Evidence map›Paper›PMID 25689829›Full record

ArticlePloS one2015

Microbiota-Independent Ameliorative Effects of Antibiotics on Spontaneous Th2-Associated Pathology of the Small Intestine.

Daehee Han, Matthew C Walsh, Kwang Soon Kim, Sung-Wook Hong, Junyoung Lee, Jaeu Yi, Gloriany Rivas, Charles D Surh, Yongwon Choi

Erratum issuedAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Microbiota and Food Allergy.Clinical reviews in allergy & immunology · 2019
    Review
  9. Article
  10. Review
  11. Article
  12. The Influence of the Microbiome on Allergic Sensitization to Food.Journal of immunology (Baltimore, Md. : 1950) · 2017
    Review
  13. Article
  14. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Daehee HanAcademy of Immunology and Microbiology, Institute for Basic Science, Pohang, 790-784, Republic of Korea; Department of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang, 790-784, Republic of Korea.
Matthew C WalshDepartment of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, 19104, United States of America.
Kwang Soon KimAcademy of Immunology and Microbiology, Institute for Basic Science, Pohang, 790-784, Republic of Korea; Department of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang, 790-784, Republic of Korea.
Sung-Wook HongAcademy of Immunology and Microbiology, Institute for Basic Science, Pohang, 790-784, Republic of Korea; Department of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang, 790-784, Republic of Korea.
Junyoung LeeAcademy of Immunology and Microbiology, Institute for Basic Science, Pohang, 790-784, Republic of Korea; Department of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang, 790-784, Republic of Korea.
Jaeu YiAcademy of Immunology and Microbiology, Institute for Basic Science, Pohang, 790-784, Republic of Korea; Department of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang, 790-784, Republic of Korea.
Gloriany RivasDepartment of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, 19104, United States of America.
Charles D SurhAcademy of Immunology and Microbiology, Institute for Basic Science, Pohang, 790-784, Republic of Korea; Department of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang, 790-784, Republic of Korea; Division of Developmental Immunology, La Jolla Institute for Allergy and Immunology, La Jolla, California, 92037, United States of America.
Yongwon ChoiDepartment of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, 19104, United States of America.

Funding

TRAF6 and the fate of T cellsR01AI064909 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI CHOI, YONGWON · 2006 to 2017
$3.9M
Interaction between microbiota and dendritic cells in mucosal toleranceR21AI108627 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI CHOI, YONGWON · 2014 to 2015
$440k
NIAID NIH HHS AI064909NIAID NIH HHS AI108627NIAID NIH HHS R01 AI064909NIAID NIH HHS R21 AI108627
6 · The paper itself

Abstract

We have previously generated a mouse model of spontaneous Th2-associated disease of the small intestine called TRAF6ΔDC, in which dendritic cell (DC)-intrinsic expression of the signaling mediator TRAF6 is ablated. Interestingly, broad-spectrum antibiotic treatment ameliorates TRAF6ΔDC disease, implying a role for commensal microbiota in disease development. However, the relationship between the drug effects and commensal microbiota status remains to be formally demonstrated. To directly assess this relationship, we have now generated TRAF6ΔDC bone marrow chimera mice under germ-free (GF) conditions lacking commensal microbiota, and found, unexpectedly, that Th2-associated disease is actually exacerbated in GF TRAF6ΔDC mice compared to specific pathogen-free (SPF) TRAF6ΔDC mice. At the same time, broad-spectrum antibiotic treatment of GF TRAF6ΔDC mice has an ameliorative effect similar to that observed in antibiotics-treated SPF TRAF6ΔDC mice, implying a commensal microbiota-independent effect of broad-spectrum antibiotic treatment. We further found that treatment of GF TRAF6ΔDC mice with broad-spectrum antibiotics increases Foxp3+ Treg populations in lymphoid organs and the small intestine, pointing to a possible mechanism by which treatment may directly exert an immunomodulatory effect. To investigate links between the exacerbated phenotype of the small intestines of GF TRAF6ΔDC mice and local microbiota, we performed microbiotic profiling of the luminal contents specifically within the small intestines of diseased TRAF6ΔDC mice, and, when compared to co-housed control mice, found significantly increased total bacterial content characterized by specific increases in Firmicutes Lactobacillus species. These data suggest a protective effect of Firmicutes Lactobacillus against the spontaneous Th2-related inflammation of the small intestine of the TRAF6ΔDC model, and may represent a potential mechanism for related disease phenotypes.

Indexed as

MicrobiotaAnimalsAnti-Bacterial AgentsDendritic CellsGene Expression RegulationGerm-Free LifeHomeostasisIntestinal DiseasesIntestine, SmallMiceT-Lymphocytes, RegulatoryTNF Receptor-Associated Factor 6Anti-Bacterial AgentsTNF Receptor-Associated Factor 6

Identifiers

PMID25689829
PMCPMC4331505

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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.