Evidence map›Paper›PMID 25114116›Full record

ArticleInfection and immunity2014

Blockade of indoleamine 2,3-dioxygenase reduces mortality from peritonitis and sepsis in mice by regulating functions of CD11b+ peritoneal cells.

Masato Hoshi, Yosuke Osawa, Hiroyasu Ito, Hirofumi Ohtaki, Tatsuya Ando, Manabu Takamatsu, Akira Hara, Kuniaki Saito, Mitsuru Seishima

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Switch of NAD Salvage toFrontiers in immunology · 2019
    Article
  16. Article
  17. Observational
  18. Article
  19. Therapeutic targeting of inflammation and tryptophan metabolism in colon and gastrointestinal cancer.Translational research : the journal of laboratory and clinical medicine · 2016
    Review
  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

9 authors at 3 institutions in 1 country.

Masato HoshiFaculty of Medical Science, Suzuka University of Medical Science, Suzuka, Japan Department of Informative Clinical Medicine, Gifu University Graduate School of Medicine, Gifu, Japan mhoshi@suzuka-u.ac.jp.
Yosuke OsawaDepartment of Hepatology, Tokyo Metropolitan Cancer and Infectious Diseases Center, Komagome Hospital, Tokyo, Japan.
Hiroyasu ItoDepartment of Informative Clinical Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Hirofumi OhtakiDepartment of Informative Clinical Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Tatsuya AndoDepartment of Informative Clinical Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Manabu TakamatsuDepartment of Tumor Pathology, Gifu University Graduate School of Medicine, Gifu, Japan.
Akira HaraDepartment of Tumor Pathology, Gifu University Graduate School of Medicine, Gifu, Japan.
Kuniaki SaitoHuman Health Sciences, Kyoto University Graduate School of Medicine and Faculty of Medicine, Kyoto, Japan.
Mitsuru SeishimaDepartment of Informative Clinical Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Gifu University · JPKyoto University · JPTokyo Metropolitan Komagome Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Indoleamine 2,3-dioxygenase-1 (Ido), which catalyzes the first and limiting step of tryptophan catabolism, has been implicated in immune tolerance. However, the roles of Ido in systemic bacterial infection are complicated and remain controversial. To explore this issue, we examined the roles of Ido in bacterial peritonitis and sepsis after cecal ligation and puncture (CLP) in mice by using the Ido inhibitor 1-methyl-d,l-tryptophan (1-MT), by comparing Ido(+/+) and Ido(-/-) mice, or by using chimeric mice in which Ido in the bone marrow-derived cells was deficient. Ido expression in the peritoneal CD11b(+) cells and its metabolite l-kynurenine in the serum were increased after CLP. 1-MT treatment or Ido deficiency, especially in bone marrow-derived cells, reduced mortality after CLP. Compared to Ido(+/+) mice, Ido(-/-) mice showed increased recruitment of neutrophils and mononuclear cells into the peritoneal cavity and a decreased bacterial count in the blood accompanied by increased CXCL-2 and CXCL-1 mRNA in the peritoneal cells. Ido has an inhibitory effect on LPS-induced CXCL-2 and CXCL-1 production in cultured peritoneal cells. These findings indicate that inhibition of Ido reduces mortality from peritonitis and sepsis after CLP via recruitment of neutrophils and mononuclear cells by chemokine production in peritoneal CD11b(+) cells. Thus, blockade of Ido plays a beneficial role in host protection during bacterial peritonitis and sepsis.

Indexed as

AnimalsBacterial InfectionsCD11b AntigenGene Expression Regulation, EnzymologicIndoleamine-Pyrrole 2,3,-DioxygenaseLeukocytes, MononuclearMaleMiceMice, KnockoutNeutrophilsPeritoneumPeritonitisRNA, MessengerSepsisCD11b AntigenIDO1 protein, mouseIndoleamine-Pyrrole 2,3,-DioxygenaseRNA, Messenger

Identifiers

PMID25114116
PMCPMC4249307
OpenAlexW2147055311

What OpenQuestion holds

Textmetadata
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.