ArticlePLoS pathogens2017
Helicobacter pylori gene silencing in vivo demonstrates urease is essential for chronic infection.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- Efficacy and safety of probiotic-supplemented bismuth quadruple therapy for the treatment ofThe Journal of international medical research · 2023Pooled it
- Comparative phylogenomics of bacterial urease systems reveals architectural conservation, lineage-specific specialization, and candidate horizontal transfer.Molecular genetics and genomics : MGG · 2026Article
- ANKRD1 expression and functional mechanism in stomach adenocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Enhancing 3-O-methylfunicone production by endophytic Talaromyces pinophilus J6 through culture optimization and its anti-Helicobacter pylori activity.Archives of microbiology · 2026Article
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- Urease inhibitors: current advances, therapeutic potentials, and clinical challenges.Future medicinal chemistry · 2026Review
- Reduced MGE burden, virulence optimization, and acid stress tolerance shape the clonal succession of MRSA ST59.Science advances · 2026Article
- Structural landscape of bacterial urease: implications for catalyst and adaptation.Archives of microbiology · 2026Review
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- Pathogenicity and virulence ofVirulence · 2025Review
- Recent advances in the mechanisms of PD-L1 expression in gastric cancer: a review.Biological research · 2025Review
- Menadione reduces the expression of virulence- and colonization-associated genes inMicrobiology (Reading, England) · 2025Article
- Helicobacter pylori and gastric cancer: mechanisms and new perspectives.Journal of hematology & oncology · 2025Review
- Research progress on the impact and mechanisms of helicobacter pylori infection on the efficacy of immunotherapy for gastric cancer.Frontiers in oncology · 2025Review
- Beyond the stomach: the association betweenFrontiers in cellular and infection microbiology · 2025Review
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- Developing a potent vaccine againstExpert reviews in molecular medicine · 2024Review
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- In vitro anti-Helicobacter pylori activity and antivirulence activity of cetylpyridinium chloride.PloS one · 2024Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori infection causes chronic active gastritis that after many years of infection can develop into peptic ulceration or gastric adenocarcinoma. The bacterium is highly adapted to surviving in the gastric environment and a key adaptation is the virulence factor urease. Although widely postulated, the requirement of urease expression for persistent infection has not been elucidated experimentally as conventional urease knockout mutants are incapable of colonization. To overcome this constraint, conditional H. pylori urease mutants were constructed by adapting the tetracycline inducible expression system that enabled changing the urease phenotype of the bacteria during established infection. Through tight regulation we demonstrate that urease expression is not only required for establishing initial colonization but also for maintaining chronic infection. Furthermore, successful isolation of tet-escape mutants from a late infection time point revealed the strong selective pressure on this gastric pathogen to continuously express urease in order to maintain chronic infection. In addition to mutations in the conditional gene expression system, escape mutants were found to harbor changes in other genes including the alternative RNA polymerase sigma factor, fliA, highlighting the genetic plasticity of H. pylori to adapt to a changing niche. The tet-system described here opens up opportunities to studying genes involved in the chronic stage of H. pylori infection to gain insight into bacterial mechanisms promoting immune escape and life-long infection. Furthermore, this genetic tool also allows for a new avenue of inquiry into understanding the importance of various virulence determinants in a changing biological environment when the bacterium is put under duress.
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