ReviewWorld journal of gastroenterology2014
Structural modifications of Helicobacter pylori lipopolysaccharide: an idea for how to live in peace.
Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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
33 citing papers in PubMed, 52 citations in OpenAlex.
- Interplay between pathogen-mediated immune evasion and innate immune negative regulation in gastrointestinal tumors.Frontiers in immunology · 2026Review
- New concepts of chitosan-based mucosal formulations for supporting control of the gastric pathogenFrontiers in microbiology · 2026Review
- Endotoxin's Impact on Organism: From Immune Activation to Tolerance and Beyond.Journal of clinical medicine · 2025Review
- Diversity, Complexity, and Specificity of Bacterial Lipopolysaccharide (LPS) Structures Impacting Their Detection and Quantification.International journal of molecular sciences · 2024Article
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- Article
- The multifaceted role of c-di-AMP signaling in the regulation ofFrontiers in cellular and infection microbiology · 2024Article
- Outer Membrane Vesicles (OMVs) as Biomedical Tools and Their Relevance as Immune-Modulating Agents againstInternational journal of molecular sciences · 2023Review
- The Roles of Innate Lymphoid Cells in the Gastric Mucosal Immunology and Oncogenesis of Gastric Cancer.International journal of molecular sciences · 2023Review
- The Association Between Oral Helicobacter pylori and Gastric Complications: A Comprehensive Review.Cureus · 2022Review
- Sweet impersonators: Molecular mimicry of host glycans by bacteria.Glycobiology · 2022Review
- Helicobacter pylori binds human Annexins via Lipopolysaccharide to interfere with Toll-like Receptor 4 signaling.PLoS pathogens · 2022Article
- TLR2 and TLR4 Signaling Pathways and Gastric Cancer: Insights from Transcriptomics and Sample ValidationIranian biomedical journal · 2022Article
- Small RNA mediated gradual control of lipopolysaccharide biosynthesis affects antibiotic resistance in Helicobacter pylori.Nature communications · 2021Article
- Helicobacter pylori-derived outer membrane vesicles stimulate interleukin 8 secretion through nuclear factor kappa B activation.The Korean journal of internal medicine · 2021Article
- Infections as Novel Risk Factors of Atherosclerotic Cardiovascular Diseases: Pathophysiological Links and Therapeutic Implications.Journal of clinical medicine · 2021Review
- Interference of LPSCells · 2021Article
- Acceptive Immunity: The Role of Fucosylated Glycans in Human Host-Microbiome Interactions.International journal of molecular sciences · 2021Review
- Use of Fourier-Transform Infrared Spectroscopy (FT-IR) for Monitoring ExperimentalInternational journal of molecular sciences · 2020Article
- Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this review, we discuss the findings and concepts underlying the "persistence mechanisms" of Helicobacter pylori (H. pylori), a spiral-shaped, Gram-negative rod bacterium that was discovered as a gastric pathogen by Marshall and Warren in 1984. H. pylori colonizes the gastric mucosa of nearly half of the human population. Infections appear in early childhood and, if not treated, persist for life. The presence or absence of symptoms and their severity depend on multiple bacterial components, host susceptibility and environmental factors, which allow H. pylori to switch between pathogenicity and commensalism. Many studies have shown that H. pylori components may facilitate the colonization process and the immune response of the host during the course of H. pylori infection. These H. pylori-driven interactions might result from positive or negative modulation. Among the negative immunomodulators, a prominent position is occupied by a vacuolating toxin A (VacA) and cytotoxin-associated gene A (CagA) protein. However, in light of the recent studies that are presented in this review, it is necessary to enrich this panel with H. pylori lipopolysaccharide (LPS). Together with CagA and VacA, LPS suppresses the elimination of H. pylori bacteria from the gastric mucosa by interfering with the activity of innate and adaptive immune cells, diminishing the inflammatory response, and affecting the adaptive T lymphocyte response, thus facilitating the development of chronic infections. The complex strategy of H. pylori bacteria for survival in the gastric mucosa of the host involves both structural modifications of LPS lipid A to diminish its endotoxic properties and the expression and variation of Lewis determinants, arranged in O-specific chains of H. pylori LPS. By mimicking host components, this phenomenon leaves these bacteria "invisible" to immune cells. Together, these mechanisms allow H. pylori to survive and live for many years within their hosts.
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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.