Sodium Chloride Affects
            <i>Helicobacter pylori</i>
            Growth and Gene Expression

Gancz, Hanan; Jones, Kathleen R.; Merrell, D. Scott

doi:10.1128/jb.01728-07

Cited by 66 publications

(76 citation statements)

References 33 publications

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“…jejuni formed long, helical filaments under hyperosmotic stress. This "defective" cell division is commonly observed for numerous bacterial species under stress conditions (10,37), for instance, during hyperosmotic stress for the C. jejuni-related epsilonproteobacterium H. pylori and the deltaproteobacterium Desulfovibrio vulgaris (15,42). Other biological stresses such as heat and oxidative shock, certain antibiotics, DNA damage, exposure to grazing by single-celled eukaryotes, and mutation or alteration of the stoichiometry of cell division components also give rise to filamentous morphologies (25).…”

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confidence: 99%

“…Upregulation of heat shock genes may account for this decreased ability to respond to heat upshock, as increased heat sensitivity was also observed for a C. jejuni mutant with a mutation in the heat shock gene repressor hspR (1). Expression of heat shock genes is not a typical response to osmotic stress in E. coli (17) but has been observed for H. pylori (15,53) and Lactococcus lactis (28), suggesting that heat shock proteins are deployed by a wide variety of bacteria to counter hyperosmotic stress-induced protein misfolding and other damage (1, 21, 30, 43, 53).…”

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confidence: 99%

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Hyperosmotic Stress Response of Campylobacter jejuni

et al. 2012

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The diarrheal pathogen Campylobacter jejuni and other gastrointestinal bacteria encounter changes in osmolarity in the environment, through exposure to food processing, and upon entering host organisms, where osmotic adaptation can be associated with virulence. In this study, growth profiles, transcriptomics, and phenotypic, mutant, and single-cell analyses were used to explore the effects of hyperosmotic stress exposure on C. jejuni. Increased growth inhibition correlated with increased osmotic concentration, with both ionic and nonionic stressors inhibiting growth at 0.620 total osmol liter ؊1 . C. jejuni adaptation to a range of osmotic stressors and concentrations was accompanied by severe filamentation in subpopulations, with microscopy indicating septum formation and phenotypic diversity between individual cells in a filament. Population heterogeneity was also exemplified by the bifurcation of colony morphology into small and large variants on salt stress plates. Flow cytometry of C. jejuni harboring green fluorescent protein (GFP) fused to the ATP synthase promoter likewise revealed bimodal subpopulations under hyperosmotic stress. We also identified frequent hyperosmotic stress-sensitive variants within the clonal wild-type population propagated on standard laboratory medium. Microarray analysis following hyperosmotic upshift revealed enhanced expression of heat shock genes and genes encoding enzymes for synthesis of potential osmoprotectants and cross-protective induction of oxidative stress genes. The capsule export gene kpsM was also upregulated, and an acapsular mutant was defective for growth under hyperosmotic stress. For C. jejuni, an organism lacking most conventional osmotic response factors, these data suggest an unusual hyperosmotic stress response, including likely "bet-hedging" survival strategies relying on the presence of stress-fit individuals in a heterogeneous population.

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confidence: 99%

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confidence: 99%

Hyperosmotic Stress Response of Campylobacter jejuni

et al. 2012

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“…The observation that bacteria sense their environment and respond, potentially in a way to enhance virulence, is not new (1,15). In other bacteria, such as Escherichia coli, Pseudomonas aeruginosa, and M. tuberculosis, sensor kinases of 2-component regulatory systems detect environmental changes, which lead to phosphorylation of the response regulator, and this induces a conformational change that permits binding of the response regulator to promoters of the DNA, resulting in changes in gene expression and phenotype (16,21,33).…”

Section: Discussionmentioning

confidence: 99%

Mimicry of the Pathogenic Mycobacterium VacuoleIn VitroElicits the Bacterial Intracellular Phenotype, Including Early-Onset Macrophage Death

Early

Bermudez

2011

Infect Immun

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Mycobacterium avium complex (MAC) within macrophages undergoes a phenotype change that allows for more efficient entry into surrounding host cells. We hypothesized that, by developing an in vitro system resembling the intravacuolar environment, one could generate insights into the mycobacterial intracellular phenotype. MAC was incubated in "elemental mixtures" that reproduce metal concentrations and pH in the vacuoles at different time points and then used to infect fresh macrophages. Incubation of MAC with the mixture corresponding to the vacuole environment 24 h postinfection infected macrophages at a significantly higher rate than bacteria that were incubated in Middlebrook 7H9 broth. Uptake occurred by macropinocytosis, similar to the uptake of bacteria passed through macrophages. Genes reported to be upregulated in intracellular bacteria, such as Mav1365, Mav2409, Mav4487, and Mav0996, were upregulated in MAC incubated in the 24-h elemental mixture. Like MAC obtained from macrophages, the vacuoles of bacteria from the 24-h elemental mixture were more likely to contain lysosome-associated membrane protein 1 (LAMP-1). A stepwise reduction scheme of the 24-h elemental mixture indicated that incubation in physiologically relevant concentrations of potassium chloride, calcium chloride, and manganese chloride was sufficient to induce characteristics of the intracellular phenotype. It was demonstrated that bacteria harboring the intracellular phenotype induced early-onset macrophage death more efficiently than bacteria grown in broth. This new trace elemental mixture mimicking the condition of the vacuole at different time points has the potential to become an effective laboratory tool for the study of the MAC and Mycobacterium tuberculosis disease process, increasing the understanding of the interaction with macrophages.

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“…The selection of ranges for those variables was based on a wide literature research (2,9,10,(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25). Coded and real values of variables are shown in Table I.…”

Section: Response Surface Methodology (Rsm): Box-behnken Designmentioning

confidence: 99%

Optimization and Culture Conditions to Improve Helicobacter Pylori Growth in HAM's F-12 Medium by Response Surface Methodology

Bessa

Correia

Cellini

et al. 2012

Int J Immunopathol Pharmacol

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Helicobacter pylori is a gastroduodenal pathogen that colonizes the human stomach and is the causal agent of gastric diseases. From the clinical and epidemiological point of view, enhancing and improving the growth of this bacterium in liquid media is an important goal to achieve in order to allow the performance of accurate physiological studies. The aim of this work was to optimize three culture conditions that influence the growth of H. pylori in the defined medium Ham's F-12 supplemented with 5% fetal bovine serum by using response surface methodology as a statistical technique to obtain the optimal conditions. The factors studied in this experimental design (Box-Behnken design) were the pH of the medium, the shaking speed (rpm) and the percentage of atmospheric oxygen, in a total of 17 experiments. The biomass specific growth rate (J1) was the response measured. The model was validated for pH and shaking speed. The percentage of atmospheric oxygen did not influence the growth for the range of values studied. At the optimal values found for pH and shaking speed, 8 and 130 rpm, respectively, a specific growth rate value of 0.164 hot, corresponding to a maximal concentration of approximately 1.5xl0 8 CFU/ml, was reached after 8 h. The experimental design strategy allowed, for the first time, the optimization of H. pylori growth in a semi-synthetic medium, which may be important to improve physiological and metabolic studies of this "fastidious" bacterium.

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Sodium Chloride Affects Helicobacter pylori Growth and Gene Expression

Cited by 66 publications

References 33 publications

Hyperosmotic Stress Response of Campylobacter jejuni

Hyperosmotic Stress Response of Campylobacter jejuni

Mimicry of the Pathogenic Mycobacterium VacuoleIn VitroElicits the Bacterial Intracellular Phenotype, Including Early-Onset Macrophage Death

Optimization and Culture Conditions to Improve Helicobacter Pylori Growth in HAM's F-12 Medium by Response Surface Methodology

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