Evidence map›Paper›PMID 30235279›Full record

ArticlePloS one2018

Propionate-producing bacteria in the intestine may associate with skewed responses of IL10-producing regulatory T cells in patients with relapsing polychondritis.

Jun Shimizu, Takao Kubota, Erika Takada, Kenji Takai, Naruyoshi Fujiwara, Nagisa Arimitsu, Masanori A Murayama, Yuji Ueda, Sueshige Wakisaka, Tomoko Suzuki and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 91 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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

11 authors at 1 institution in 1 country.

Jun ShimizuDepartment of Immunology and Medicine, St. Marianna University School of Medicine, Kawasaki, Japan.
Takao KubotaDepartment of Immunology and Medicine, St. Marianna University School of Medicine, Kawasaki, Japan.
Erika TakadaDepartment of Immunology and Medicine, St. Marianna University School of Medicine, Kawasaki, Japan.
Kenji TakaiDepartment of Immunology and Medicine, St. Marianna University School of Medicine, Kawasaki, Japan.
Naruyoshi FujiwaraDepartment of Immunology and Medicine, St. Marianna University School of Medicine, Kawasaki, Japan.
Nagisa ArimitsuDepartment of Immunology and Medicine, St. Marianna University School of Medicine, Kawasaki, Japan.
Masanori A MurayamaDepartment of Immunology and Medicine, St. Marianna University School of Medicine, Kawasaki, Japan.
Yuji UedaDepartment of Immunology and Medicine, St. Marianna University School of Medicine, Kawasaki, Japan.
Sueshige WakisakaDepartment of Immunology and Medicine, St. Marianna University School of Medicine, Kawasaki, Japan.
Tomoko SuzukiDepartment of Immunology and Medicine, St. Marianna University School of Medicine, Kawasaki, Japan.
Noboru SuzukiDepartment of Immunology and Medicine, St. Marianna University School of Medicine, Kawasaki, Japan.ORCID 0000-0001-7090-7415
St. Marianna University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Relapsing polychondritis (RP) is an inflammatory disease of unknown causes, characterized by recurrent inflammation in cartilaginous tissues of the whole body. Recently, researchers have reported that, in mouse experiments, altered gut microbe-dependent T cell differentiation occurred in gut associated lymphoid tissues. Here, we investigated whether gut microbe alteration existed, and if so, the alteration affected peripheral T cell differentiation in patients with RP. In an analysis of gut microbiota, we found increased annotated species numbers in RP patients compared with normal individuals. In the RP gut microbiota, we observed several predominant species, namely Veillonella parvula, Bacteroides eggerthii, Bacteroides fragilis, Ruminococcus bromii, and Eubacterium dolichum, all species of which were reported to associate with propionate production in human intestine. Propionate is a short-chain fatty acid and is suggested to associate with interleukin (IL)10-producing regulatory T (Treg) cell differentiation in gut associated lymphoid tissues. IL10 gene expressions were moderately higher in freshly isolated peripheral blood mononuclear cells (PBMC) of RP patients than those of normal individuals. Six hours after the initiation of the cell culture, regardless of the presence and absence of mitogen stimulation, IL10 gene expressions were significantly lower in RP patients than those in normal individuals. It is well known that PBMC of patients with autoimmune and inflammatory diseases show hyporesponsiveness to mitogen stimulation. We suggest that, in RP patients, continuous stimulation of intestinal T cells by excessive propionate leads to the spontaneous IL10 production and a subsequent refractory period of T cells in patients with RP. The hyporesponsiveness of Treg cells upon activation may associate with inflammatory cytokine production of PBMC and subsequently relate to chondritis in RP patients.

Indexed as

Gastrointestinal MicrobiomeCell DifferentiationFemaleHumansInterleukin-10MaleMiddle AgedPolychondritis, RelapsingPropionatesT-LymphocytesIL10 protein, humanInterleukin-10Propionates

Identifiers

PMID30235279
PMCPMC6147427
OpenAlexW2892367196

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.