ArticleJournal of translational medicine2025
Changes of gastric microflora and metabolites in patients with chronic atrophic gastritis.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Review
- Gastric Microbiota Dysbiosis and Microbiome-Based Interventions in Chronic Atrophic Gastritis.Nutrients · 2026Review
- Herbal Medicine and the Gastrointestinal Microbiota in Gastric Precancerous Lesions and Gastric Cancer: Mechanistic Evidence and Translational Challenges.Cancer management and research · 2026Review
- The oral-gut axis in chronic atrophic gastritis: current perspectives and integrated strategies.Frontiers in immunology · 2025Review
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9 authors.
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Abstract
backgroundChronic atrophic gastritis (CAG) is related to the body's microbial and metabolic systems. Combined studies of microbiome and metabolomics can clarify the mechanisms of disease occurrence and progression. We used 16S rRNA sequencing, metagenomics sequencing and metabolomics sequencing to depict the landscapes of bacterium and metabolites, construct correlation networks of different bacterium and metabolites describe potential pathogenic mechanisms of chronic atrophic gastritis.
methodsThe gastric juices of 30 non-atrophic gastritis (NAG) patients and 30 CAG patients were collected. Gastric microflora was analyzed by 16S rRNA sequencing and metagenomics sequencing. Gastric metabolites were analyzed by LC-MS analysis. Different bioinformatics methods were used to analyze the data of microbiome and metabolome, and to analyze the relationship between them.
resultsIn atrophic gastritis, bacteria diversity decreased. The genera with a mean decrease in Gini greater than 1.5 included peptostreptococcus, fusobacterium, prevotella, sphingomonas and bacteroides. KEGG pathway included renal cell carcinoma, proximal tubule bicarbonate reclamation, citrate cycle and aldosterone synthesis and secretion with significant enrichment of differential metabolites. Peptostreptococcus, fusobacterium, prevotella and sphingomonas were in pivot positions of the correlation network of differential metabolites and differential bacterium. Viral carcinogenesis, glycine serine and threonine metabolism, RNA polymerase, galactose metabolism and retinol metabolism were enriched in chronic atrophic gastritis based on the metagenomic sequencing data.
conclusionPeptostreptococcus, fusobacterium, prevotella, sphingomonas and bacteroides were the essential features that distinguish atrophic gastritis from non-atrophic gastritis, and caused disease by altering various metabolic pathways. Viral carcinogenesis, glycine serine and threonine metabolism, RNA polymerase, galactose metabolism and retinol metabolism may be related to the occurrence and progression of CAG.
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