Virulence gene expression in vivo

2004 ◽  
Vol 7 (3) ◽  
pp. 283-289 ◽  
Author(s):  
S SHELBURNE ◽  
J MUSSER
Keyword(s):  
Gene Expression ◽  
Virulence Gene ◽  
Virulence Gene Expression

Vibrio harveyi virulence gene expression in vitro and in vivo during infection in black tiger shrimp Penaeus monodon

2020 ◽  
Vol 139 ◽  
pp. 153-160
Author(s):  
S Peeralil ◽  
TC Joseph ◽  
V Murugadas ◽  
PG Akhilnath ◽  
VN Sreejith ◽  
...  
Keyword(s):  
Gene Expression ◽  
Virulence Genes ◽  
Vibrio Harveyi ◽  
Penaeus Monodon ◽  
Challenge Test ◽  
Virulence Gene ◽  
Economic Losses ◽  
Virulence Gene Expression

Luminescent Vibrio harveyi is common in sea and estuarine waters. It produces several virulence factors and negatively affects larval penaeid shrimp in hatcheries, resulting in severe economic losses to shrimp aquaculture. Although V. harveyi is an important pathogen of shrimp, its pathogenicity mechanisms have yet to be completely elucidated. In the present study, isolates of V. harveyi were isolated and characterized from diseased Penaeus monodon postlarvae from hatcheries in Kerala, India, from September to December 2016. All 23 tested isolates were positive for lipase, phospholipase, caseinase, gelatinase and chitinase activity, and 3 of the isolates (MFB32, MFB71 and MFB68) showed potential for significant biofilm formation. Based on the presence of virulence genes, the isolates of V. harveyi were grouped into 6 genotypes, predominated by vhpA+ flaB+ ser+ vhh1- luxR+ vopD- vcrD+ vscN-. One isolate from each genotype was randomly selected for in vivo virulence experiments, and the LD50 ranged from 1.7 ± 0.5 × 103 to 4.1 ± 0.1 × 105 CFU ml-1. The expression of genes during the infection in postlarvae was high in 2 of the isolates (MFB12 and MFB32), consistent with the result of the challenge test. However, in MFB19, even though all genes tested were present, their expression level was very low and likely contributed to its lack of virulence. Because of the significant variation in gene expression, the presence of virulence genes alone cannot be used as a marker for pathogenicity of V. harveyi.

scholarly journals EnterotoxigenicE. colivirulence gene regulation in human infections

2018 ◽  
Vol 115 (38) ◽  
pp. E8968-E8976 ◽  
Author(s):  
Alexander A. Crofts ◽  
Simone M. Giovanetti ◽  
Erica J. Rubin ◽  
Frédéric M. Poly ◽  
Ramiro L. Gutiérrez ◽  
...  
Keyword(s):  
Gene Expression ◽  
Virulence Factor ◽  
Virulence Gene ◽  
Human Infection ◽  
Anaerobic Growth ◽  
Infection Model ◽  
Low Oxygen ◽  
Virulence Gene Expression ◽  
Factor Expression

EnterotoxigenicEscherichia coli(ETEC) is a global diarrheal pathogen that utilizes adhesins and secreted enterotoxins to cause disease in mammalian hosts. Decades of research on virulence factor regulation in ETEC has revealed a variety of environmental factors that influence gene expression, including bile, pH, bicarbonate, osmolarity, and glucose. However, other hallmarks of the intestinal tract, such as low oxygen availability, have not been examined. Further, determining how ETEC integrates these signals in the complex host environment is challenging. To address this, we characterized ETEC’s response to the human host using samples from a controlled human infection model. We found ETEC senses environmental oxygen to globally influence virulence factor expression via the oxygen-sensitive transcriptional regulator fumarate and nitrate reduction (FNR) regulator. In vitro anaerobic growth replicates the in vivo virulence factor expression profile, and deletion offnrin ETEC strain H10407 results in a significant increase in expression of all classical virulence factors, including the colonization factor antigen I (CFA/I) adhesin operon and both heat-stable and heat-labile enterotoxins. These data depict a model of ETEC infection where FNR activity can globally influence virulence gene expression, and therefore proximity to the oxygenated zone bordering intestinal epithelial cells likely influences ETEC virulence gene expression in vivo. Outside of the host, ETEC biofilms are associated with seasonal ETEC epidemics, and we find FNR is a regulator of biofilm production. Together these data suggest FNR-dependent oxygen sensing in ETEC has implications for human infection inside and outside of the host.

scholarly journals 18β-Glycyrrhetinic Acid Inhibits Methicillin-Resistant Staphylococcus aureus Survival and Attenuates Virulence Gene Expression

2012 ◽  
Vol 57 (1) ◽  
pp. 241-247 ◽  
Author(s):  
Danyelle R. Long ◽  
Julia Mead ◽  
Jay M. Hendricks ◽  
Michele E. Hardy ◽  
Jovanka M. Voyich
Keyword(s):  
Gene Expression ◽  
Staphylococcus Aureus ◽  
Virulence Gene ◽  
Glycyrrhetinic Acid ◽  
Licorice Root ◽  
Methicillin Resistant ◽  
Content Type ◽  
Virulence Gene Expression

ABSTRACTMethicillin-resistantStaphylococcus aureus(MRSA) has become a major source of infection in hospitals and in the community. Increasing antibiotic resistance inS. aureusstrains has created a need for alternative therapies to treat disease. A component of the licorice rootGlycyrrhizaspp., 18β-glycyrrhetinic acid (GRA), has been shown to have antiviral, antitumor, and antibacterial activity. This investigation explores thein vitroandin vivoeffects of GRA on MRSA pulsed-field gel electrophoresis (PFGE) type USA300. GRA exhibited bactericidal activity at concentrations exceeding 0.223 μM. Upon exposure ofS. aureusto sublytic concentrations of GRA, we observed a reduction in expression of key virulence genes, includingsaeRandhla. In murine models of skin and soft tissue infection, topical GRA treatment significantly reduced skin lesion size and decreased the expression ofsaeRandhlagenes. Our investigation demonstrates that at high concentrations GRA is bactericidal to MRSA and at sublethal doses it reduces virulence gene expression inS. aureusbothin vitroandin vivo.

scholarly journals Role of the Histone-Like Nucleoid Structuring Protein in Colonization, Motility, and Bile-Dependent Repression of Virulence Gene Expression in Vibrio cholerae

2006 ◽  
Vol 74 (5) ◽  
pp. 3060-3064 ◽  
Author(s):  
Amalendu Ghosh ◽  
Kalidas Paul ◽  
Rukhsana Chowdhury
Keyword(s):  
Gene Expression ◽  
Vibrio Cholerae ◽  
Virulence Factors ◽  
Virulence Gene ◽  
Virulence Gene Expression

ABSTRACT Bile-mediated repression of virulence gene expression is relieved in a Vibrio cholerae hns mutant. The mutant also exhibited reduced motility due to lower flrA expression, higher in vivo production of the virulence factors, and lower colonization efficiency. The colonization defect of the mutant was due to low FlrA production.

scholarly journals Activation of theListeria monocytogenesVirulence Program by a Reducing Environment

mBio ◽  
2017 ◽  
Vol 8 (5) ◽  
Author(s):  
Jonathan L. Portman ◽  
Samuel B. Dubensky ◽  
Bret N. Peterson ◽  
Aaron T. Whiteley ◽  
Daniel A. Portnoy
Keyword(s):  
Gene Expression ◽  
Synthetic Medium ◽  
Virulence Gene ◽  
Intracellular Pathogen ◽  
Intracellular Pathogens ◽  
Virulence Gene Expression ◽  
Cell Cytosol ◽  
Host Cell Cytosol

ABSTRACTUpon entry into the host cell cytosol, the facultative intracellular pathogenListeria monocytogenescoordinates the expression of numerous essential virulence factors by allosteric binding of glutathione (GSH) to the Crp-Fnr family transcriptional regulator PrfA. Here, we report that robust virulence gene expression can be recapitulated by growing bacteria in a synthetic medium containing GSH or other chemical reducing agents. Bacteria grown under these conditions were 45-fold more virulent in an acute murine infection model and conferred greater immunity to a subsequent lethal challenge than bacteria grown in conventional media. During cultivationin vitro, PrfA activation was completely dependent on the intracellular levels of GSH, as a glutathione synthase mutant (ΔgshF) was activated by exogenous GSH but not reducing agents. PrfA activation was repressed in a synthetic medium supplemented with oligopeptides, but the repression was relieved by stimulation of the stringent response. These data suggest that cytosolicL. monocytogenesinterprets a combination of metabolic and redox cues as a signal to initiate robust virulence gene expressionin vivo.IMPORTANCEIntracellular pathogens are responsible for much of the worldwide morbidity and mortality from infectious diseases. These pathogens have evolved various strategies to proliferate within individual cells of the host and avoid the host immune response. Through cellular invasion or the use of specialized secretion machinery, all intracellular pathogens must access the host cell cytosol to establish their replicative niches. Determining how these pathogens sense and respond to the intracellular compartment to establish a successful infection is critical to our basic understanding of the pathogenesis of each organism and for the rational design of therapeutic interventions.Listeria monocytogenesis a model intracellular pathogen with robustin vitroandin vivoinfection models. Studies of the host-sensing and downstream signaling mechanisms evolved byL. monocytogenesoften describe themes of pathogenesis that are broadly applicable to less tractable pathogens. Here, we describe how bacteria use external redox states as a cue to activate virulence.

scholarly journals Genome-Wide Identification of Genes Regulated by the Rcs Phosphorelay System in Erwinia amylovora

2012 ◽  
Vol 25 (1) ◽  
pp. 6-17 ◽  
Author(s):  
Dongping Wang ◽  
Mingsheng Qi ◽  
Bernarda Calla ◽  
Schuyler S. Korban ◽  
Steven J. Clough ◽  
...  
Keyword(s):  
Gene Expression ◽  
Erwinia Amylovora ◽  
Virulence Gene ◽  
Luria Bertani ◽  
Regulatory Genes ◽  
Bacterial Cells ◽  
Virulence Gene Expression ◽  
Genome Wide

The exopolysaccharide amylovoran is one of the major pathogenicity factors in Erwinia amylovora, the causal agent of fire blight of apples and pears. We have previously demonstrated that the RcsBCD phosphorelay system is essential for virulence by controlling amylovoran biosynthesis. We have also found that the hybrid sensor kinase RcsC differentially regulates amylovoran production in vitro and in vivo. To further understand how the Rcs system regulates E. amylovora virulence gene expression, we conducted genome-wide microarray analyses to determine the regulons of RcsB and RcsC in liquid medium and on immature pear fruit. Array analyses identified a total of 648 genes differentially regulated by RcsCB in vitro and in vivo. Consistent with our previous findings, RcsB acts as a positive regulator in both conditions, while RcsC positively controls expression of amylovoran biosynthetic genes in vivo but negatively controls expression in vitro. Besides amylovoran biosynthesis and regulatory genes, cell-wall and cell-envelope (membrane) as well as regulatory genes were identified as the major components of the RcsBC regulon, including many novel genes. We have also demonstrated that transcripts of rcsA, rcsC, and rcsD genes but not the rcsB gene were up-regulated when bacterial cells were grown in minimal medium or following infection of pear fruits compared with those grown in Luria Bertani medium. Furthermore, using the genome of E. amylovora ATCC 49946, a hidden Markov model predicted 60 genes with a candidate RcsB binding site in the intergenic region, 28 of which were identified in the microarray assay. Based on these findings as well as previous reported data, a working model has been proposed to illustrate how the Rcs phosphorelay system regulates virulence gene expression in E. amylovora.

scholarly journals Identification of fevR, a Novel Regulator of Virulence Gene Expression in Francisella novicida

2008 ◽  
Vol 76 (8) ◽  
pp. 3473-3480 ◽  
Author(s):  
Anna Brotcke ◽  
Denise M. Monack
Keyword(s):  
Gene Expression ◽  
Regulatory Gene ◽  
Constitutive Expression ◽  
Virulence Gene ◽  
Virulence Gene Expression ◽  
Francisella Novicida ◽  
Expression Of Genes ◽  
Bacterial Replication ◽  
Virulence Gene Regulation

ABSTRACT Francisella tularensis infects wild animals and humans to cause tularemia. This pathogen targets the cytosol of macrophages, where it replicates using the genes in the Francisella pathogenicity island (FPI). Virulence gene regulation in Francisella is complex, but transcriptional regulators MglA and SspA have been shown to regulate the expression of approximately 100 genes, including the entire FPI. We utilized a Francisella novicida transposon mutant library to identify additional regulatory factors and identified five additional genes that are essential for virulence gene expression. One regulatory gene, FTN_0480 (fevR, Francisella effector of virulence regulation), present in all Francisella species, is required for expression of the FPI genes and other genes in the MglA/SspA regulon. The expression of fevR is positively regulated by MglA. However, constitutive expression of fevR in an mglA mutant strain did not restore expression of the MglA/SspA regulon, demonstrating that mglA and fevR act in parallel to positively regulate virulence gene expression. Virulence studies revealed that fevR is essential for bacterial replication in macrophages and in mice, where we additionally show that fevR is required for the expression of genes in the MglA/SspA regulon in vivo. Thus, fevR is a crucial virulence gene in Francisella, required for the expression of virulence factors known to be essential for this pathogen's subversion of host defenses and pathogenesis in vivo.

scholarly journals A Systems Biology Approach To Modeling Vibrio cholerae Gene Expression under Virulence-Inducing Conditions

2010 ◽  
Vol 192 (17) ◽  
pp. 4300-4310 ◽  
Author(s):  
Sanjat Kanjilal ◽  
Robert Citorik ◽  
Regina C. LaRocque ◽  
Marco F. Ramoni ◽  
Stephen B. Calderwood
Keyword(s):  
Gene Expression ◽  
Systems Biology ◽  
Vibrio Cholerae ◽  
Regulation Of Gene Expression ◽  
Virulence Gene ◽  
Temporal Separation ◽  
New Members ◽  
Virulence Gene Expression

ABSTRACT Vibrio cholerae is a Gram-negative bacillus that is the causative agent of cholera. Pathogenesis in vivo occurs through a series of spatiotemporally controlled events under the control of a gene cascade termed the ToxR regulon. Major genes in the ToxR regulon include the master regulators toxRS and tcpPH, the downstream regulator toxT, and virulence factors, the ctxAB and tcpA operons. Our current understanding of the dynamics of virulence gene expression is limited to microarray analyses of expression at selected time points. To better understand this process, we utilized a systems biology approach to examine the temporal regulation of gene expression in El Tor V. cholerae grown under virulence-inducing conditions in vitro (AKI medium), using high-resolution time series genomic profiling. Results showed that overall gene expression in AKI medium mimics that of in vivo studies but with less clear temporal separation between upstream regulators and downstream targets. Expression of toxRS was unaffected by growth under virulence-inducing conditions, but expression of toxT was activated shortly after switching from stationary to aerating conditions. The tcpA operon was also activated early during mid-exponential-phase growth, while the ctxAB operon was turned on later, after the rise in toxT expression. Expression of ctxAB continued to rise despite an eventual decrease in toxT. Cluster analysis of gene expression highlighted 15 hypothetical genes and six genes related to environmental information processing that represent potential new members of the ToxR regulon. This study applies systems biology tools to analysis of gene expression of V. cholerae in vitro and provides an important comparator for future studies done in vivo.

scholarly journals Differential expression of key pneumococcal virulence genes in vivo

Microbiology ◽  
2006 ◽  
Vol 152 (2) ◽  
pp. 305-311 ◽  
Author(s):  
Kim S. LeMessurier ◽  
Abiodun David Ogunniyi ◽  
James C. Paton
Keyword(s):  
Gene Expression ◽  
Virulence Genes ◽  
Virulence Gene ◽  
Rt Pcr ◽  
Dynamic Nature ◽  
Virulence Gene Expression ◽  
Bacterial Rna ◽  
Significant Difference ◽  
Time Point

Few studies have examined in vivo virulence gene expression in Streptococcus pneumoniae. In this study, expression of key pneumococcal virulence genes cbpA, pspA, ply, psaA, cps2A, piaA, nanA and spxB in the nasopharynx, lungs and bloodstream of mice was investigated, following intranasal challenge with the serotype 2 strain D39. Bacterial RNA was extracted, linearly amplified and assayed by real-time RT-PCR. At 72 h, cbpA mRNA was present at higher levels in the nasopharynx and lungs than in the blood. At this time-point, the mRNAs for PspA and PiaA were most abundant in the nasopharynx, whereas no significant difference in gene expression between niches was observed for ply, psaA and cps2A. Both nanA and spxB mRNAs were present in higher amounts in the nasopharynx than in the lungs or blood. These findings illustrate the dynamic nature of pneumococcal virulence gene expression in vivo.

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