ReviewBioMed research international2015
Interplay of the Gastric Pathogen Helicobacter pylori with Toll-Like Receptors.
Review in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 82 citations in OpenAlex.
- Cardiovascular and Neurological Diseases and Association with Helicobacter Pylori Infection-An Overview.Diagnostics (Basel, Switzerland) · 2024Review
- Review
- Article
- Trimer stability of Helicobacter pylori HtrA is regulated by a natural mutation in the protease domain.Medical microbiology and immunology · 2023Article
- Immune Biology and Persistence of Helicobacter pylori in Gastric Diseases.Current topics in microbiology and immunology · 2023Article
- Clinical Pathogenesis, Molecular Mechanisms of Gastric Cancer Development.Current topics in microbiology and immunology · 2023Article
- Linking dysbiosis to precancerous stomach through inflammation: Deeper than and beyond imaging.Frontiers in immunology · 2023Review
- Helicobacter pylori-Induced Host Cell DNA Damage and Genetics of Gastric Cancer Development.Current topics in microbiology and immunology · 2023Article
- Gastric Epithelial Barrier Disruption, Inflammation and Oncogenic Signal Transduction by Helicobacter pylori.Current topics in microbiology and immunology · 2023Review
- Pathogenomics of Helicobacter pylori.Current topics in microbiology and immunology · 2023Review
- Biomarker Characterization and Prediction of Virulence and Antibiotic Resistance fromBiomolecules · 2022Review
- Article
- Unique TLR9 Activation by Helicobacter pylori Depends on the cag T4SS, But Not on VirD2 Relaxases or VirD4 Coupling Proteins.Current microbiology · 2022Article
- NOD1 rs2075820 (p.E266K) polymorphism is associated with gastric cancer among individuals infected with cagPAI-positive H. pylori.Biological research · 2021Article
- An Overview of Helicobacter pylori Infection.Methods in molecular biology (Clifton, N.J.) · 2021Review
- Infection and atherosclerosis: TLR-dependent pathways.Cellular and molecular life sciences : CMLS · 2020Review
- Article
- T Cell Cytokines Impact Epithelial Cell Responses duringJournal of immunology (Baltimore, Md. : 1950) · 2020Review
- Evaluation of toll-like receptors as prognostic biomarkers in gastric cancer: high tissue TLR5 predicts a better outcome.Scientific reports · 2019Article
- The Role of Toll-Like Receptors in Oncotherapy.Oncology research · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Toll-like receptors (TLRs) are crucial for pathogen recognition and downstream signaling to induce effective immunity. The gastric pathogen Helicobacter pylori is a paradigm of persistent bacterial infections and chronic inflammation in humans. The chronicity of inflammation during H. pylori infection is related to the manipulation of regulatory cytokines. In general, the early detection of H. pylori by TLRs and other pattern recognition receptors (PRRs) is believed to induce a regulatory cytokine or chemokine profile that eventually blocks the resolution of inflammation. H. pylori factors such as LPS, HSP-60, NapA, DNA, and RNA are reported in various studies to be recognized by specific TLRs. However, H. pylori flagellin evades the recognition of TLR5 by possessing a conserved N-terminal motif. Activation of TLRs and resulting signal transduction events lead to the production of pro- and anti-inflammatory mediators through activation of NF-κB, MAP kinases, and IRF signaling pathways. The genetic polymorphisms of these important PRRs are also implicated in the varied outcome and disease progression. Hence, the interplay of TLRs and bacterial factors highlight the complexity of innate immune recognition and immune evasion as well as regulated processes in the progression of associated pathologies. Here we will review this important aspect of H. pylori infection.
Indexed as
Identifiers
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.