ArticleNature communications2023
Helicobacter pylori initiates successful gastric colonization by utilizing L-lactate to promote complement resistance.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Characterization ofJournal of bacteriology · 2026Article
- Pathogenicity and virulence ofVirulence · 2025Review
- Review
- Specificities of chemosensory receptors in the human gut microbiota.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Lactate promotes invasive Klebsiella pneumoniae liver abscess syndrome by increasing capsular polysaccharide biosynthesis via the PTS-CRP axis.Nature communications · 2025Article
- The dynamic oral-gastric microbial axis connects oral and gastric health: current evidence and disputes.NPJ biofilms and microbiomes · 2025Review
- Review
- Metabolic reprogramming inFrontiers in cellular and infection microbiology · 2025Review
- Biochemical characterization of paralyzed flagellum proteins A (PflA) and B (PflB) from Helicobacter pylori flagellar motor.Bioscience reports · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The complement system has long been appreciated for its role in bloodborne infections, but its activities in other places, including the gastrointestinal tract, remain elusive. Here, we report that complement restricts gastric infection by the pathogen Helicobacter pylori. This bacterium colonized complement-deficient mice to higher levels than wild-type counterparts, particularly in the gastric corpus region. H. pylori uses uptake of the host molecule L-lactate to create a complement-resistant state that relies on blocking the deposition of the active complement C4b component on H. pylori's surface. H. pylori mutants unable to achieve this complement-resistant state have a significant mouse colonization defect that is largely corrected by mutational removal of complement. This work highlights a previously unknown role for complement in the stomach, and has revealed an unrecognized mechanism for microbial-derived complement resistance.
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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.