Evidence map›Paper›PMID 40301773›Full record

Observational studyBMC gastroenterology2025

Dysregulated gastric microbial communities and functional shifts in chronic atrophic versus non-atrophic gastritis: a Helicobacter pylori-Negative observational study.

Hong Yao, Tingting Liu, Yiming Chen, Ling She, Tingfeng Wu, Dongsong Liu, Yuhong Deng, Yubin Han, Kai Chen, Jianmin Deng and 3 more

Abstract readObservational Study
In one paragraph

Observational study in BMC gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Review
  2. IntratumoralAnimals : an open access journal from MDPI · 2026
    Article
  3. Article
  4. Article
  5. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Hong YaoGuangzhou University of Chinese Medicine, Guangzhou, 510405, Guangdong, People's Republic of China.
Tingting LiuThe Eighth Clinical Medical College of Guangzhou University of Chinese Medicine, Foshan, 528000, Guangdong, People's Republic of China.
Yiming ChenThe Eighth Clinical Medical College of Guangzhou University of Chinese Medicine, Foshan, 528000, Guangdong, People's Republic of China.
Ling SheThe Eighth Clinical Medical College of Guangzhou University of Chinese Medicine, Foshan, 528000, Guangdong, People's Republic of China.
Tingfeng WuThe Eighth Clinical Medical College of Guangzhou University of Chinese Medicine, Foshan, 528000, Guangdong, People's Republic of China.
Dongsong LiuThe Eighth Clinical Medical College of Guangzhou University of Chinese Medicine, Foshan, 528000, Guangdong, People's Republic of China.
Yuhong DengThe Eighth Clinical Medical College of Guangzhou University of Chinese Medicine, Foshan, 528000, Guangdong, People's Republic of China.
Yubin HanThe Eighth Clinical Medical College of Guangzhou University of Chinese Medicine, Foshan, 528000, Guangdong, People's Republic of China.
Kai ChenThe Eighth Clinical Medical College of Guangzhou University of Chinese Medicine, Foshan, 528000, Guangdong, People's Republic of China.
Jianmin DengThe Eighth Clinical Medical College of Guangzhou University of Chinese Medicine, Foshan, 528000, Guangdong, People's Republic of China.
Jue ZhangThe Eighth Clinical Medical College of Guangzhou University of Chinese Medicine, Foshan, 528000, Guangdong, People's Republic of China.
Jinfeng ChenThe Eighth Clinical Medical College of Guangzhou University of Chinese Medicine, Foshan, 528000, Guangdong, People's Republic of China. fscjf@sina.com.
Fengbin LiuLingnan Institute of Spleen and Stomach Diseases, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510405, Guangdong, People's Republic of China. liufengbin163@163.com.

Funding

Foshan Hospital Of Traditional Chinese Medicine 20233002Foshan Science and Technology Bureau 2220001005125
6 · The paper itself

Abstract

backgroundHelicobacter pylori (H. pylori) infection was identified as a substantial risk factor for gastric cancer development, but the eradication of H. pylori did not necessarily lead to a reduction in the incidence of gastric cancer. Non-Helicobacter pylori (non-H. pylori) bacteria in the stomach are involved in the transformation of gastritis carcinoma. The aim of this study was to characterize the microbiome composition of the gastric mucosa and its functions in non-H. pylori (H. pylori-negative) patients with chronic atrophic gastritis (CAG) and chronic non-atrophic gastritis (CNAG).

methodsFourteen CNAG samples and twenty-three CAG samples were collected. The composition of the gastric microbiome was analyzed using 16 S rDNA gene sequencing. The bioinformatic analysis was performed using alpha and beta diversity analyses, PICRUSt2, and linear discriminant analysis effect size (LEfSe).

resultsThe two groups shared the same most abundant bacterial phyla (Pseudomonadota, Bacillota, Actinomycetota, and Bacteroidota). The top 5 most abundant bacterial genera in the CAG group were Sphingomonas, Ralstonia, Brevundimonas, Methyloversatilis, and Pseudomonas. In the CNAG group, the top genera were Brevundimonas, Ralstonia, Sphingomonas, Methyloversatilis, and Acinetobacter. Differential analysis revealed distinct genera between groups: the CAG group showed enrichment in Sphingomonas, Ralstonia, Bradyrhizobium, Roseateles, and Acidithiobacillus, while the CNAG group was enriched in Brevundimonas, Rhodococcus, Hydrogenophaga, Bacteroides, and Leifsonia (p < 0.05). Sphingomonas exhibited a positive correlation with Acidithiobacillus but negative correlations with Brevundimonas, Hydrogenophaga, and Leifsonia. Pathways related to xenobiotic biodegradation, metabolism, signal transduction, cofactor/vitamin metabolism, cancer, infectious diseases, and digestive system were enriched in the CAG group. In contrast, the CNAG group showed enrichment in amino acid metabolism, translation, replication/repair, and terpenoid/polyketide metabolism.

conclusionGastric mucosal microbiota dysbiosis and functional shifts are significantly associated with chronic atrophic gastritis. Taxa such as Sphingomonas and Ralstonia, enriched in CAG patients, may indicate microbial signatures associated with early atrophic transition and provide candidates for further mechanistic validation.

Indexed as

Gastric MucosaGastritisGastritis, AtrophicGastrointestinal MicrobiomeAdultAgedChronic DiseaseFemaleHelicobacter pyloriHumansMaleMiddle Aged16S rDNA sequencingChronic atrophic gastritisGastric microbiota dysbiosisHelicobacter pylori-negative gastritisMetabolic prediction

Identifiers

PMID40301773
PMCPMC12039101

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.