ReviewGut microbes2015
Helicobacter pylori activates the TLR2/NLRP3/caspase-1/IL-18 axis to induce regulatory T-cells, establish persistent infection and promote tolerance to allergens.
Review in Gut microbes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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.
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
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- Association Between Gut Microbiota and Autoimmune Thyroid Disease: A Systematic Review and Meta-Analysis.Frontiers in endocrinology · 2021Pooled it
- Beyond Infection: Mitochondrial Reprogramming and Immunometabolic Adaptation inDiseases (Basel, Switzerland) · 2026Article
- [Molecular mechanisms of chronic gastric mucosal inflammation induced byZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026Review
- Helicobacter pylori-linked gene CFAP73 rewires epithelial programs and shapes the gastric cancer microenvironment.Discover oncology · 2026Article
- Mitochondrial Stress inAntioxidants (Basel, Switzerland) · 2026Review
- CirculatingFrontiers in cellular and infection microbiology · 2026Article
- Immunoinformatics-Based Multi-Epitope Vaccine Targeting Helicobacter Pylori.Cancer reports (Hoboken, N.J.) · 2026Article
- Jatrorrhizine attenuates inflammatory response in Helicobacter pylori-induced gastritis by suppressing NLRP3 inflammasomes and NF-κB signaling pathway.Archives of microbiology · 2025Article
- Helicobacter pylori infection promotes M1 macrophage polarization and gastric inflammation by activation of NLRP3 inflammasome via TNF/TNFR1 axis.Cell communication and signaling : CCS · 2025Article
- Microbiota and gastric cancer: from molecular mechanisms to therapeutic strategies.Frontiers in cellular and infection microbiology · 2025Review
- The association between Helicobacter pylori infection and the risk for gout in hyperuricemia patients in China - A cross-sectional study.Gut pathogens · 2024Article
- CLEC4E upregulation in gastric cancer: A potential therapeutic target correlating with tumor-associated macrophages.Heliyon · 2024Article
- The 'speck'-tacular oversight of the NLRP3-pyroptosis pathway on gastrointestinal inflammatory diseases and tumorigenesis.Journal of biomedical science · 2023Review
- NOD-like Receptor Signaling Pathway in Gastrointestinal Inflammatory Diseases and Cancers.International journal of molecular sciences · 2023Review
- Gut dysbiosis contributes to chlamydial induction of hydrosalpinx in the upper genital tract.Frontiers in microbiology · 2023Article
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- Characterization of Pathogenic CD8Infection and immunity · 2022Article
- The Efficacy of Cancer Immunotherapies Is Compromised byFrontiers in immunology · 2022Review
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
No grant is acknowledged in the PubMed record.
Abstract
The Gram-negative bacterium Helicobacter pylori is both a normal constituent of the human gastric microbiota as well as a pathogen tightly associated with severe gastric disorders. The ability of H. pylori to activate the inflammasome and caspase-1 in antigen-presenting and other cells, and the resulting processing and release of caspase-1-dependent cytokines, impacts both the immunomodulatory and pathogenic activities of H. pylori. This article summarizes recent insights by us and others on the bacterial and host prerequisites of inflammasome activation. H. pylori predominantly activates the NLRP3 inflammasome through a process that requires TLR2-dependent licensing. We identified the urease enzyme, a colonization determinant known to be required for acid adaptation, as critically required for activation of the TLR2/NLRP3/caspase-1 axis. The phenotypes of urease mutants, as well as mouse strains defective for TLR2 or NLRP3, are discussed with respect to their ability to support persistent colonization, immune tolerance and immunity to H. pylori.
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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.