ReviewInflammopharmacology2017
Role of LPS-elicited signaling in triggering gastric mucosal inflammatory responses to H. pylori: modulatory effect of ghrelin.
Review in Inflammopharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 54 citations in OpenAlex.
- Trial
- Dendritic Cells Derived MMP9 Fuels Sepsis-Induced Cardiac Dysfunction Through JNK/AP1 Driven Pro-Inflammatory Cytokine and Nitric Oxide Storm.Inflammation · 2026Article
- Acupuncture-associated gastric mucosal repair and the EGF-EGFR-related signaling network: evidence, limitations, and prospects.Frontiers in immunology · 2026Review
- The hemopexin domain of matrix metalloproteinase-9 attenuates lipopolysaccharide-induced interleukin-6 secretion in liver.Scientific reports · 2025Article
- Metformin Inhibits the Development of Helicobacter pylori-Associated Gastritis by Regulating the ERK-MMP10-IL-1β Axis.Cell biochemistry and biophysics · 2025Article
- Fine Particulate Matter (PM2.5) Disrupts Intestinal Barrier Function by Inducing Oxidative Stress and PI3K/AKT-Mediated Inflammation in Caco-2 Cells.International journal of molecular sciences · 2025Article
- Functional potential and applications of Ureibacillus massiliensis based on whole-genome sequencing analysis.BMC microbiology · 2025Article
- Ghrelin in Depression: A Promising Therapeutic Target.Molecular neurobiology · 2025Review
- Obesity and the gut microbiota: implications of neuroendocrine and immune signaling.The FEBS journal · 2025Review
- Beyond weight loss: exploring the neurological ramifications of altered gut microbiota post-bariatric surgery.Journal of translational medicine · 2025Review
- Advances in Helicobacter pylori lipopolysaccharide structure and function.FEMS microbiology reviews · 2025Review
- A comprehensive overview of the effects of probiotics, prebiotics and synbiotics on the gut-brain axis.Frontiers in microbiology · 2025Review
- Toll-like Receptor 4 Signaling Mediates Gastritis and Gastric Cancer.Current molecular medicine · 2025Review
- Influence of Bariatric Surgery on Gut Microbiota Composition and Its Implication on Brain and Peripheral Targets.Nutrients · 2024Review
- Herbal melanin modulates PGE2 and IL-6 gastroprotective markers through COX-2 and TLR4 signaling in the gastric cancer cell line AGS.BMC complementary medicine and therapies · 2023Article
- Estrogen receptor subtype mediated anti-inflammation and vasorelaxationFrontiers in endocrinology · 2023Article
- Impact of the microenvironment on the pathogenesis of mucosa-associated lymphoid tissue lymphomas.World journal of gastrointestinal oncology · 2022Review
- Article
- Galectin-1 Inhibited LPS-Induced Autophagy and Apoptosis of Human Periodontal Ligament Stem Cells.Inflammation · 2021Article
- Gut peptides and the microbiome: focus on ghrelin.Current opinion in endocrinology, diabetes, and obesity · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection with Helicobacter pylori is a primary culprit in the etiology of gastric disease, and its cell-wall lipopolysaccharide (LPS) is recognized as a potent endotoxin responsible for triggering a pattern of the mucosal inflammatory responses. The engagement by the LPS of gastric mucosal Toll-like receptor 4 (TLR4) leads to initiation of signal transduction events characterized by the activation of mitogen-activated protein kinase (MAPK) cascade, induction of phosphoinositide-specific phospholipase C (PLC)/protein kinase C (PKC)/phosphatidylinositol 3-kinase (PI3K) pathway, and up-regulation in Src/Akt. These signaling events in turn exert their influence over H. pylori-elicited excessive generation of NO and PGE2 caused by the disturbances in nitric oxide synthase and cyclooxygenase isozyme systems, increase in epidermal growth factor receptor transactivation, and the induction in matrix metalloproteinase-9 (MMP-9) release. Interestingly, the extent of gastric mucosal inflammatory response to H. pylori is influenced by a peptide hormone, ghrelin, the action of which relays on the growth hormone secretagogue receptor type 1a (GHS-R1a)-mediated mobilization of G-protein dependent transduction pathways. Yet, the signals triggered by TLR-4 activation as well as those arising through GHS-R1a stimulation converge at MAPK and PLC/PKC/PI3K pathways that form a key integration node for proinflammatory signals generated by H. pylori LPS as well as for those involved in modulation of inflammation by ghrelin. Hence, therapeutic targeting these signals' convergence and integration node could provide a novel and attractive opportunities for developing more effective treatments of H. pylori-related gastric disease.
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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.