The DOI matches its Crossref record; 76 of the 76 references it cites were found in a registry or an index.
Growth Phase-Dependent Response of Helicobacter pylori to Iron Starvation
Open accessAbstract
Iron is an essential nutrient that is often found in extremely limited available quantities within eukaryotic hosts. Because of this, many pathogenic bacteria have developed regulated networks of genes important for iron uptake and storage. In addition, it has been shown that many bacteria use available iron concentrations as a signal to regulate virulence gene expression. We have utilized DNA microarray technology to identify genes of the human pathogen Helicobacter pylori that are differentially regulated on a growth-inhibiting shift to iron starvation conditions. In addition, the growth phase-dependent expression of these genes was investigated by examining both exponential and stationary growth phase cultures. We identified known iron-regulated genes, as well as a number of genes whose regulation by iron concentration was not previously appreciated. Included in the list of regulated factors were the known virulence genes cagA, vacA, and napA. We examined the effect of iron starvation on the motility of H. pylori and found that exponential- and stationary-phase cultures responded differently to the stress. We further found that while growing cells are rapidly killed by iron starvation, stationary-phase cells show a remarkable ability to survive iron depletion. Finally, bioinformatic analysis of the predicted promoter regions of the differentially regulated genes led to identification of several putative Fur boxes, suggesting a direct role for Fur in iron-dependent regulation of these genes.
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“In either case, iron deficiency increases H. pylori expression of the Cag pathogenicity island that encodes for a type 4 secretion system used to deliver CagA into host cells (Merrell et al., 2003).”
From The Impact of Dietary Transition Metals on Host-Bacterial Interactions (2018) · cites this paper as Merrell et al., 2003
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Pathogenesis of Helicobacter pylori Infection
Kusters, J. G., van Vliet, A. H. M., & Kuipers, E. J. (2006) · Clinical Microbiology Reviews · doi:10.1128/cmr.00054-05 · Cited by 2,526
THE PATHOGENESIS OFHELICOBACTER PYLORI–INDUCED GASTRO-DUODENAL DISEASES
Atherton, J. C. (2006) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev.pathol.1.110304.100125 · Cited by 582
Pathogenesis of Helicobacter pylori infection
Camilo, V., Sugiyama, T., & Touati, E. (2017) · Helicobacter · doi:10.1111/hel.12405 · Cited by 377
An Overview of Helicobacter pylori VacA Toxin Biology
Foegeding, N. J., Caston, R. R., McClain, M. S., Ohi, M. D., & Cover, T. L. (2016) · Toxins · doi:10.3390/toxins8060173 · Cited by 244
Iron limitation induces SpoT‐dependent accumulation of ppGpp in Escherichia coli
Vinella, D., Albrecht, C. H., Cashel, M., & D’Ari, R. (2005) · Molecular Microbiology · doi:10.1111/j.1365-2958.2005.04601.x · Cited by 221
Metadata
- Authors
- Merrell, D. S., Thompson, L. J., Kim, C. C., Mitchell, H., Tompkins, L. S., Lee, A., & Falkow, S.
- Affiliations
- Stanford Medicine (US)
- UNSW Sydney (AU)
- Venue
- Infection and Immunity
- Publisher
- American Society for Microbiology
- Published
- 2003-11
- Volume
- 71
- Issue
- 11
- Pages
- 6510-6525
- ISSN
- 0019-9567 (ISSN-L)
- 1098-5522
- PMC
- PMC219544
- OpenAlex
- W2139704756
- Cited by
- 149
- References
- 76
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 3 · 2023: 5 · 2022: 2 · 2021: 5 · 2020: 2 · 2019: 2 · 2018: 3 · 2017: 6 · 2016: 8 · 2015: 3 · 2014: 9 · 2013: 8 · 2012: 12
- FWCI
- 10.23
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Infection and Immunity (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- Damon Runyon Cancer Research Foundation
- University of New South Wales
- National Institutes of Health (DK56339)
- Medical Research Council
- National Health and Medical Research Council (CA92229, AI38459)
- National Cancer Institute (CA 92229, R01CA092229)
- National Institute of Allergy and Infectious Diseases (AI 38459, AI 07502-06, R01AI038459, T32AI007502)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-56339, P30DK056339)
- Topics
- Health Sciences › Medicine › Gastroenterology › Helicobacter pylori-related gastroenterology studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Bacterial Genetics and Biotechnology
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Keywords
- Helicobacter pylori, iron starvation, iron regulation, growth phase, virulence gene expression, CagA, VacA, napA, bacterial motility, Fur protein, Fur box, promoter analysis, iron absorption, stationary phase survival
- MeSH terms
- Base Sequence, Biological Transport, Flagellin, Iron, Molecular Sequence Data, Nitrogen, Protein Biosynthesis, Gene Expression Regulation, Bacterial, Helicobacter pylori, Computational Biology, Oligonucleotide Array Sequence Analysis, Virulence Factors
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