scholarly journals Spatiotemporal Analysis of Acid Adaptation-Mediated Vibrio cholerae Hyperinfectivity

2004 ◽  
Vol 72 (4) ◽  
pp. 2405-2407 ◽  
Author(s):  
Michael J. Angelichio ◽  
D. Scott Merrell ◽  
Andrew Camilli
Keyword(s):  
Small Intestine ◽  
Vibrio Cholerae ◽  
Spatiotemporal Analysis ◽  
Rapid Onset ◽  
Multiplication Rate ◽  
Acid Adaptation ◽  
Infant Mouse ◽  
Mouse Intestine ◽  
Kinetics Of ◽  
Transcriptional Induction

ABSTRACT Acid adaptation has previously been shown to increase the infectivity of Vibrio cholerae in the infant mouse model. To better understand this phenomenon, we monitored the spatial distribution and temporal changes in the ratios of acid-adapted cells to unadapted V. cholerae cells in the small intestine, as well as the timing of virulence factor expression. We found that the competitive advantage afforded by acid adaptation does not become manifest until greater than 3 h postinfection; thus, acid adaptation does not increase V. cholerae passage through the gastric acid barrier. Additionally, acid-adapted and unadapted V. cholerae cells colonize the same sections of the small intestine and show similar kinetics of transcriptional induction of the virulence genes tcpA and ctxA. These studies suggest that the increased infectivity of acid-adapted V. cholerae is due to a more rapid onset of multiplication and/or to an increased multiplication rate within the infant mouse intestine.

scholarly journals Characterization of Ferric and Ferrous Iron Transport Systems in Vibrio cholerae

2006 ◽  
Vol 188 (18) ◽  
pp. 6515-6523 ◽  
Author(s):  
Elizabeth E. Wyckoff ◽  
Alexandra R. Mey ◽  
Andreas Leimbach ◽  
Carolyn F. Fisher ◽  
Shelley M. Payne
Keyword(s):  
Vibrio Cholerae ◽  
Transport System ◽  
Iron Transport ◽  
Iron Acquisition ◽  
Shigella Flexneri ◽  
Transport Systems ◽  
Infant Mouse ◽  
Mouse Intestine ◽  
Dependent Transport

ABSTRACT Vibrio cholerae has multiple iron acquisition systems, including TonB-dependent transport of heme and of the catechol siderophore vibriobactin. Strains defective in both of these systems grow well in laboratory media and in the infant mouse intestine, indicating the presence of additional iron acquisition systems. Previously uncharacterized potential iron transport systems, including a homologue of the ferrous transporter Feo and a periplasmic binding protein-dependent ATP binding cassette (ABC) transport system, termed Fbp, were identified in the V. cholerae genome sequence. Clones encoding either the Feo or the Fbp system exhibited characteristics of iron transporters: both repressed the expression of lacZ cloned under the control of a Fur-regulated promoter in Escherichia coli and also conferred growth on a Shigella flexneri mutant that has a severe defect in iron transport. Two other ABC transporters were also evaluated but were negative by these assays. Transport of radioactive iron by the Feo system into the S. flexneri iron transport mutant was stimulated by the reducing agent ascorbate, consistent with Feo functioning as a ferrous transporter. Conversely, ascorbate inhibited transport by the Fbp system, suggesting that it transports ferric iron. The growth of V. cholerae strains carrying mutations in one or more of the potential iron transport genes indicated that both Feo and Fbp contribute to iron acquisition. However, a mutant defective in the vibriobactin, Fbp, and Feo systems was not attenuated in a suckling mouse model, suggesting that at least one other iron transport system can be used in vivo.

scholarly journals DNA Damage and Reactive Nitrogen Species are Barriers to Vibrio cholerae Colonization of the Infant Mouse Intestine

2011 ◽  
Vol 7 (2) ◽  
pp. e1001295 ◽  
Author(s):  
Bryan W. Davies ◽  
Ryan W. Bogard ◽  
Nicole M. Dupes ◽  
Tyler A. I. Gerstenfeld ◽  
Lyle A. Simmons ◽  
...  
Keyword(s):  
Dna Damage ◽  
Vibrio Cholerae ◽  
Reactive Nitrogen Species ◽  
Reactive Nitrogen ◽  
Nitrogen Species ◽  
Infant Mouse ◽  
Mouse Intestine

scholarly journals Sialic Acid Catabolism Confers a Competitive Advantage to Pathogenic Vibrio cholerae in the Mouse Intestine

2009 ◽  
Vol 77 (9) ◽  
pp. 3807-3816 ◽  
Author(s):  
Salvador Almagro-Moreno ◽  
E. Fidelma Boyd
Keyword(s):  
Sialic Acid ◽  
Vibrio Cholerae ◽  
Sialic Acids ◽  
Infant Mouse ◽  
Pathogenic Vibrio ◽  
Important Relationship ◽  
Mouse Intestine ◽  
El Tor ◽  
Mouse Model Of Infection ◽  
Competition Assays

ABSTRACT Sialic acids comprise a family of nine-carbon ketosugars that are ubiquitous on mammalian mucous membranes. However, sialic acids have a limited distribution among Bacteria and are confined mainly to pathogenic and commensal species. Vibrio pathogenicity island 2 (VPI-2), a 57-kb region found exclusively among pathogenic strains of Vibrio cholerae, contains a cluster of genes (nan-nag) putatively involved in the scavenging (nanH), transport (dctPQM), and catabolism (nanA, nanE, nanK, and nagA) of sialic acid. The capacity to utilize sialic acid as a carbon and energy source might confer an advantage to V. cholerae in the mucus-rich environment of the gut, where sialic acid availability is extensive. In this study, we show that V. cholerae can utilize sialic acid as a sole carbon source. We demonstrate that the genes involved in the utilization of sialic acid are located within the nan-nag region of VPI-2 by complementation of E scherichia coli mutants and gene knockouts in V. cholerae N16961. We show that nanH, dctP, nanA, and nanK are highly expressed in V. cholerae grown on sialic acid. By using the infant mouse model of infection, we show that V. cholerae ΔnanA strain SAM1776 is defective in early intestinal colonization stages. In addition, SAM1776 shows a decrease in the competitive index in colonization-competition assays comparing the mutant strain with both O1 El Tor and classical strains. Our data indicate an important relationship between the catabolism of sialic acid and bacterial pathogenesis, stressing the relevance of the utilization of the resources found in the host's environment.

scholarly journals PhoB Regulates Motility, Biofilms, and Cyclic di-GMP in Vibrio cholerae

2009 ◽  
Vol 191 (21) ◽  
pp. 6632-6642 ◽  
Author(s):  
Jason T. Pratt ◽  
EmilyKate McDonough ◽  
Andrew Camilli
Keyword(s):  
Small Intestine ◽  
Life Cycle ◽  
Vibrio Cholerae ◽  
Late Stage ◽  
Signaling Mechanism ◽  
Infant Mouse ◽  
Mouse Small Intestine ◽  
External Stimuli ◽  
Late Stages

ABSTRACT Signaling through the second messenger cyclic di-GMP (c-di-GMP) is central to the life cycle of Vibrio cholerae. However, relatively little is known about the signaling mechanism, including the specific external stimuli that regulate c-di-GMP concentration. Here, we show that the phosphate responsive regulator PhoB regulates an operon, acgAB, which encodes c-di-GMP metabolic enzymes. We show that induction of acgAB by PhoB positively regulates V. cholerae motility in vitro and that PhoB regulates expression of acgAB at late stages during V. cholerae infection in the infant mouse small intestine. These data support a model whereby PhoB becomes activated at a late stage of infection in preparation for dissemination of V. cholerae to the aquatic environment and suggest that the concentration of exogenous phosphate may become limited at late stages of infection.

scholarly journals Hyperinfectivity of Human-Passaged Vibrio cholerae Can Be Modeled by Growth in the Infant Mouse

2005 ◽  
Vol 73 (10) ◽  
pp. 6674-6679 ◽  
Author(s):  
Ashfaqul Alam ◽  
Regina C. LaRocque ◽  
Jason B. Harris ◽  
Cecily Vanderspurt ◽  
Edward T. Ryan ◽  
...  
Keyword(s):  
Mouse Model ◽  
Competitive Advantage ◽  
Vibrio Cholerae ◽  
Type Iv Pili ◽  
Human Intestine ◽  
Epidemic Spread ◽  
Infant Mouse ◽  
Type Iv ◽  
Mouse Intestine ◽  
Human Stool

ABSTRACT It has previously been shown that passage of Vibrio cholerae through the human intestine imparts a transient hyperinfectious phenotype that may contribute to the epidemic spread of cholera. The mechanism underlying this human-passaged hyperinfectivity is incompletely understood, in part due to inherent difficulties in recovering and studying organisms that are freshly passed in human stool. Here, we demonstrate that passage of V. cholerae through the infant mouse intestine leads to an equivalent degree of hyperinfectivity as passage through the human host. We have used this infant mouse model of host-passaged hyperinfectivity to characterize the timing and the anatomic location of the competitive advantage of mouse-passaged V. cholerae as well as the contribution of three type IV pili to the phenotype.

scholarly journals The Vibrio cholerae FlgM Homologue Is an Anti-σ28 Factor That Is Secreted through the Sheathed Polar Flagellum

2004 ◽  
Vol 186 (14) ◽  
pp. 4613-4619 ◽  
Author(s):  
Nidia E. Correa ◽  
Jeffrey R. Barker ◽  
Karl E. Klose
Keyword(s):  
Vibrio Cholerae ◽  
Transcriptional Activity ◽  
Human Pathogen ◽  
Class Iii ◽  
Nonstructural Proteins ◽  
Infant Mouse ◽  
Repressive Effect ◽  
Flagellar Assembly ◽  
Mouse Intestine ◽  
Flagellar Genes

ABSTRACT Vibrio cholerae has a single polar sheathed flagellum that propels the cells of this bacterium. Flagellar synthesis, motility, and chemotaxis have all been linked to virulence in this human pathogen. V. cholerae expresses flagellar genes in a hierarchy consisting of σ54- and σ28-dependent transcription. In other bacteria, σ28 transcriptional activity is controlled by an anti-σ28 factor, FlgM. We demonstrate that the V. cholerae FlgM homologue (i) physically interacts with σ28, (ii) has a repressive effect on some V. cholerae σ28-dependent flagellar promoters, and (iii) is secreted through the polar sheathed flagellum, consistent with anti-σ28 activity. Interestingly, FlgM does not have a uniform repressive effect on all σ28-dependent promoters, as determined by measurement of σ28-dependent transcription in cells either lacking FlgM (ΔflgM) or incapable of secretion (ΔfliF). Further analysis of a ΔfliF strain revealed that this flagellar assembly block causes a decrease in class III (FlrC- and σ54-dependent) and class IV (σ28-dependent), but not class II (FlrA- and σ54-dependent), flagellar transcription. V. cholerae flgM and fliA (encodes σ28) mutants were only modestly affected in their ability to colonize the infant mouse intestine, a measure of virulence. Our results demonstrate that V. cholerae FlgM functions as an anti-σ28 factor and that the sheathed flagellum is competent for secretion of nonstructural proteins.

scholarly journals The ompU Paralogue vca1008 Is Required for Virulence of Vibrio cholerae

2004 ◽  
Vol 186 (15) ◽  
pp. 5167-5171 ◽  
Author(s):  
Carlos G. Osorio ◽  
Hector Martinez-Wilson ◽  
Andrew Camilli
Keyword(s):  
Mouse Model ◽  
Vibrio Cholerae ◽  
Intestinal Infection ◽  
Infant Mouse ◽  
Mouse Infection ◽  
Necessary And Sufficient ◽  
Transcriptional Induction

ABSTRACT We made single and combined mutations in ompU, ompT, and the two putative porin genes vca1008 and vc0972. The fitness of the strains was tested in vitro and in the infant mouse model of intestinal infection. We also studied the transcriptional induction of vca1008 in vitro and during mouse infection. We show that vca1008 is induced during infection and is necessary and sufficient (in the absence of ompU, ompT, and vc0972) for infection.

scholarly journals ToxR-Independent Expression of Cholera Toxin from the Replicative Form of CTXφ

1998 ◽  
Vol 66 (1) ◽  
pp. 394-397 ◽  
Author(s):  
Sara Lazar ◽  
Matthew K. Waldor
Keyword(s):  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Toxin Production ◽  
Recipient Strain ◽  
Replicative Form ◽  
Filamentous Bacteriophage ◽  
Infant Mouse ◽  
Mouse Intestine

ABSTRACT The ctxAB operon, which encodes cholera toxin, resides in the genome of CTXφ, a filamentous bacteriophage. WithinVibrio cholerae cells, the CTXφ genome can exist either as a replicating plasmid or as a prophage integrated into the chromosome. Previous work established that ToxR is required for chromosomal ctxAB expression. We have learned that strains harboring the CTXφ replicative form produce cholera toxin under all conditions tested, independently of ToxR. During passage of CTXφ lysogens through the infant mouse intestine, transduction of CTXφ to a recipient strain can be detected, indicating that phage excision and replication occur in vivo. These results suggest that phage induction might provide a novel mechanism for the regulation of cholera toxin production.

scholarly journals Role of Cyclic Di-GMP during El Tor Biotype Vibrio cholerae Infection: Characterization of the In Vivo-Induced Cyclic Di-GMP Phosphodiesterase CdpA

2008 ◽  
Vol 76 (4) ◽  
pp. 1617-1627 ◽  
Author(s):  
Rita Tamayo ◽  
Stefan Schild ◽  
Jason T. Pratt ◽  
Andrew Camilli
Keyword(s):  
Small Intestine ◽  
Vibrio Cholerae ◽  
Biofilm Formation ◽  
Virulence Gene ◽  
Virulence Gene Expression ◽  
Infant Mouse

ABSTRACT In Vibrio cholerae, the second messenger cyclic di-GMP (c-di-GMP) positively regulates biofilm formation and negatively regulates virulence and is proposed to play an important role in the transition from persistence in the environment to survival in the host. Herein we describe a characterization of the infection-induced gene cdpA, which encodes both GGDEF and EAL domains, which are known to mediate diguanylate cyclase and c-di-GMP phosphodiesterase (PDE) activities, respectively. CdpA is shown to possess PDE activity, and this activity is regulated by its inactive degenerate GGDEF domain. CdpA inhibits biofilm formation but has no effect on colonization of the infant mouse small intestine. Consistent with these observations, cdpA is expressed during in vitro growth in a biofilm but is not expressed in vivo until the late stage of infection, after colonization has occurred. To test for a role of c-di-GMP in the early stages of infection, we artificially increased c-di-GMP and observed reduced colonization. This was attributed to a significant reduction in toxT transcription during infection. Cumulatively, these results support a model of the V. cholerae life cycle in which c-di-GMP must be down-regulated early after entering the small intestine and maintained at a low level to allow virulence gene expression, colonization, and motility at appropriate stages of infection.

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