Nutritional Requirements and Antibiotic Resistance Patterns of<i>Helicobacter</i>Species in Chemically Defined Media

Testerman, Traci L.; Conn, P. Brian; Mobley, Harry L. T.; McGee, David J.

doi:10.1128/jcm.44.5.1650-1658.2006

Cited by 64 publications

(87 citation statements)

References 26 publications

(30 reference statements)

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“…H. pylori requires zinc for growth in vitro (Testerman et al, 2001(Testerman et al, , 2006. We do not know whether zinc is limiting in the stomach, but studies have found that H. pylori infection lowers mucosal zinc concentrations (Sempértegui et al, 2007), possibly due to the presence of neutrophils, which produce the zinc-chelating agent calprotectin (Kehl-Fie & Skaar, 2010).…”

Section: Discussionmentioning

confidence: 99%

“…pylori does not require additional nickel for growth (Testerman et al, 2001(Testerman et al, , 2006, although it requires nickel as a cofactor for two critical enzymes: urease, which mediates pH homeostasis, and hydrogenase, which is used for hydrogen metabolism . The basal level of nickel in the medium is apparently sufficient for these enzymes, but it is not yet known whether in vivo nickel is limiting or toxic.…”

Section: Discussionmentioning

confidence: 99%

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A supplemented soft agar chemotaxis assay demonstrates the Helicobacter pylori chemotactic response to zinc and nickel

2013

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Department of Microbiology and Environmental Toxicology at the University of California at Santa Cruz, Santa Cruz, CA, USA Directed motility, or chemotaxis, is required for Helicobacter pylori to establish infection in the stomach, although the full repertoire of this bacterium's chemotactic responses is not yet known. Here we report that H. pylori responds to zinc as an attractant and nickel as a repellent. To reach this conclusion, we employed both a temporal chemotaxis assay based on bacterial reversals and a supplemented soft agar spatial assay. We refined the temporal assay using a previously described chemorepellent, acid, and found that H. pylori requires rich media with serum to maintain optimal swimming motility. Surprisingly, we found that some strains respond to acid as an attractant, and that the TlpC chemoreceptor correlated with whether acid was sensed as an attractant or repellent. Using this same assay, we detected weak repellent responses to nickel and copper, and a varied response to zinc. We thus developed an alternative spatial chemotactic assay called the supplemented soft agar assay, which utilizes soft agar medium supplemented with the test compound. With Escherichia coli, the attractant serine slowed overall bacterial migration, while the repellent nickel increased the speed of overall migration. In H. pylori we detected slowed migration with doubled tryptone media, as well as zinc, consistent with an attractant response. In contrast, nickel increased migration, consistent with repulsion.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

A supplemented soft agar chemotaxis assay demonstrates the Helicobacter pylori chemotactic response to zinc and nickel

2013

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“…It is regarded as a major etiologic factor in the development of chronic gastritis, peptic ulcer and gastric cancer (Lopez-Saez et al, 2010). In more detail, H. pylori are the main risk factor in 65-80% of gastric cancers, but in only 2% of such infections (You et al, 2000;Testerman et al, 2006;Vilchis et al, 2009;Janjetic et al, 2010;Zamani et al, 2011). That is to say, despite the worldwide distribution of H pylori infection in patients with gastric disease, only a few number of infected individuals develop gastric cancer, It is important to clarify other factors that may determine risk among those infected with H. pylori (Hisaki et al, 1988;Lin et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Serum Zinc Status and Helicobacter Pylori Infection in Gastric Disease Patients

Zhang¹,

Wu²,

Niu³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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The role of Helicobacter pylori status and serum zinc value in gastric disease patients and healthy controls were investigated. Cases used in this work were 45 gastric cancer patients, 44 with peptic ulcers, 52 suffering gastritis and 64 healthy controls, all diagnosed histologically with the controls undergoing medical checkups. Helicobacter pylori status and serum levels of Zn were determined by 13C-urea breath test and flame atomic absorption spectrophotometer, respectively. Our study showed that Helicobacter pylori infection has no change in gastritis, peptic ulcer and gastric cancer group, on the contrast, serum levels of Zn were significantly reduced in gastritis, peptic ulcer and gastric cancer group, compared with healthy controls, and the higher the Zn levels are, the more increased risk of gastric cancer. Helicobacter pylori infection is a cause of gastritis, peptic ulcers and even gastric cancer, while serum zinc level is an indicator of protection of gastric membranes against damage.

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“…It was more recently shown that purines are required for growth in Reynolds and Penn's defined medium for strain G27 (17), and that catalase was incapable of restoring growth in purine-free media. Similar studies utilizing the tissue culture medium Ham's F12 and subsequent derivations have also shown that purines are essential for the growth of H. pylori strain 26695 (18,19), and this has been recently reconfirmed by researchers utilizing a series of mutants for purine nucleotide metabolism (20,21).…”

mentioning

confidence: 89%

Helicobacter pylori Salvages Purines from Extracellular Host Cell DNA Utilizing the Outer Membrane-Associated Nuclease NucT

Liechti

Goldberg

2013

J Bacteriol

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Helicobacter pylori is a bacterial pathogen that establishes life-long infections in humans, and its presence in the gastric epithelium is strongly associated with gastritis, peptic ulcer disease, and gastric cancer. Having evolved in this specific gastric niche for hundreds of thousands of years, this microbe has become dependent on its human host. Bioinformatic analysis reveals that H. pylori has lost several genes involved in the de novo synthesis of purine nucleotides, and without this pathway present, H. pylori must salvage purines from its environment in order to grow. While the presence and abundance of free purines in various mammalian tissues has been loosely quantified, the concentration of purines present within the gastric mucosa remains unknown. There is evidence, however, that a significant amount of extracellular DNA is present in the human gastric mucosal layer as a result of epithelial cell turnover, and this DNA has the potential to serve as an adequate purine source for gastric purine auxotrophs. In this study, we characterize the ability of H. pylori to grow utilizing only DNA as a purine source. We show that this ability is independent of the ComB DNA uptake system, and that H. pylori utilization of DNA as a purine source is largely influenced by the presence of an outer membrane-associated nuclease (NucT). A ⌬nucT mutant exhibits significantly reduced extracellular nuclease activity and is deficient in growth when DNA is provided as the sole purine source in laboratory growth media. These growth defects are also evident when this nuclease mutant is grown in the presence of AGS cells or in purine-free tissue culture medium that has been conditioned by AGS cells in the absence of fetal bovine serum. Taken together, these results indicate that the salvage of purines from exogenous host cell DNA plays an important role in allowing H. pylori to meet its purine requirements for growth.

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Nutritional Requirements and Antibiotic Resistance Patterns ofHelicobacterSpecies in Chemically Defined Media

Cited by 64 publications

References 26 publications

A supplemented soft agar chemotaxis assay demonstrates the Helicobacter pylori chemotactic response to zinc and nickel

A supplemented soft agar chemotaxis assay demonstrates the Helicobacter pylori chemotactic response to zinc and nickel

Serum Zinc Status and Helicobacter Pylori Infection in Gastric Disease Patients

Helicobacter pylori Salvages Purines from Extracellular Host Cell DNA Utilizing the Outer Membrane-Associated Nuclease NucT

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