Evidence map›Paper›PMID 41816355›Full record

ArticleFrontiers in cellular and infection microbiology2026

Periodontitis promotes intestinal inflammation through gut microbiota-mediated suppression of GPR109A.

Xinyue Wang, Zhonghan Xu, Yujie Yao, Hui Jia, Meng Du, Shuangzheng Wang, Fuhua Yan, Lili Li

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in cellular and infection microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–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

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. 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

8 authors.

Xinyue Wang *Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Zhonghan Xu *Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Yujie YaoNanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Hui JiaNanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Meng DuNanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Shuangzheng WangSchool of Medicine, Nankai University, Tianjin, China.
Fuhua YanNanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Lili LiNanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: To determine whether periodontitis promotes intestinal inflammation through gut microbiota-mediated suppression of the GPR109A receptor. Methods: Periodontitis was induced by ligatures in C57BL/6J mice under normal chow or high-fructose diet. Periodontal destruction was evaluated by micro-computed tomography and hematoxylin and eosin staining. Colonic GPR109A expression, intestinal epithelial integrity, as well as intestinal and systemic inflammation were assessed by histology and immunostaining, quantitative polymerase chain reaction (qPCR) and enzyme-linked immunosorbent assay (ELISA). Short-chain fatty acids (SCFAs) in colonic contents were quantified by GC-MS/MS. Further, the probiotic strain CBM588 was supplemented to two groups of mice (CP/LP group) to alleviate periodontitis-induced inflammation, and GPR109A expression was detected. To investigate the role of periodontitis-associated gut microbiota, fecal microbiota from control (GF-CON) and ligatured (GF-LIG) mice were transplanted into germ-free recipients, and colonic GPR109A levels and inflammatory responses were analyzed. Finally, GPR109A function was modulated by administration of GSK256073 and mepenzolate bromide in ligatured mice, and corresponding changes in tight junctional integrity as well as intestinal and systemic inflammation were evaluated. Results: Periodontitis significantly downregulated the expression of colonic GPR109A and disrupted the localization of ZO-1 and Occludin. Probiotic supplementation restored GPR109A expression and rescued ZO-1 distribution. Fecal microbiota transplantation from periodontitis donors led to GPR109A suppression, tight junction impairment, and inflammatory upregulation in germ-free mice, confirming a microbiota-dependent mechanism. Activation of GPR109A reversed barrier disruption and reduced pro-inflammatory cytokine levels. Conclusion: Periodontitis promotes colonic inflammation by gut microbiota-induced suppression of GPR109A receptor, leading to the destruction of the epithelial barrier. Activation of GPR109A restores barrier function and attenuates inflammation.

Indexed as

Gastrointestinal MicrobiomeInflammationPeriodontitisReceptors, G-Protein-CoupledReceptors, NicotinicAnimalsColonDisease Models, AnimalFatty Acids, VolatileIntestinal Barrier FunctionIntestinal MucosaMaleMiceMice, Inbred C57BLOccludinZonula Occludens-1 ProteinFatty Acids, VolatileHcar2 protein, mouseOccludinReceptors, G-Protein-CoupledReceptors, NicotinicTjp1 protein, mouseZonula Occludens-1 ProteinGPR109Agut microbiotaintestinal barrierintestinal inflammationoral-gut axisperiodontitis

Identifiers

PMID41816355
PMCPMC12971913

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.