwide and is highly resistant to cationic antimicrobial peptides, like polymyxin B. This resistance arises from the attachment of one or two glycine residues to the lipid A domain of lipopolysaccharide, a major surface component of Gram-negative bacteria. Here, we identify the VprAB two-component system that regulates the charge of the bacterial surface by directly controlling the expression of genes required for glycine addition to lipid A. The VprAB-dependent lipid A modification confers polymyxin B resistance and contributes significantly to pathogenesis. This finding is relevant for understanding howVibrio choleraehas evolved mechanisms to facilitate the evasion of the host immune system and increase bacterial fitness.

scholarly journals Genome Sequence of a Pathogenic Vibrio cholerae O1 El Tor Strain Defective for the Entire Vibrio Pathogenicity Island 1, Isolated in Eastern Democratic Republic of the Congo

2020 ◽  
Vol 9 (26) ◽  
Author(s):  
Leonid M. Irenge ◽  
Jean-François Durant ◽  
Jérôme Ambroise ◽  
Prudence N. Mitangala ◽  
Bertrand Bearzatto ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Genome Sequence ◽  
Democratic Republic ◽  
Pathogenicity Island ◽  
Content Type ◽  
Pathogenic Vibrio ◽  
Republic Of The Congo ◽  
Vibrio Cholerae O1 ◽  
El Tor ◽  
North Kivu

ABSTRACT We report here a complete genome sequence of a Vibrio cholerae O1 El Tor (Inaba; sequence type 515 [ST515]) strain isolated from a cholera patient in North Kivu Province, Democratic Republic of the Congo (DRC), which showed a complete deletion (∼80 kb) of the Vibrio pathogenicity island 1.

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