Lactobacillus bulgaricus, Lactobacillus rhamnosus and Lactobacillus paracasei Attenuate Salmonella Enteritidis, Salmonella Heidelberg and Salmonella Typhimurium Colonization and Virulence Gene Expression In Vitro

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.

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Interplay between the QseC and QseE Bacterial Adrenergic Sensor Kinases in Salmonella enterica Serovar Typhimurium Pathogenesis

Infection and Immunity ◽

10.1128/iai.00803-12 ◽

2012 ◽

Vol 80 (12) ◽

pp. 4344-4353 ◽

Cited By ~ 34

Author(s):

Cristiano G. Moreira ◽

Vanessa Sperandio

Keyword(s):

Gene Expression ◽

Epithelial Cells ◽

Salmonella Enterica ◽

Double Mutant ◽

Virulence Gene ◽

Virulence Gene Expression ◽

Regulatory Cascade ◽

Serovar Typhimurium ◽

Sensor Kinases

ABSTRACTThe bacterial adrenergic sensor kinases QseC and QseE respond to epinephrine and/or norepinephrine to initiate a complex phosphorelay regulatory cascade that modulates virulence gene expression in several pathogens. We have previously shown that QseC activates virulence gene expression inSalmonella entericaserovar Typhimurium. Here we report the role of QseE inS. Typhimurium pathogenesis as well as the interplay between these two histidine sensor kinases in gene regulation. AnS. TyphimuriumqseEmutant is hampered in the invasion of epithelial cells and intramacrophage replication. The ΔqseCstrain is highly attenuated for intramacrophage survival but has only a minor defect in invasion. However, the ΔqseECstrain has only a slight attenuation in invasion, mirroring the ΔqseCstrain, and has an intermediary intramacrophage replication defect in comparison to the ΔqseEand ΔqseCstrains. The expressions of thesipAandsopBgenes, involved in the invasion of epithelial cells, are activated by epinephrine via QseE. The expression levels of these genes are still decreased in the ΔqseECdouble mutant, albeit to a lesser extent, congruent with the invasion phenotype of this mutant. The expression level of thesifAgene, important for intramacrophage replication, is decreased in theqseEmutant and the ΔqseECdouble mutant grownin vitro. However, as previously reported by us, the epinephrine-dependent activation of this gene occurs via QseC. In the systemic model ofS. Typhimurium infection of BALB/c mice, theqseCandqseEmutants are highly attenuated, while the double mutant has an intermediary phenotype. Altogether, these data suggest that both adrenergic sensors play an important role in modulating several aspects ofS. Typhimurium pathogenesis.

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

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.01023-12 ◽

2012 ◽

Vol 57 (1) ◽

pp. 241-247 ◽

Cited By ~ 32

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.

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Adherence and associated virulence gene expression in acid-treated Escherichia coli O157 : H7 in vitro and in ligated pig intestine

Microbiology ◽

10.1099/mic.0.056101-0 ◽

2012 ◽

Vol 158 (4) ◽

pp. 1084-1093 ◽

Cited By ~ 11

Author(s):

Xianhua Yin ◽

Yanni Feng ◽

Yang Lu ◽

James R. Chambers ◽

Joshua Gong ◽

...

Keyword(s):

Gene Expression ◽

Escherichia Coli ◽

Virulence Gene ◽

Escherichia Coli O157 ◽

Virulence Gene Expression

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Erratum to “The GadX regulon affects virulence gene expression and adhesion of porcine enteropathogenic Escherichia coli in vitro” [Vet. Anim. Sci. 3C (2017) 10–17]

Veterinary and Animal Science ◽

10.1016/j.vas.2020.100093 ◽

2020 ◽

Vol 9 ◽

pp. 100093

Author(s):

Hannah-Sophie Braun ◽

Gerhard Sponder ◽

Jörg R. Aschenbach ◽

Katharina Kerner ◽

Rolf Bauerfeind ◽

...

Keyword(s):

Gene Expression ◽

Escherichia Coli ◽

Virulence Gene ◽

Enteropathogenic Escherichia Coli ◽

Virulence Gene Expression

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Activation of theListeria monocytogenesVirulence Program by a Reducing Environment

mBio ◽

10.1128/mbio.01595-17 ◽

2017 ◽

Vol 8 (5) ◽

Cited By ~ 15

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.

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Role of Staphylococcus aureus Global Regulators sae and σB in Virulence Gene Expression during Device-Related Infection

Infection and Immunity ◽

10.1128/iai.73.6.3415-3421.2005 ◽

2005 ◽

Vol 73 (6) ◽

pp. 3415-3421 ◽

Cited By ~ 79

Author(s):

Christiane Goerke ◽

Ursula Fluckiger ◽

Andrea Steinhuber ◽

Vittoria Bisanzio ◽

Martina Ulrich ◽

...

Keyword(s):

Gene Expression ◽

Staphylococcus Aureus ◽

Virulence Gene ◽

Northern Analysis ◽

Virulence Gene Expression ◽

Global Regulators ◽

Reverse Transcription Pcr ◽

Direct Cross

ABSTRACT The ability of Staphylococcus aureus to adapt to different environments is due to a regulatory network comprising several loci. Here we present a detailed study of the interaction between the two global regulators sae and σB of S. aureus and their influence on virulence gene expression in vitro, as well as during device-related infection. The expression of sae, asp23, hla, clfA, coa, and fnbA was determined in strain Newman and its isogenic saeS/R and sigB mutants by Northern analysis and LightCycler reverse transcription-PCR. There was no indication of direct cross talk between the two regulators. sae had a dominant effect on target gene expression during device-related infection. σB seemed to be less active throughout the infection than under induced conditions in vitro.

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