Evidence map›Paper›PMID 42254009›Full record

ArticleFrontiers in immunology2026

Pasteurized

Si Chen, Chenyang Zhang, Xue Liu, Yiying Zhu, Chenguang Niu, Wanqi Lv

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Si ChenDepartment of Multidisciplinary Consultant Center, Shanghai Stomatological Hospital and School of Stomatology, Fudan University, Shanghai, China.
Chenyang ZhangShanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Fudan University, Shanghai, China.
Xue LiuDepartment of Multidisciplinary Consultant Center, Shanghai Stomatological Hospital and School of Stomatology, Fudan University, Shanghai, China.
Yiying ZhuShanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Fudan University, Shanghai, China.
Chenguang NiuDepartment of Endodontics, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, College of Stomatology, Shanghai Jiao Tong University, National Clinical Research Center for Oral Diseases, National Center for Stomatology, Shanghai Key Laboratory of Stomatology, Shanghai, China.
Wanqi LvDepartment of Multidisciplinary Consultant Center, Shanghai Stomatological Hospital and School of Stomatology, Fudan University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Obesity, a global epidemic, disrupts bone metabolism via gut microbiota dysbiosis, and probiotic/postbiotic supplementation emerges as a promising intervention. Akkermansia muciniphila (Akk), a next-generation probiotic, exerts metabolic benefits in obesity, yet its effects on bone homeostasis-especially in pasteurized form (pAkk)-and underlying mechanisms remain unclear. Methods: High-fat diet (HFD)-induced obese mice were used to establish bone loss models, with fecal microbiota transplantation to verify gut microbiota's role. Mice were gavaged with live Akk, pAkk, or control for 4 weeks. Bone microarchitecture was assessed via micro-computed tomography (μCT), and bone formation/resorption were detected by histomorphometry, ELISA, and TRAP staining. Flow cytometry, immunofluorescence, and qRT-PCR analyzed regulatory T (Treg) cell differentiation. RNA sequencing identified key genes, and Nr4a1 knockout mice validated the mechanism. Cell coculture confirmed pAkk-induced Tregs' inhibitory effect on osteoclastogenesis. Results: Obesity-related gut microbiota induced trabecular bone loss, with reduced intestinal Akk abundance. pAkk (but not live Akk) rescued HFD-induced bone loss, increased bone formation marker (P1NP), decreased resorption marker (β-CTX), and inhibited osteoclast differentiation. pAkk promoted CD4 Conclusion: Pasteurized Akkermansia muciniphila alleviates HFD-induced bone loss in obese mice by promoting intestinal and systemic Treg differentiation to inhibit osteoclastogenesis, dependent on the nuclear hormone receptor Nr4a1. Our findings identify pAkk as a promising postbiotic for obesity-related bone loss and uncover a novel Nr4a1/Treg axis linking gut microbiota to bone homeostasis.

Indexed as

Bone ResorptionNuclear Receptor Subfamily 4, Group A, Member 1ProbioticsT-Lymphocytes, RegulatoryAkkermansiaAnimalsCell DifferentiationDiet, High-FatDisease Models, AnimalGastrointestinal MicrobiomeMaleMiceMice, Inbred C57BLMice, KnockoutObesityOsteoclastsNr4a1 protein, mouseNuclear Receptor Subfamily 4, Group A, Member 1Akkermansia muciniphilabone metabolismgut microbiotaNr4a1obesityosteoclastogenesisTreg differentiation

Identifiers

PMID42254009
PMCPMC13236502

What OpenQuestion holds

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Registered trials

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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.