scholarly journals Impact of a human gut microbe on Vibrio cholerae host colonization through biofilm enhancement

2021 ◽  
Author(s):  
Kelsey Barrasso ◽  
Denise Chac ◽  
Meti D. Debela ◽  
Jason B. Harris ◽  
Regina C. LaRocque ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Intestinal Microbiota ◽  
Diarrheal Disease ◽  
Disease Outcome ◽  
Host Colonization ◽  
Ample Evidence ◽  
Infant Mouse ◽  
Enteric Infections ◽  
Gut Microbe ◽  
Colonization Model

AbstractThe human intestinal microbiota plays a crucial role in protection against the infection of Vibrio cholerae, the etiological agent of the diarrheal disease cholera. A rare commensal bacterium, Paracoccus aminovorans, was previously identified to bloom in the intestines during V. cholerae infection in a cohort of patients exposed to the pathogen. However, how P. aminovorans interacts with V. cholerae has not been experimentally determined; moreover, whether any association between this bacterium alters the behaviors of V. cholerae to affect the disease outcome is also unclear. Here we show that P. aminovorans and V. cholerae together form dual-species biofilm structures with previously uncharacterized novel features. Using an infant mouse colonization model, we demonstrate that the presence of P. aminovorans within the murine small intestine enhances V. cholerae colonization in the same niche that is dependent on the production of the Vibrio exopolysaccharide (VPS), a major component of mature V. cholerae biofilm. Our study has identified a novel mechanism by which a microbiota species increases V. cholerae virulence, and we establish a plausible explanation for the increased abundance of specific microbiota species in individuals during V. cholerae infection.Significance StatementWhile ample evidence suggests that the outcome of various enteric infections can be affected by the intestinal microbiota, how specific gut microbes change the behaviors of a pathogen is unclear. Here we characterize the interaction between Vibrio cholerae and a rare gut microbe, Paracoccus aminovorans, that is known to bloom in the intestines during active V. cholerae infection. These two bacteria form a dual-species biofilm structure and increases the host colonization efficiency of V. cholerae. To our knowledge, no prior study has demonstrated that an individual microbe increases V. cholerae virulence. Importantly, our study illustrates a novel mechanism of gut microbe-pathogen interaction that has the potential to alter the disease outcome.

scholarly journals Serotype has a significant impact on the virulence of 7th pandemic Vibrio cholerae O1

2020 ◽  
Author(s):  
Stefan L Nordqvist ◽  
Kaisa Thorell ◽  
Frida Nilsson ◽  
Madeleine Löfstrand ◽  
Arvid Hagelberg ◽  
...  
Keyword(s):  
Gene Expression ◽  
Vibrio Cholerae ◽  
Virulence Genes ◽  
Diarrheal Disease ◽  
Selective Pressure ◽  
Infection Model ◽  
Infant Mouse ◽  
Mouse Infection Model ◽  
Vibrio Cholerae O1 ◽  
El Tor

AbstractOf over 200 different identified Vibrio cholerae serogroups only the O1 serogroup is consistently associated with endemic and epidemic cholera disease. The O1 serogroup has two serologically distinguishable variants, the Ogawa and Inaba serotypes, which differ only by a methyl group present on the terminal sugar of the Ogawa O-antigen but absent from Inaba strains. This methylation is catalyzed by a methyltransferase encoded by the wbeT gene, which in Inaba strains is disrupted by mutation. It is currently thought that there is little difference between the two serotypes. However, here we show, using isogenic pairs of O1 El Tor V. cholerae, that Inaba strains show significantly different patterns of gene expression and are significantly less able than the corresponding Ogawa strains to cause cholera in an infant mouse infection model. Our results suggest that changes in gene expression resulting from the loss of the wbeT gene lead to reduced virulence and possibly also reduced survival fitness outside the human host.Author SummaryThe bacterium Vibrio cholerae causes the pandemic diarrheal disease cholera. Despite many identified serotypes of V. cholerae only one, O1, causes pandemic cholera. The O1 serotype of pandemic V. cholerae has two distinguishable variants (called Ogawa and Inaba) long considered to be clinically and epidemiologically equivalent. Cholera outbreaks consist only of one the two variants at any time. In general, Ogawa strains cause the majority of outbreaks with relatively short-lived Inaba outbreaks occurring sporadically. We have suggested earlier that Inaba outbreaks occur during periods of environmental selective pressure against the Ogawa serotype. We demonstrate here that the two variants are not clinically equivalent. The Ogawa serotype is better able to respond to infection in an animal model by up regulating the expression of virulence genes essential for disease development. We suggest that this phenomenon is the result of wider ranging differences in gene expression resulting from the mutation that converts Ogawa into Inaba strains, and may help to explain the dominance of the Ogawa serotype in nature.

scholarly journals The Vibrio cholerae Pst2 Phosphate Transport System Is Upregulated in Biofilms and Contributes to Biofilm-Induced Hyperinfectivity

2012 ◽  
Vol 80 (5) ◽  
pp. 1794-1802 ◽  
Author(s):  
Benjamin Mudrak ◽  
Rita Tamayo
Keyword(s):  
Vibrio Cholerae ◽  
Diarrheal Disease ◽  
Phosphate Transport ◽  
Uptake System ◽  
Content Type ◽  
Infant Mouse ◽  
Membrane Complex ◽  
Inner Membrane Complex ◽  
Infectious Form

ABSTRACTVibrio choleraeis the causative agent of the deadly diarrheal disease cholera. As part of its life cycle,V. choleraepersists in marine environments, where it forms surface-attached communities commonly described as biofilms. Evidence indicates that these biofilms constitute the infectious form of the pathogen during outbreaks. Previous work has shown that biofilm-derivedV. choleraecells, even when fully dispersed from the biofilm matrix, are vastly more infectious than planktonic (free-living) cells. Here, we sought to identify factors that contribute to biofilm-induced hyperinfectivity inV. cholerae, and we present evidence for one aspect of the molecular basis of this phenotype. We identified proteins upregulated during growth in biofilms and determined their contributions to the hyperinfectivity phenotype. We found that PstS2, the periplasmic component of the Pst2 phosphate uptake system, was enriched in biofilms. Another gene in thepst2locus was transcriptionally upregulated in biofilms. Using the infant mouse model, we found that mutation of twopst2components resulted in impaired colonization. Importantly, deletion of the Pst2 inner membrane complex caused a greater colonization defect after growth in a biofilm compared to shaking culture. Based on these data, we propose thatV. choleraecells in biofilms upregulate the Pst2 system and therefore gain an advantage upon entry into the host. Further characterization of factors contributing to biofilm-induced hyperinfectivity inV. choleraewill improve our understanding of the transmission of the bacteria from natural aquatic habitats to the human host.

scholarly journals Nonredundant Roles of Iron Acquisition Systems in Vibrio cholerae

2015 ◽  
Vol 84 (2) ◽  
pp. 511-523 ◽  
Author(s):  
Eric D. Peng ◽  
Elizabeth E. Wyckoff ◽  
Alexandra R. Mey ◽  
Carolyn R. Fisher ◽  
Shelley M. Payne
Keyword(s):  
Vibrio Cholerae ◽  
Diarrheal Disease ◽  
Iron Acquisition ◽  
Growth Conditions ◽  
Growth Defect ◽  
Null Mutant ◽  
Content Type ◽  
Infant Mouse ◽  
Iron Transporter

Vibrio cholerae, the causative agent of the severe diarrheal disease cholera, thrives in both marine environments and the human host. To do so, it must encode the tools necessary to acquire essential nutrients, including iron, under these vastly different conditions. A number ofV. choleraeiron acquisition systems have been identified; however, the precise role of each system is not fully understood. To test the roles of individual systems, we generated a series of mutants in which only one of the four systems that support iron acquisition on unsupplemented LB agar, Feo, Fbp, Vct, and Vib, remains functional. Analysis of these mutants under different growth conditions showed that these systems are not redundant. The strain carrying only the ferrous iron transporter Feo grew well at acidic, but not alkaline, pH, whereas the ferric iron transporter Fbp promoted better growth at alkaline than at acidic pH. A strain defective in all four systems (null mutant) had a severe growth defect under aerobic conditions but accumulated iron and grew as well as the wild type in the absence of oxygen, suggesting the presence of an additional, unidentified iron transporter inV. cholerae. In support of this, the null mutant was only moderately attenuated in an infant mouse model of infection. While the null mutant used heme as an iron sourcein vitro, we demonstrate that heme is not available toV. choleraein the infant mouse intestine.

scholarly journals Vibrio cholerae Represses Polysaccharide Synthesis To Promote Motility in Mucosa

2015 ◽  
Vol 83 (3) ◽  
pp. 1114-1121 ◽  
Author(s):  
Zhenyu Liu ◽  
Yuning Wang ◽  
Shengyan Liu ◽  
Ying Sheng ◽  
Karl-Gustav Rueggeberg ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Epithelial Surface ◽  
Semisolid Medium ◽  
Content Type ◽  
Infant Mouse ◽  
Genome Wide ◽  
Polysaccharide Synthesis ◽  
A Genome ◽  
Rapid Spread ◽  
Colonization Model

The viscoelastic mucus layer of gastrointestinal tracts is a host defense barrier that a successful enteric pathogen, such asVibrio cholerae, must circumvent.V. cholerae, the causative agent of cholera, is able to penetrate the mucosa and colonize the epithelial surface of the small intestine. In this study, we found that mucin, the major component of mucus, promotedV. choleraemovement on semisolid medium and in liquid medium. A genome-wide screen revealed thatVibriopolysaccharide (VPS) production was inversely correlated with mucin-enhanced motility. Mucin adhesion assays indicated that VPS bound to mucin. Moreover, we found thatvpsexpression was reduced upon exposure to mucin. In an infant mouse colonization model, mutants that overexpressed VPS colonized less effectively than wild-type strains in more distal intestinal regions. These results suggest thatV. choleraeis able to sense mucosal signals and modulatevpsexpression accordingly so as to promote fast motion in mucus, thus allowing for rapid spread throughout the intestines.

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 Identification of the Vibrio cholerae Enterobactin Receptors VctA and IrgA: IrgA Is Not Required for Virulence

2002 ◽  
Vol 70 (7) ◽  
pp. 3419-3426 ◽  
Author(s):  
Alexandra R. Mey ◽  
Elizabeth E. Wyckoff ◽  
Amanda G. Oglesby ◽  
Eva Rab ◽  
Ronald K. Taylor ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Mutant Strain ◽  
Genomic Sequence ◽  
Iron Acquisition ◽  
Lethal Dose ◽  
Single Mutation ◽  
Periplasmic Binding Protein ◽  
Infant Mouse ◽  
Abc Transport ◽  
Important Virulence Factor

ABSTRACT The gram-negative enteric pathogen Vibrio cholerae requires iron for growth. V. cholerae has multiple iron acquisition systems, including utilization of heme and hemoglobin, synthesis and transport of the catechol siderophore vibriobactin, and transport of several siderophores that it does not itself make. One siderophore that V. cholerae transports, but does not make, is enterobactin. Enterobactin transport requires TonB and is independent of the vibriobactin receptor ViuA. In this study, two candidate enterobactin receptor genes, irgA (VC0475) and vctA (VCA0232), were identified by analysis of the V. cholerae genomic sequence. A single mutation in either of these genes did not significantly impair enterobactin utilization, but a strain defective in both genes did not use enterobactin. When either irgA or vctA was supplied on a plasmid, the ability of the irgA vctA double mutant to use enterobactin was restored. This indicates that both VctA and IrgA transport enterobactin. We also identify the genes vctPDGC, which are linked to vctA and encode a periplasmic binding protein-dependent ABC transport system that functions in the utilization of both enterobactin and vibriobactin (VCA0227-0230). An irgA::TnphoA mutant strain, MBG40, was shown in a previous study to be highly attenuated and to have a strong colonization defect in an infant mouse model of V. cholerae infection (M. B. Goldberg, V. J. DiRita, and S. B. Calderwood, Infect. Immun. 58:55-60, 1990). In this work, a new irgA mutation was constructed, and this mutant strain was not significantly impaired in its ability to compete with the parental strain in infant mice and was not attenuated for virulence in an assay of 50% lethal dose. These data indicate that the virulence defect in MBG40 is not due to the loss of irgA function and that irgA is unlikely to be an important virulence factor.

THE MANAGEMENT OF THE CRITICALLY ILL CHILD WITH DEHYDRATION SECONDARY TO DIARRHEA

PEDIATRICS ◽  
1970 ◽  
Vol 45 (6) ◽  
pp. 1029-1036
Author(s):  
Laurence Finberg
Keyword(s):  
Diarrheal Disease ◽  
Oral Intake ◽  
The Body ◽  
Critical Stage ◽  
Water Losses ◽  
Subcutaneous Infusion ◽  
Routes Of Administration ◽  
Parenteral Route ◽  
Trained Personnel ◽  
Enteric Infections

Diarrhea and vomiting, which so frequently complicate diarrheal diseases, occur in a variety of disorders affecting infants. Although enteric infections cause these symptoms more often than all other diseases combined, noninfectious causes may occasionally also occur. While each cause may have specific other effects, the discussion here will deliberately be limited to the management of the physiologic disturbances that accompany excessive loss of water and salts from tile gastrointestinal tract. Etiologic considerations, however important they may be, will not be further pursued. This emphasis is appropriate since survival following critical dehydration depends far more upon the correction of the physiologic disturbance than upon the removal of the cause. A critical stage in diarrheal disease may be defined as occurring when a volume of fluid equal in mass to about 10% of the body weight has been lost over a period of a day or two. Clinically, this usually occurs shortly after anorexia or vomiting has precluded oral intake. At this stage of illness, parenteral fluid therapy should be employed. Oral intake should be curtailed during the early hours of therapy. The use of milk or other foods high in calories and solute complicates management by markedly increasing stool water losses. Even if severe undernutrition coexists with tile diarrhea, the first 6 to 8 hours should be a period of brief starvation; the parenteral glucose will provide emergency calories. Although such routes of administration as intragastric drip and subcutaneous infusion have been employed successfully, their usage should be restricted to places where a deficiency of supplies or trained personnel interdicts the preferred parenteral route—continuous intravenous infusion.

scholarly journals Sugar-mediated regulation of a c-di-GMP phosphodiesterase in Vibrio cholerae

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Kyoo Heo ◽  
Young-Ha Park ◽  
Kyung-Ah Lee ◽  
Joonwon Kim ◽  
Hyeong-In Ham ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Biofilm Formation ◽  
Carbon Sources ◽  
Phosphotransferase System ◽  
Host Colonization ◽  
Host Immune Responses ◽  
Gut Colonization ◽  
Host Diet ◽  
Underlying Mechanisms ◽  
Cyclic Dinucleotide

AbstractBiofilm formation protects bacteria from stresses including antibiotics and host immune responses. Carbon sources can modulate biofilm formation and host colonization in Vibrio cholerae, but the underlying mechanisms remain unclear. Here, we show that EIIAGlc, a component of the phosphoenolpyruvate (PEP):carbohydrate phosphotransferase system (PTS), regulates the intracellular concentration of the cyclic dinucleotide c-di-GMP, and thus biofilm formation. The availability of preferred sugars such as glucose affects EIIAGlc phosphorylation state, which in turn modulates the interaction of EIIAGlc with a c-di-GMP phosphodiesterase (hereafter referred to as PdeS). In a Drosophila model of V. cholerae infection, sugars in the host diet regulate gut colonization in a manner dependent on the PdeS-EIIAGlc interaction. Our results shed light into the mechanisms by which some nutrients regulate biofilm formation and host colonization.

scholarly journals Growth Phase Regulation of Vibrio cholerae RTX Toxin Export

2006 ◽  
Vol 189 (5) ◽  
pp. 1827-1835 ◽  
Author(s):  
Bethany Kay Boardman ◽  
Brian M. Meehan ◽  
Karla J. Fullner Satchell
Keyword(s):  
Stationary Phase ◽  
Vibrio Cholerae ◽  
Growth Phase ◽  
Diarrheal Disease ◽  
Outer Membrane Vesicles ◽  
Transcriptional Level ◽  
Type I ◽  
Bacterial Membranes ◽  
Rtx Toxin ◽  
Phase Regulation

ABSTRACT Vibrio cholerae, the causative agent of the severe diarrheal disease cholera, secretes several “accessory” toxins, including RTX toxin, which causes the cross-linking of the actin cytoskeleton. RTX toxin is exported to the extracellular milieu by an atypical type I secretion system (T1SS), and we previously noted that RTX-associated activity is detectable only in supernatant fluids from log phase cultures. Here, we investigate the mechanisms for regulating RTX toxin activity in supernatant fluids. We find that exported proteases are capable of destroying RTX activity and may therefore play a role in the growth phase regulation of toxin activity. We determined that the absence of RTX toxin in stationary-phase culture supernatant fluids is also due to a lack of toxin secretion and not attributable to solely proteolytic degradation. We ascertained that the T1SS apparatus is regulated at the transcriptional level by growth phase control that is independent of quorum sensing, unlike other virulence factors of V. cholerae. Additionally, in stationary-phase cultures, all RTX toxin activity is associated with bacterial membranes or outer membrane vesicles.

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