Evidence map›Paper›PMID 39374734›Full record

ArticleJournal of advanced research2025

Elevated muramyl dipeptide by sialic acid-facilitated postantibiotic pathobiont expansion contributes to gut dysbiosis-induced mastitis in mice.

Min Qiu, Cong Ye, Lijuan Bao, Keyi Wu, Yihong Zhao, Xiaotong Zhao, Ruibo Tang, Ruping Shang, Shan Shang, Chongshan Yuan and 5 more

Abstract read
In one paragraph

Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Anthocyanins Prevent Mastitis Exacerbation by Inhibiting PANoptosis Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  7. Article
  8. 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

15 authors.

Min QiuDepartment of Gynecology, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin Province, China; Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun 130062, Jilin Province, China.
Cong YeDepartment of Gynecology, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin Province, China.
Lijuan BaoDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun 130062, Jilin Province, China.
Keyi WuDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun 130062, Jilin Province, China.
Yihong ZhaoDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun 130062, Jilin Province, China.
Xiaotong ZhaoDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun 130062, Jilin Province, China.
Ruibo TangDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun 130062, Jilin Province, China.
Ruping ShangDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun 130062, Jilin Province, China.
Shan ShangDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun 130062, Jilin Province, China.
Chongshan YuanDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun 130062, Jilin Province, China.
Xiaoyu HuDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun 130062, Jilin Province, China.
Naisheng ZhangDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun 130062, Jilin Province, China.
Yunhe FuDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun 130062, Jilin Province, China. Electronic address: fuyunhesky@163.com.
Jun WangCollege of Animal Science and Technology, Jilin Agricultural University, Changchun 130118, Jilin Province, China. Electronic address: Junwang2004@126.com.
Caijun ZhaoDepartment of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun 130062, Jilin Province, China. Electronic address: zhaocj2001@sina.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionIn responses to antibiotics exposure, gut dysbiosis is a risk factor not only for pathogen infection but also for facilitating pathobiont expansion, resulting in increased inflammatory responses in the gut and distant organs. However, how this process is regulated has not been fully elucidated.

objectivesIn this study, we investigated the role of sialic acid, a host-derived carbohydrate, in the pathogenesis of gut dysbiosis-derived inflammation in distant organs.

methodsAmpicillin (Amp)-induced gut dysbiotic mice were treated with N-glycolylneuraminic acid (Neu5Gc) and N-acetylneuraminic acid (Neu5Ac) for three weeks to assess the role of sialic acids in mastitis. The underlying mechanism by which sialic acids regulate mastitis was explored using 16S rRNA sequencing, transcriptomics and employed multiple molecular approaches.

resultsAdministration of Neu5Ac and Neu5Gc exacerbated gut dysbiosis-induced mastitis and systemic inflammation. The gut dysbiosis caused by Amp was also aggravated by sialic acid. Notably, increased Enterococcus expansion, which was positively correlated with inflammatory markers, was observed in both Neu5Ac- and Neu5Gc-treated gut dysbiotic mice. Treatment of mice with Enterococcus cecorum (E. cecorum) aggravated gut dysbiosis-induced mastitis. Mechanically, sialic acid-facilitated E. cecorum expansion promoted muramyl dipeptide (MDP) release, which induced inflammatory responses by activating the NOD2-RIP2-NF-κB axis.

conclusionsCollectively, our data reveal a role of sialic acid-facilitated postantibiotic pathobiont expansion in gut dysbiosis-associated inflammation, highlighting a potential strategy for disease prevention by regulating the MDP-NOD2-RIP2 axis.

Indexed as

DysbiosisGastrointestinal MicrobiomeMastitisN-Acetylneuraminic AcidAmpicillinAnimalsAnti-Bacterial AgentsDisease Models, AnimalFemaleInflammationMiceNeuraminic AcidsNod2 Signaling Adaptor ProteinRNA, Ribosomal, 16SAmpicillinAnti-Bacterial AgentsN-Acetylneuraminic AcidNeuraminic AcidsN-glycolylneuraminic acidNod2 Signaling Adaptor ProteinRNA, Ribosomal, 16SEnterococcus cecorumGut dysbiosisMastitisMuramyl dipeptideSialic acid

Identifiers

PMID39374734
PMCPMC12302661

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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.