Regulation of <i>Helicobacter pylori cagA</i> Expression in Response to Salt

Loh, John T.; Torres, Victor J.; Cover, Timothy L.

doi:10.1158/0008-5472.can-06-4746

Cited by 131 publications

(130 citation statements)

References 46 publications

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“…We also observed that infection with 60190ΔcagA significantly reduced IL-8 induction, whereas 60190ΔcagE showed no induction at all. This is in agreement with previous results in which cagAmutants did not completely revert the induction of IL-8 but cagEmutants maintained basal IL-8 expression levels (29)(30)(31).…”

Section: Discussionsupporting

confidence: 93%

Helicobacter pylori induces β3GnT5 in human gastric cell lines, modulating expression of the SabA ligand sialyl–Lewis x

Marcos¹,

Magalhães²,

Ferreira³

et al. 2008

J. Clin. Invest.

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Section: Discussionsupporting

confidence: 93%

Helicobacter pylori induces β3GnT5 in human gastric cell lines, modulating expression of the SabA ligand sialyl–Lewis x

Marcos¹,

Magalhães²,

Ferreira³

et al. 2008

J. Clin. Invest.

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“…Monomeric DprB and dimeric RuvC may differ in their affinity to differing DNA structures within bacterial cells. Microarray studies showed that dprB and ruvC have similar transcription levels in free-living H. pylori 26695 strains (44), suggesting that differences in function between the two proteins, rather than abundance, account for the differing phenotypes.…”

Section: Discussionmentioning

confidence: 99%

DprB Facilitates Inter- and Intragenomic Recombination in Helicobacter pylori

Zhang

2012

J Bacteriol

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For naturally competent microorganisms, such as Helicobacter pylori, the steps that permit recombination of exogenous DNA are not fully understood. Immediately downstream of an H. pylori gene (dprA) that facilitates high-frequency natural transformation is HP0334 (dprB), annotated to be a putative Holliday junction resolvase (HJR). We showed that the HP0334 (dprB) gene product facilitates high-frequency natural transformation. We determined the physiologic roles of DprB by genetic analyses. DprB controls in vitro growth, survival after exposure to UV or fluoroquinolones, and intragenomic recombination. dprB ruvC double deletion dramatically decreases both homologous and homeologous transformation and survival after exposure to DNAdamaging agents. Moreover, the DprB protein binds to synthetic Holliday junction structures rather than double-stranded or single-stranded DNA. These results demonstrate that the dprB product plays important roles affecting inter-and intragenomic recombination. We provide evidence that the two putative H. pylori HJRs (DprB and RuvC) have overlapping but distinct functions involving intergenomic (primarily DprB) and intragenomic (primarily RuvC) recombination. Genetic diversity, a characteristic of many bacterial populations, maximizes survival when ecological niches change and reflects the major impact of horizontal gene transfer (18, 69). The Gram-negative slow-growing bacterium Helicobacter pylori, which colonizes the human stomach and resists gastric inflammation and whose persistence affects the risk of gastrointestinal diseases (10), is naturally competent for DNA uptake. H. pylori isolates from individual hosts have remarkable genetic diversity, reflecting adaptation to their gastric habitats and to inflammation (2,29,43,46,50,66); their ability to be transformed contributes to the development of variation (12,26,28,39), and recombination involves multiple mechanisms (31,73).Natural transformation of bacterial cells involves three steps: exogenous DNA binding, uptake and translocation, and recombination with genomic DNA (15). The early steps of H. pylori natural transformation require comB genes that encode homologs of a type IV secretion system facilitating DNA uptake (26). A DprAfamily protein encoded by HP0333 plays roles in high-frequency uptake and translocation of exogenous DNA (4, 62, 63), and RecA (HP0153) is required for the homologous recombination inherent in H. pylori transformation (55, 70). Expression of H. pylori natural competence genes can be induced by DNA damage, further increasing transformation frequency (TF) and gene exchange (20).In H. pylori, natural transformation is suppressed by the DNA helicases RuvB and RecG (30,32). Holliday junctions (HJs), fourway branched DNA intermediates produced at the last step of homologous recombination, are recognized by Holliday junction resolvases (HJRs), specialized DNA-binding proteins that are required to complete recombination (59). HJ structures that are typically formed by the crossover of parental and invading stran...

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“…In keeping with this, a recent study showed that elevated salt concentrations result in alterations in expression of the virulence factor CagA in H. pylori strain 26695 (16). Loh et al showed that an increased salt concentration slows H. pylori growth and affects expression of a large number of genes (16). Concomitant studies by our group that explored this effect in further detail are described here.…”

mentioning

confidence: 88%

Sodium Chloride Affects Helicobacter pylori Growth and Gene Expression

2008

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Epidemiological evidence links high-salt diets and Helicobacter pylori infection with increased risk of developing gastric maladies. The mechanism by which elevated sodium chloride content causes these manifestations is unclear. Here we characterize the response of H. pylori to temporal changes in sodium chloride concentration and show that growth, cell morphology, survival, and virulence factor expression are all altered by increased salt concentration.

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Regulation of Helicobacter pylori cagA Expression in Response to Salt

Abstract: Helicobacter pylori infection and a high dietary salt intake are risk factors for the development of gastric adenocarcinoma.

Cited by 131 publications

References 46 publications

Helicobacter pylori induces β3GnT5 in human gastric cell lines, modulating expression of the SabA ligand sialyl–Lewis x

Helicobacter pylori induces β3GnT5 in human gastric cell lines, modulating expression of the SabA ligand sialyl–Lewis x

DprB Facilitates Inter- and Intragenomic Recombination in Helicobacter pylori

Sodium Chloride Affects Helicobacter pylori Growth and Gene Expression

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