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.

Two regulatory factors of Vibrio cholerae activating the mannose-sensitive haemagglutinin pilus expression is important for biofilm formation and colonization in mice

Microbiology ◽  
2021 ◽  
Vol 167 (10) ◽  
Author(s):  
Mengting Shi ◽  
Yue Zheng ◽  
Xianghong Wang ◽  
Zhengjia Wang ◽  
Menghua Yang
Keyword(s):  
Mouse Model ◽  
Vibrio Cholerae ◽  
Biofilm Formation ◽  
Type Species ◽  
Wild Type ◽  
Expression Library ◽  
Content Type ◽  
Genomic Expression ◽  
Infant Mouse ◽  
Link Type

Vibrio cholerae the causative agent of cholera, uses a large number of coordinated transcriptional regulatory events to transition from its environmental reservoir to the host intestine, which is its preferred colonization site. Transcription of the mannose-sensitive haemagglutinin pilus (MSHA), which aids the persistence of V. cholerae in aquatic environments, but causes its clearance by host immune defenses, was found to be regulated by a yet unknown mechanism during the infection cycle of V. cholerae . In this study, genomic expression library screening revealed that two regulators, VC1371 and VcRfaH, are able to positively activate the transcription of MSHA operon. VC1371 is localized and active in the cell membrane. Deletion of vc1371 or VcrfaH genes in V. cholerae resulted in less MshA protein production and less efficiency of biofilm formation compared to that in the wild-type strain. An adult mouse model showed that the mutants with vc1371 or VcrfaH deletion colonized less efficiently than the wild-type; the VcrfaH deletion mutant showed less colonization efficiency in the infant mouse model. The findings strongly suggested that the two regulators, namely VC1371 and VcRfaH, which are involved in the regulation of MSHA expression, play an important role in V. cholerae biofilm formation and colonization in mice.

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 Role of Vibrio cholerae O139 Surface Polysaccharides in Intestinal Colonization

2002 ◽  
Vol 70 (11) ◽  
pp. 5990-5996 ◽  
Author(s):  
Jutta Nesper ◽  
Stefan Schild ◽  
Crystal M. Lauriano ◽  
Anita Kraiss ◽  
Karl E. Klose ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Capsular Polysaccharide ◽  
Genetically Engineered ◽  
Side Chain ◽  
Intestinal Colonization ◽  
Core Oligosaccharide ◽  
Infant Mouse ◽  
Surface Polysaccharides

ABSTRACT Since the first occurrence of O139 Vibrio cholerae as a cause of cholera epidemics, this serogroup has been investigated intensively, and it has been found that its pathogenicity is comparable to that of O1 El Tor strains. O139 isolates express a thin capsule, composed of a polymer of repeating units structurally identical to the lipopolysaccharide (LPS) O side chain. In this study, we investigated the role of LPS O side chain and capsular polysaccharide (CPS) in intestinal colonization by with genetically engineered mutants. We constructed CPS-negative, CPS/LPS O side chain-negative, and CPS-positive/LPS O side chain-negative mutants. Furthermore, we constructed two mutants with defects in LPS core oligosaccharide (OS) assembly. Loss of LPS O side chain or CPS resulted in a ≈30-fold reduction in colonization of the infant mouse small intestine, indicating that the presence of both LPS O side chain and CPS is important during the colonization process. The strain lacking both CPS and LPS O side chain and a CPS-positive, LPS O side chain-negative core OS mutant were both essentially unable to colonize. To characterize the role of surface polysaccharides in survival in the host intestine, resistance to several antimicrobial substances was investigated in vitro. These investigations revealed that the presence of CPS protects the cell against attack of the complement system and that an intact core OS is necessary for survival in the presence of bile.

scholarly journals Upregulation of virulence genes promotes Vibrio cholerae biofilm hyperinfectivity

2020 ◽  
Vol 117 (20) ◽  
pp. 11010-11017 ◽  
Author(s):  
A. L. Gallego-Hernandez ◽  
W. H. DePas ◽  
J. H. Park ◽  
J. K. Teschler ◽  
R. Hartmann ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Three Dimensional ◽  
Planktonic Cells ◽  
Infant Mouse ◽  
Enhanced Production ◽  
Quantitative Image ◽  
Virulence Factor Gene ◽  
Colonization Patterns

Vibrio cholerae remains a major global health threat, disproportionately impacting parts of the world without adequate infrastructure and sanitation resources. In aquatic environments, V. cholerae exists both as planktonic cells and as biofilms, which are held together by an extracellular matrix. V. cholerae biofilms have been shown to be hyperinfective, but the mechanism of hyperinfectivity is unclear. Here we show that biofilm-grown cells, irrespective of the surfaces on which they are formed, are able to markedly outcompete planktonic-grown cells in the infant mouse. Using an imaging technique designed to render intestinal tissue optically transparent and preserve the spatial integrity of infected intestines, we reveal and compare three-dimensional V. cholerae colonization patterns of planktonic-grown and biofilm-grown cells. Quantitative image analyses show that V. cholerae colonizes mainly the medial portion of the small intestine and that both the abundance and localization patterns of biofilm-grown cells differ from that of planktonic-grown cells. In vitro biofilm-grown cells activate expression of the virulence cascade, including the toxin coregulated pilus (TCP), and are able to acquire the cholera toxin-carrying CTXФ phage. Overall, virulence factor gene expression is also higher in vivo when infected with biofilm-grown cells, and modulation of their regulation is sufficient to cause the biofilm hyperinfectivity phenotype. Together, these results indicate that the altered biogeography of biofilm-grown cells and their enhanced production of virulence factors in the intestine underpin the biofilm hyperinfectivity phenotype.

scholarly journals The Alternative Sigma Factor σE Plays an Important Role in Intestinal Survival and Virulence in Vibrio cholerae

2002 ◽  
Vol 70 (10) ◽  
pp. 5355-5362 ◽  
Author(s):  
Gabriela Kovacikova ◽  
Karen Skorupski
Keyword(s):  
Vibrio Cholerae ◽  
Sigma Factor ◽  
Parental Strain ◽  
Time Course ◽  
Lethal Dose ◽  
Alternative Sigma Factor ◽  
Growth And Survival ◽  
Infant Mouse

ABSTRACT The alternative sigma factor σΕ (RpoE) is involved in the response to extracytoplasmic stress and plays a role in the virulence of a variety of different bacteria. To assess the role of σΕ in Vibrio cholerae pathogenesis, a ΔrpoE mutant was constructed and analyzed using the infant mouse model. The results here show that σΕ contributes significantly to the virulence of V. cholerae. The ΔrpoE mutant was highly attenuated with a 50% lethal dose more than 3 logs higher than that for the parental strain, and its ability to colonize the intestine was reduced approximately 30-fold. A time course of infection revealed that the number of CFU of the ΔrpoE mutant was approximately 1 log lower than that of the parental strain by 12 h postinoculation and decreased further by 24 h. The defect in virulence in the ΔrpoE mutant thus appears to be a diminished ability to survive within the intestinal environment. The results here also show that σΕ is not required for growth and survival of V. cholerae in vitro at high temperatures but is required under other stressful conditions, such as in the presence of 3% ethanol. As in Escherichia coli, the expression of rpoE in V. cholerae is dependent upon two promoters located upstream of the gene, P1 and P2. P1 appears to be σ70 dependent, whereas the downstream promoter, P2, is positively autoregulated by σΕ.

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.

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