scholarly journals Salmonella enterica Serovar Enteritidis tatB and tatC Mutants Are Impaired in Caco-2 Cell Invasion In Vitro and Show Reduced Systemic Spread in Chickens

2010 ◽  
Vol 78 (8) ◽  
pp. 3493-3505 ◽  
Author(s):  
Claudia Silva Mickael ◽  
Po-King S. Lam ◽  
Emil M. Berberov ◽  
Brenda Allan ◽  
Andrew A. Potter ◽  
...  
Keyword(s):  
Salmonella Enterica ◽  
Sodium Dodecyl ◽  
Systemic Infection ◽  
Poultry Meat ◽  
Salmonella Enterica Serovar Enteritidis ◽  
Systemic Spread ◽  
Essential Components ◽  
Tat System ◽  
Folded Proteins

ABSTRACT Salmonella enterica subsp. enterica serovar Enteritidis is a leading causative agent of gastroenteritis in humans. This pathogen also colonizes the intestinal tracts of poultry and can spread systemically in chickens. Transfer to humans usually occurs through undercooked or improperly handled poultry meat or eggs. The bacterial twin-arginine transport (Tat) pathway is responsible for the translocation of folded proteins across the cytoplasmic membrane. In order to study the role of the Tat system in the infection and colonization of chickens by Salmonella Enteritidis, we constructed chromosomal deletion mutants of the tatB and tatC genes, which are essential components of the Tat translocon. We observed that the tat mutations affected bacterial cell morphology, motility, and sensitivity to albomycin, sodium dodecyl sulfate (SDS), and EDTA. In addition, the mutant strains showed reduced invasion of polarized Caco-2 cells. The wild-type phenotype was restored in all our Salmonella Enteritidis tat mutants by introducing episomal copies of the tatABC genes. When tested in chickens by use of a Salmonella Enteritidis ΔtatB strain, the Tat system inactivation did not substantially affect cecal colonization, but it delayed systemic infection. Taken together, our data demonstrated that the Tat system plays a role in Salmonella Enteritidis pathogenesis.

scholarly journals Salmonella enterica Serovar Enteritidis Pathogenicity Island 1 Is Not Essential for but Facilitates Rapid Systemic Spread in Chickens

2009 ◽  
Vol 77 (7) ◽  
pp. 2866-2875 ◽  
Author(s):  
Taseen S. Desin ◽  
Po-King S. Lam ◽  
Birgit Koch ◽  
Claudia Mickael ◽  
Emil Berberov ◽  
...  
Keyword(s):  
Salmonella Enterica ◽  
Systemic Infection ◽  
Poultry Meat ◽  
Wild Type ◽  
Secretion Systems ◽  
Salmonella Enterica Serovar Enteritidis ◽  
Systemic Spread ◽  
Mutant Strains ◽  
Vitro Analysis

ABSTRACT Salmonella enterica subsp. enterica serovar Enteritidis is a leading cause of human food-borne illness that is mainly associated with the consumption of contaminated poultry meat and eggs. To cause infection, S. Enteritidis is known to use two type III secretion systems, which are encoded on two salmonella pathogenicity islands, SPI-1 and SPI-2, the first of which is thought to play a major role in invasion and bacterial uptake. In order to study the role of SPI-1 in the colonization of chicken, we constructed deletion mutants affecting the complete SPI-1 region (40 kb) and the invG gene. Both ΔSPI-1 and ΔinvG mutant strains were impaired in the secretion of SipD, a SPI-1 effector protein. In vitro analysis using polarized human intestinal epithelial cells (Caco-2) revealed that both mutant strains were less invasive than the wild-type strain. A similar observation was made when chicken cecal and small intestinal explants were coinfected with the wild-type and ΔSPI-1 mutant strains. Oral challenge of 1-week-old chicken with the wild-type or ΔSPI-1 strains demonstrated that there was no difference in chicken cecal colonization. However, systemic infection of the liver and spleen was delayed in birds that were challenged with the ΔSPI-1 strain. These data demonstrate that SPI-1 facilitates systemic infection but is not essential for invasion and systemic spread of the organism in chickens.

scholarly journals Antimicrobial Photodynamic Inactivation Inhibits Candida albicans Virulence Factors and ReducesIn VivoPathogenicity

2012 ◽  
Vol 57 (1) ◽  
pp. 445-451 ◽  
Author(s):  
Ilka Tiemy Kato ◽  
Renato Araujo Prates ◽  
Caetano Padial Sabino ◽  
Beth Burgwyn Fuchs ◽  
George P. Tegos ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Virulence Factors ◽  
Sodium Dodecyl ◽  
Systemic Infection ◽  
Tube Formation ◽  
Photodynamic Inactivation ◽  
Content Type ◽  
Daughter Cells

ABSTRACTThe objective of this study was to evaluate whetherCandida albicansexhibits altered pathogenicity characteristics following sublethal antimicrobial photodynamic inactivation (APDI) and if such alterations are maintained in the daughter cells.C. albicanswas exposed to sublethal APDI by using methylene blue (MB) as a photosensitizer (0.05 mM) combined with a GaAlAs diode laser (λ 660 nm, 75 mW/cm2, 9 to 27 J/cm2).In vitro, we evaluated APDI effects onC. albicansgrowth, germ tube formation, sensitivity to oxidative and osmotic stress, cell wall integrity, and fluconazole susceptibility.In vivo, we evaluatedC. albicanspathogenicity with a mouse model of systemic infection. Animal survival was evaluated daily. Sublethal MB-mediated APDI reduced the growth rate and the ability ofC. albicansto form germ tubes compared to untreated cells (P< 0.05). Survival of mice systemically infected withC. albicanspretreated with APDI was significantly increased compared to mice infected with untreated yeast (P< 0.05). APDI increasedC. albicanssensitivity to sodium dodecyl sulfate, caffeine, and hydrogen peroxide. The MIC for fluconazole forC. albicanswas also reduced following sublethal MB-mediated APDI. However, none of those pathogenic parameters was altered in daughter cells ofC. albicanssubmitted to APDI. These data suggest that APDI may inhibit virulence factors and reducein vivopathogenicity ofC. albicans. The absence of alterations in daughter cells indicates that APDI effects are transitory. The MIC reduction for fluconazole following APDI suggests that this antifungal could be combined with APDI to treatC. albicansinfections.

scholarly journals Caveolin-1-Deficient Mice Show Defects in Innate Immunity and Inflammatory Immune Response during Salmonella enterica Serovar Typhimurium Infection

2006 ◽  
Vol 74 (12) ◽  
pp. 6665-6674 ◽  
Author(s):  
Freddy A. Medina ◽  
Cecilia J. de Almeida ◽  
Elliott Dew ◽  
Jiangwei Li ◽  
Gloria Bonuccelli ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Salmonella Enterica ◽  
Inflammatory Responses ◽  
Systemic Infection ◽  
Bacterial Invasion ◽  
Chemokine Production ◽  
Caveolin 1 ◽  
Serovar Typhimurium ◽  
Deficient Mice

ABSTRACT A number of studies have shown an association of pathogens with caveolae. To this date, however, there are no studies showing a role for caveolin-1 in modulating immune responses against pathogens. Interestingly, expression of caveolin-1 has been shown to occur in a regulated manner in immune cells in response to lipopolysaccharide (LPS). Here, we sought to determine the role of caveolin-1 (Cav-1) expression in Salmonella pathogenesis. Cav-1−/− mice displayed a significant decrease in survival when challenged with Salmonella enterica serovar Typhimurium. Spleen and tissue burdens were significantly higher in Cav-1−/− mice. However, infection of Cav-1−/− macrophages with serovar Typhimurium did not result in differences in bacterial invasion. In addition, Cav-1−/− mice displayed increased production of inflammatory cytokines, chemokines, and nitric oxide. Regardless of this, Cav-1−/− mice were unable to control the systemic infection of Salmonella. The increased chemokine production in Cav-1−/− mice resulted in greater infiltration of neutrophils into granulomas but did not alter the number of granulomas present. This was accompanied by increased necrosis in the liver. However, Cav-1−/− macrophages displayed increased inflammatory responses and increased nitric oxide production in vitro in response to Salmonella LPS. These results show that caveolin-1 plays a key role in regulating anti-inflammatory responses in macrophages. Taken together, these data suggest that the increased production of toxic mediators from macrophages lacking caveolin-1 is likely to be responsible for the marked susceptibility of caveolin-1-deficient mice to S. enterica serovar Typhimurium.

scholarly journals The absence of murine cathelicidin-related antimicrobial peptide impacts host responses enhancing Salmonella enterica serovar Typhimurium infection

Gut Pathogens ◽  
2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Danisa M. Bescucci ◽  
Sandra T. Clarke ◽  
Catherine L. J. Brown ◽  
Valerie F. Boras ◽  
Tony Montina ◽  
...  
Keyword(s):  
Antimicrobial Peptide ◽  
Salmonella Enterica ◽  
Systemic Infection ◽  
Cell Loss ◽  
Host Responses ◽  
Post Inoculation ◽  
Systemic Dissemination ◽  
Serovar Typhimurium ◽  
The Impact

Abstract Background Cathelicidins are a class of antimicrobial peptide, and the murine cathelicidin-related antimicrobial peptide (mCRAMP) has been demonstrated in vitro to impair Salmonella enterica serovar Typhimurium proliferation. However, the impact of mCRAMP on host responses and the microbiota following S. Typhimurium infection has not been determined. In this study mCRAMP−/− and mCRAMP+/+ mice (± streptomycin) were orally inoculated with S. enterica serovar Typhimurium DT104 (SA +), and impacts on the host and enteric bacterial communities were temporally evaluated. Results Higher densities of the pathogen were observed in cecal digesta and associated with mucosa in SA+/mCRAMP−/− mice that were pretreated (ST+) and not pretreated (ST−) with streptomycin at 24 h post-inoculation (hpi). Both SA+/ST+/mCRAMP−/− and SA+/ST−/mCRAMP−/− mice were more susceptible to infection exhibiting greater histopathologic changes (e.g. epithelial injury, leukocyte infiltration, goblet cell loss) at 48 hpi. Correspondingly, immune responses in SA+/ST+/mCRAMP–/− and SA+/ST−/mCRAMP–/− mice were affected (e.g. Ifnγ, Kc, Inos, Il1β, RegIIIγ). Systemic dissemination of the pathogen was characterized by metabolomics, and the liver metabolome was affected to a greater degree in SA+/ST+/mCRAMP–/− and SA+/ST−/mCRAMP–/− mice (e.g. taurine, cadaverine). Treatment-specific changes to the structure of the enteric microbiota were associated with infection and mCRAMP deficiency, with a higher abundance of Enterobacteriaceae and Veillonellaceae observed in infected null mice. The microbiota of mice that were administered the antibiotic and infected with Salmonella was dominated by Proteobacteria. Conclusion The study findings showed that the absence of mCRAMP modulated both host responses and the enteric microbiota enhancing local and systemic infection by Salmonella Typhimurium.

scholarly journals QseC Mediates Salmonella enterica Serovar Typhimurium Virulence In Vitro and In Vivo

2009 ◽  
Vol 78 (3) ◽  
pp. 914-926 ◽  
Author(s):  
Cristiano G. Moreira ◽  
David Weinshenker ◽  
Vanessa Sperandio
Keyword(s):  
Epithelial Cells ◽  
Salmonella Enterica ◽  
Systemic Disease ◽  
Systemic Infection ◽  
Flagellar Motility ◽  
Signaling System ◽  
Interkingdom Signaling ◽  
Serovar Typhimurium

ABSTRACT The autoinducer-3 (AI-3)/epinephrine (Epi)/norepinephrine (NE) interkingdom signaling system mediates chemical communication between bacteria and their mammalian hosts. The three signals are sensed by the QseC histidine kinase (HK) sensor. Salmonella enterica serovar Typhimurium is a pathogen that uses HKs to sense its environment and regulate virulence. Salmonella serovar Typhimurium invades epithelial cells and survives within macrophages. Invasion of epithelial cells is mediated by the type III secretion system (T3SS) encoded in Salmonella pathogenicity island 1 (SPI-1), while macrophage survival and systemic disease are mediated by the T3SS encoded in SPI-2. Here we show that QseC plays an important role in Salmonella serovar Typhimurium pathogenicity. A qseC mutant was impaired in flagellar motility, in invasion of epithelial cells, and in survival within macrophages and was attenuated for systemic infection in 129x1/SvJ mice. QseC acts globally, regulating expression of genes within SPI-1 and SPI-2 in vitro and in vivo (during infection of mice). Additionally, dopamine β-hydroxylase knockout (Dbh − / −) mice that do not produce Epi or NE showed different susceptibility to Salmonella serovar Typhimurium infection than wild-type mice. These data suggest that the AI-3/Epi/NE signaling system is a key factor during Salmonella serovar Typhimurium pathogenesis in vitro and in vivo. Elucidation of the role of this interkingdom signaling system in Salmonella serovar Typhimurium should contribute to a better understanding of the complex interplay between the pathogen and the host during infection.

scholarly journals Inactivation of Rv2525c, a Substrate of the Twin Arginine Translocation (Tat) System of Mycobacterium tuberculosis, Increases β-Lactam Susceptibility and Virulence

2006 ◽  
Vol 188 (18) ◽  
pp. 6669-6679 ◽  
Author(s):  
Brigitte Saint-Joanis ◽  
Caroline Demangel ◽  
Mary Jackson ◽  
Priscille Brodin ◽  
Laurent Marsollier ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Biochemical Analysis ◽  
Species Conservation ◽  
Knockout Mutant ◽  
Orthologous Genes ◽  
Twin Arginine Translocation ◽  
Cell Wall Biogenesis ◽  
Tat System ◽  
Folded Proteins

ABSTRACT The twin arginine translocation (Tat) system is used by many bacteria to export fully folded proteins containing cofactors. Here, we show genetically that this system is essential for Mycobacterium tuberculosis, as the tatAC operon and tatB genes could be inactivated only in partially diploid strains. Using comparative genomics, the rv2525c gene of M. tuberculosis was identified as encoding a histidine-rich protein, with a twin arginine signal peptide, and orthologous genes were shown to be present in several but not all actinobacterial species. Conservation of this gene by Mycobacterium leprae, which has undergone reductive evolution, suggested an important role for rv2525c. An rv2525c knockout mutant was constructed, and biochemical analysis indicated that the mature Rv2525c protein is secreted. Upon exposure to antituberculous drugs, rv2525c expression is significantly up-regulated together with those of other genes involved in cell wall biogenesis. Phenotypic comparison of the mutant with the parental strain revealed an increase in susceptibility to some β-lactam antibiotics and, despite slower growth in vitro, enhanced virulence in both cellular and murine models of tuberculosis. The Tat system thus contributes in multiple ways to survival of the tubercle bacillus.

scholarly journals Single passage in mouse organs enhances the survival and spread of Salmonella enterica

2015 ◽  
Vol 12 (113) ◽  
pp. 20150702 ◽  
Author(s):  
Richard Dybowski ◽  
Olivier Restif ◽  
Alexandre Goupy ◽  
Duncan J. Maskell ◽  
Piero Mastroeni ◽  
...  
Keyword(s):  
Salmonella Enterica ◽  
Probability Generating Function ◽  
Systemic Infection ◽  
Original Method ◽  
Wild Type ◽  
Immigration Process ◽  
Serovar Typhimurium ◽  
Intravenous Inoculation

Intravenous inoculation of Salmonella enterica serovar Typhimurium into mice is a prime experimental model of invasive salmonellosis. The use of wild-type isogenic tagged strains (WITS) in this system has revealed that bacteria undergo independent bottlenecks in the liver and spleen before establishing a systemic infection. We recently showed that those bacteria that survived the bottleneck exhibited enhanced growth when transferred to naive mice. In this study, we set out to disentangle the components of this in vivo adaptation by inoculating mice with WITS grown either in vitro or in vivo . We developed an original method to estimate the replication and killing rates of bacteria from experimental data, which involved solving the probability-generating function of a non-homogeneous birth–death–immigration process. This revealed a low initial mortality in bacteria obtained from a donor animal. Next, an analysis of WITS distributions in the livers and spleens of recipient animals indicated that in vivo -passaged bacteria started spreading between organs earlier than in vitro -grown bacteria. These results further our understanding of the influence of passage in a host on the fitness and virulence of Salmonella enterica and represent an advance in the power of investigation on the patterns and mechanisms of host–pathogen interactions.

Inhibitory Effects of Enterococcus Strains Obtained from a Probiotic Product on In Vitro Growth of Salmonella enterica Serovar Enteritidis Strain IFO3313

2006 ◽  
Vol 69 (9) ◽  
pp. 2258-2262 ◽  
Author(s):  
WATTHANA THEPPANGNA ◽  
KOICHI OTSUKI ◽  
TOSHIYUKI MURASE
Keyword(s):  
Salmonella Enterica ◽  
Salmonella Enteritidis ◽  
Viable Cell ◽  
Mixed Cultures ◽  
Inhibitory Effects ◽  
Salmonella Enterica Serovar Enteritidis ◽  
Cell Counts ◽  
Pure Cultures ◽  
Probiotic Product

Enterococcus faecium and Enterococcus gallinarum strains were isolated from a commercial probiotic product and the effects of these strains on the growth of Salmonella enterica serovar Enteritidis strain IFO3313 were investigated. Viable cell counts of Salmonella Enteritidis in mixed cultures with the probiotic product isolate of E. faecium were significantly (P &lt; 0.05) lower than those in pure cultures after 6, 8, and 24 h when the cultures were incubated in heart infusion broth at 37 and 41°C. Significant differences in viable cell counts of Salmonella Enteritidis in mixed cultures with the probiotic product isolate of E. gallinarum and those in pure cultures were also observed after 8 and 24 h at 37 and 41°C. Similar observations were shown in mixed cultures of Salmonella Enteritidis with the reference strains of E. faecium GIFU8355 and E. gallinarum ATCC 49573. Significant differences in viable cell counts of these enterococcal strains were not shown among pure and mixed cultures with Salmonella Enteritidis. The pH values in pure and mixed cultures were 7.0 or 7.5 throughout the experiments. E. faecium strains were found to harbor the genes encoding enterocins A and B and showed inhibitory zones with a diameter of 4 to 6 mm against growth of Salmonella Enteritidis in the enterocin production assays. However, the E. gallinarum strains possessed neither of the enterocin genes tested and exhibited no inhibition zone in the enterocin production assays. These results indicated that enterococcal strains exhibit inhibitory effects on the growth of Salmonella Enteritidis and these effects were due to both enterocin and nonenterocin factors.

scholarly journals In vitro efficacy of several disinfectants against Salmonella enterica serovar Enteritidis and Escherichia coli strains from poultry

2016 ◽  
Vol 46 (8) ◽  
pp. 1438-1442
Author(s):  
Sonia Martínez-Martínez ◽  
Sheila Yubero-Delgado ◽  
Elías-Fernando Rodríguez-Ferri ◽  
Rafael Frandoloso ◽  
Álvaro Álvarez-Estrada ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Salmonella Enterica ◽  
Environmental Control ◽  
Control Measures ◽  
In Vitro Test ◽  
Salmonella Enterica Serovar Enteritidis ◽  
Vitro Test ◽  
The Individual ◽  
Ammonium Compounds

ABSTRACT The efficacy of 28 individual or blended disinfectants against avian Salmonella enterica serovar Enteritidis and Escherichia coli strains was determined. An in vitro test in the presence and absence of serum as source of organic material was conducted. Povidone-iodine (releasing 1% available iodine), 1% potassium permanganate, 70% ethanol, 2% chlorhexidine digluconate and three commercial formulations based on quaternary ammonium compounds + formaldehyde or cresol derivates were the most effective against all strains tested and reduced bacterial counts by more than 106 times (6-log10) regardless of the presence of organic matter. These commercial compounds as well as ethanol and chlorhexidine among the individual substances tested might be helpful in the adoption of environmental control measures against these two enterobacteria in poultry industry.

scholarly journals Complete Genome Sequence of Bacteriophage MA12, Which Infects both Campylobacter jejuni and Salmonella enterica Serovar Enteritidis

2016 ◽  
Vol 4 (6) ◽  
Author(s):  
Sunjin Lee ◽  
Taesoo Kwon ◽  
Su-Jin Chae ◽  
Jong-Hyun Kim ◽  
Yeon Ho Kang ◽  
...  
Keyword(s):  
Campylobacter Jejuni ◽  
Genome Sequence ◽  
Complete Genome Sequence ◽  
Salmonella Enterica ◽  
Complete Genome ◽  
Phage Therapy ◽  
Poultry Meat ◽  
Salmonella Enterica Serovar Enteritidis

Here, we announce the complete genome sequence of Salmonella enterica serovar Enteritidis ( S . Enteritidis) bacteriophage MA12, a 41-Kb chromosome. The strain can infect both Campylobacter jejuni ( C. jejuni ) and S . Enteritidis and can be used in phage therapy experiments with poultry and poultry meat.

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