Evidence map›Paper›PMID 32061677›Full record

ArticleBone2020

Post-antibiotic gut dysbiosis-induced trabecular bone loss is dependent on lymphocytes.

Naiomy Deliz Rios-Arce, Jonathan D Schepper, Andrew Dagenais, Laura Schaefer, Connor S Daly-Seiler, Joseph D Gardinier, Robert A Britton, Laura R McCabe, Narayanan Parameswaran

Open access · greenAbstract read
In one paragraph

Article in Bone, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% of its field
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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Dysbiosis in the Gut-Liver Axis Is Associated With Low Bone Mass During Murine Cholestasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Limosilactobacillus reuteri promotes the expression and secretion of enteroendocrine- and enterocyte-derived hormones.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. bioRxiv : the preprint server for biology · 2024
    Article
  14. Article
  15. Article
  16. JBMR plus · 2023
    Article
  17. Article
  18. Article
  19. Article
  20. 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

9 authors at 3 institutions in 1 country.

Naiomy Deliz Rios-ArceComparative Medicine and Integrative Biology Program, Michigan State University, East Lansing, MI, USA; Department of Physiology, Michigan State University, East Lansing, MI, USA.
Jonathan D SchepperDepartment of Physiology, Michigan State University, East Lansing, MI, USA.
Andrew DagenaisDepartment of Physiology, Michigan State University, East Lansing, MI, USA.
Laura SchaeferDepartment of Molecular Virology and Microbiology, Alkek Center for Metagenomics and Microbiome Research, Baylor College of Medicine, Houston, TX, USA.
Connor S Daly-SeilerHenry Ford Health System-Bone and Joint Center, USA.
Joseph D GardinierHenry Ford Health System-Bone and Joint Center, USA.
Robert A BrittonDepartment of Molecular Virology and Microbiology, Alkek Center for Metagenomics and Microbiome Research, Baylor College of Medicine, Houston, TX, USA.
Laura R McCabeDepartment of Physiology, Michigan State University, East Lansing, MI, USA; Department of Radiology, Michigan State University, East Lansing, MI, USA; Biomedical Imaging Research Center, Michigan State University, East Lansing, MI, USA. Electronic address: mccabel@msu.edu.
Narayanan ParameswaranComparative Medicine and Integrative Biology Program, Michigan State University, East Lansing, MI, USA; Department of Physiology, Michigan State University, East Lansing, MI, USA. Electronic address: narap@msu.edu.
Michigan State University · USBaylor College of Medicine · USHenry Ford Health System · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
Mechanistic basis of probiotic prevention of osteoporosisR01AT007695 · NCCIH · MICHIGAN STATE UNIVERSITY · PI BRITTON, ROBERT A, MCCABE, LAURA R · 2013 to 2017
$2.2M
The Role of the Gut and Bone Microenvironment in T1D Bone LossR01DK101050 · NIDDK · MICHIGAN STATE UNIVERSITY · PI MCCABE, LAURA R, PARAMESWARAN, NARAYANAN · 2014 to 2016
$1.1M
NCCIH NIH HHS R01 AT007695NIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK101050
6 · The paper itself

Abstract

Recent studies in mouse models have shown that gut microbiota significantly influences bone health. We demonstrated that 2-week oral treatment with broad spectrum antibiotics followed by 4 weeks of recovery of the gut microbiota results in dysbiosis (microbiota imbalance)-induced bone loss in mice. Because gut microbiota is critical for the development of the immune system and since both microbiota and the immune system can regulate bone health, in this study, we tested the role of the immune system in mediating post-antibiotic dysbiosis-induced bone loss. For this, we treated wild-type (WT) and lymphocyte deficient Rag2 knockout (KO) mice with ampicillin/neomycin cocktail in water for 2 weeks followed by 4 weeks of water without antibiotics. This led to a significant bone loss (31% decrease from control) in WT mice. Interestingly, no bone loss was observed in the KO mice suggesting that lymphocytes are required for dysbiosis-induced bone loss. Bray-Curtis diversity metrics showed similar microbiota changes in both the WT and KO post-antibiotic treated groups. However, several operational taxonomic units (OTUs) classified as Lactobacillales were significantly higher in the repopulated KO when compared to the WT mice, suggesting that these bacteria might play a protective role in preventing bone loss in the KO mice after antibiotic treatment. The effect of dysbiosis on bone was therefore examined in the WT mice in the presence or absence of oral Lactobacillus reuteri treatment for 4 weeks (post-ABX treatment). As hypothesized, mice treated with L. reuteri did not display bone loss, suggesting a bone protective role for this group of bacteria. Taken together, our studies elucidate an important role for lymphocytes in regulating post-antibiotic dysbiosis-induced bone loss.

Indexed as

Anti-Bacterial AgentsBone ResorptionDysbiosisGastrointestinal MicrobiomeAnimalsCancellous BoneLymphocytesMiceMice, Inbred C57BLAnti-Bacterial AgentsAdaptive immune systemBoneLactobacillus reuteri 6475MicrobiotaProbiotics

Identifiers

PMID32061677
PMCPMC7138712
OpenAlexW3006656100

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.