Trial reportPloS one2013
Helicobacter pylori cholesteryl α-glucosides contribute to its pathogenicity and immune response by natural killer T cells.
Trial report in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 63 citations in OpenAlex.
- Bacterial lipid structural diversity mediates commensalism and pathogenesis.Nature reviews. Microbiology · 2026Review
- Intestinal mucosal immunity and type 1 diabetes: Non-negligible communication between gut and pancreas.Diabetes, obesity & metabolism · 2025Review
- Role of CD1d and iNKT cells in regulating intestinal inflammation.Frontiers in immunology · 2023Review
- Review
- The Efficacy of Cancer Immunotherapies Is Compromised byFrontiers in immunology · 2022Review
- LaryngealMicroorganisms · 2021Article
- Cholestenone functions as an antibiotic againstProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Helicobacter pylori metabolites exacerbate gastritis through C-type lectin receptors.The Journal of experimental medicine · 2021Article
- NKT Cells Contribute to the Control of Microbial Infections.Frontiers in cellular and infection microbiology · 2021Review
- Review
- Structure, metabolism and biological functions of steryl glycosides in mammals.The Biochemical journal · 2020Review
- The dialogue between unconventional T cells and the microbiota.Mucosal immunology · 2020Review
- Role of Helicobacter pylori infection in the manifestation of old age-related diseases.Molecular genetics & genomic medicine · 2020Review
- Immune Response inGastroenterology research and practice · 2020Review
- Structural basis of NKT cell inhibition using the T-cell receptor-blocking anti-CD1d antibody 1B1.The Journal of biological chemistry · 2019Article
- Helicobacter pylori Deregulates T and B Cell Signaling to Trigger Immune Evasion.Current topics in microbiology and immunology · 2019Review
- The interaction between invariant Natural Killer T cells and the mucosal microbiota.Immunology · 2018Review
- Molecular recognition of microbial lipid-based antigens by T cells.Cellular and molecular life sciences : CMLS · 2018Review
- The Janus Face of NKT Cell Function in Autoimmunity and Infectious Diseases.International journal of molecular sciences · 2018Review
- Cloning of Helicobacter suis cholesterol α-glucosyltransferase and production of an antibody capable of detecting it in formalin-fixed, paraffin-embedded gastric tissue sections.Histochemistry and cell biology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 4 institutions in 3 countries.
Funding
Abstract
Approximately 10-15% of individuals infected with Helicobacter pylori will develop ulcer disease (gastric or duodenal ulcer), while most people infected with H. pylori will be asymptomatic. The majority of infected individuals remain asymptomatic partly due to the inhibition of synthesis of cholesteryl α-glucosides in H. pylori cell wall by α1,4-GlcNAc-capped mucin O-glycans, which are expressed in the deeper portion of gastric mucosa. However, it has not been determined how cholesteryl α-glucosyltransferase (αCgT), which forms cholesteryl α-glucosides, functions in the pathogenesis of H. pylori infection. Here, we show that the activity of αCgT from H. pylori clinical isolates is highly correlated with the degree of gastric atrophy. We investigated the role of cholesteryl α-glucosides in various aspects of the immune response. Phagocytosis and activation of dendritic cells were observed at similar degrees in the presence of wild-type H. pylori or variants harboring mutant forms of αCgT showing a range of enzymatic activity. However, cholesteryl α-glucosides were recognized by invariant natural killer T (iNKT) cells, eliciting an immune response in vitro and in vivo. Following inoculation of H. pylori harboring highly active αCgT into iNKT cell-deficient (Jα18(-/-)) or wild-type mice, bacterial recovery significantly increased in Jα18(-/-) compared to wild-type mice. Moreover, cytokine production characteristic of Th1 and Th2 cells dramatically decreased in Jα18(-/-) compared to wild-type mice. These findings demonstrate that cholesteryl α-glucosides play critical roles in H. pylori-mediated gastric inflammation and precancerous atrophic gastritis.
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What OpenQuestion holds
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.