ArticleDigestive diseases and sciences2024
Porphyromonas gingivalis Lipopolysaccharide Damages Mucosal Barrier to Promote Gastritis-Associated Carcinogenesis.
Article in Digestive diseases and sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Gut microbiome alterations during gastric cancer: evidence assessment of case-control studies.Frontiers in microbiology · 2024Pooled it
- The emerging role of non-Gastroenterology report · 2026Review
- Remodeling mechanisms and intervention strategies of the oral mucosal immune barrier.Frontiers in immunology · 2026Review
- Nonlinear Relationship Between Myeloperoxidase Levels andJournal of clinical medicine · 2025Article
- Gastric cancer diagnosis and prevention: Detecting precancerous at community level.World journal of gastrointestinal oncology · 2025Article
- The dynamic oral-gastric microbial axis connects oral and gastric health: current evidence and disputes.NPJ biofilms and microbiomes · 2025Review
- The oral-gut axis in chronic atrophic gastritis: current perspectives and integrated strategies.Frontiers in immunology · 2025Review
- Inflammatory factors collaboratively linkFrontiers in immunology · 2025Review
- Microbial oncogenesis within the gastric niche: how the gastric microbiota influencesFrontiers in microbiology · 2025Review
- Article
- Probability Regarding the Tumor-Promoter Role of Porphyromonas gingivalis for the Gastric Carcinogenesis.Digestive diseases and sciences · 2024Article
- Reply to "The Probability Regarding the Tumor-promoter Role of Porphyromonas gingivalis for the Gastric Carcinogenesis".Digestive diseases and sciences · 2024Article
- Differential gene expression profile inJournal of oral biology and craniofacial researchArticle
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
backgroundRecent epidemiological studies suggested correlation between gastric cancer (GC) and periodontal disease.
aimsWe aim to clarify involvement of lipopolysaccharide of Porphyromonas gingivalis (Pg.), one of the red complex periodontal pathogens, in the GC development.
methodsTo evaluate barrier function of background mucosa against the stimulations, we applied biopsy samples from 76 patients with GC using a Ussing chamber system (UCs). K19-Wnt1/C2mE transgenic (Gan) mice and human GC cell-lines ± THP1-derived macrophage was applied to investigate the role of Pg. lipopolysaccharide in inflammation-associated carcinogenesis.
resultsIn the UCs, Pg. lipopolysaccharide reduced the impedance of metaplastic and inflamed mucosa with increases in mRNA expression of toll-like receptor (TLR) 2, tumor necrosis factor (TNF) α, and apoptotic markers. In vitro, Pg. lipopolysaccharide promoted reactive oxidative stress (ROS)-related apoptosis as well as activated TLR2-β-catenin-signaling on MKN7, and it increased the TNFα production on macrophages, respectively. TNFα alone activated TLR2-β-catenin-signaling in MKN7, while it further increased ROS and TNFα in macrophages. Under coculture with macrophages isolated after stimulation with Pg. lipopolysaccharide, β-catenin-signaling in MKN7 was activated with an increase in supernatant TNFα concentration, both of which were decreased by adding a TNFα neutralization antibody into the supernatant. In Gan mice with 15-week oral administration of Pg. lipopolysaccharide, tumor enlargement with β-catenin-signaling activation were observed with an increase in TNFα with macrophage infiltration.
conclusionsLocal exposure of Pg. lipopolysaccharide may increase ROS on premalignant gastric mucosa to induce apoptosis-associated barrier dysfunction and to secrete TNFα from activated macrophages, and both stimulation of Pg. lipopolysaccharide and TNFα might activate TLR2-β-catenin-signaling in GC.
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