ArticleInfection and immunity2007
Helicobacter pylori chemotaxis modulates inflammation and bacterium-gastric epithelium interactions in infected mice.
Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
71 citing papers in PubMed, 119 citations in OpenAlex.
- TheJournal of bacteriology · 2026Article
- Managing dangerous liaisons: lessons fromJournal of bacteriology · 2026Review
- Co-expression network analysis and systems-level mapping of hub-bottleneck regulators deciphers the virulence architecture of Helicobacter pylori.Archives of microbiology · 2026Article
- Pathogenicity and virulence ofVirulence · 2025Review
- Swarm Autonomy: From Agent Functionalization to Machine Intelligence.Advanced materials (Deerfield Beach, Fla.) · 2025Review
- Strategies ofFrontiers in cellular and infection microbiology · 2024Review
- Acquisition of Type I methyltransferase via horizontal gene transfer increases the drug resistance ofMicrobial genomics · 2023Article
- Genetic determinants of Biofilm formation of Helicobacter pylori using whole-genome sequencing.BMC microbiology · 2023Article
- Bacterial chemotaxis in human diseases.Trends in microbiology · 2023Review
- Helicobacter pylori Chronic-Stage Inflammation Undergoes Fluctuations That Are Altered inInfection and immunity · 2023Article
- CryoEM structure of a post-assembly MS-ring reveals plasticity in stoichiometry and conformation.PloS one · 2023Article
- Prediction of gastric cancer risk by a polygenic risk score ofWorld journal of gastrointestinal oncology · 2022Article
- Multiple functions of flagellar motility and chemotaxis in bacterial physiology.FEMS microbiology reviews · 2021Review
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- Small RNA mediated gradual control of lipopolysaccharide biosynthesis affects antibiotic resistance in Helicobacter pylori.Nature communications · 2021Article
- Helicobacter pylori Uses the TlpB Receptor To Sense Sites of Gastric Injury.Infection and immunity · 2019Article
- Article
- Genome-wide mutation analysis ofGut pathogens · 2019Article
- What bacteria want.Environmental microbiology · 2018Review
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The ulcer-causing pathogen Helicobacter pylori uses directed motility, or chemotaxis, to both colonize the stomach and promote disease development. Previous work showed that mutants lacking the TlpB chemoreceptor, one of the receptors predicted to drive chemotaxis, led to less inflammation in the gerbil stomach than did the wild type. Here we expanded these findings and examined the effects on inflammation of completely nonchemotactic mutants and mutants lacking each chemoreceptor. Of note, all mutants colonized mice to the same levels as did wild-type H. pylori. Infection by completely nonchemotactic mutants (cheW or cheY) resulted in significantly less inflammation after both 3 and 6 months of infection. Mutants lacking either the TlpA or TlpB H. pylori chemotaxis receptors also had alterations in inflammation severity, while mutants lacking either of the other two chemoreceptors (TlpC and HylB) behaved like the wild type. Fully nonchemotactic and chemoreceptor mutants adhered to cultured gastric epithelial cells and caused cellular release of the chemokine interleukin-8 in vitro similar to the release caused by the wild type. The situation appeared to be different in the stomach. Using silver-stained histological sections, we found that nonchemotactic cheY or cheW mutants were less likely than the wild type to be intimately associated with the cells of the gastric mucosa, although there was not a strict correlation between intimate association and inflammation. Because others have shown that in vivo adherence promotes inflammation, we propose a model in which H. pylori uses chemotaxis to guide it to a productive interaction with the stomach epithelium.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.