Evidence map›Paper›PMID 25588622›Full record

ArticleScientific reports2015

Insulin-like growth factor-1 endues monocytes with immune suppressive ability to inhibit inflammation in the intestine.

Rong-Ti Ge, Li-Hua Mo, Ruijin Wu, Jiang-Qi Liu, Huan-Ping Zhang, Zhigang Liu, Zhanju Liu, Ping-Chang Yang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. [Mechanism of Der f 1/IGF-1 nanoparticle promoting the production of regulatory T cell].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2023
    Article
  9. Article
  10. Article
  11. Survival of HT29 Cancer Cells Is Affected by IGF1R InhibitionPathology oncology research : POR · 2022
    Article
  12. Article
  13. Insulin/IGF-1 signaling promotes immunosuppression via the STAT3 pathway: impact on the aging process and age-related diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. IGF1 receptor and thyroid-associated ophthalmopathy.Journal of molecular endocrinology · 2018
    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

8 authors at 4 institutions in 2 countries.

Rong-Ti Ge1] Department of Gastroenterology, The Shanghai Tenth People's Hospital of Tongji University, Shanghai, 200072, China [2] Brain Body Institute, McMaster University, Hamilton, ON, Canada L8N 4A6.
Li-Hua MoShenzhen Key Laboratory of Allergy &Immunology, Shenzhen University School of Medicine and State Key Laboratory of Respiratory Disease for Allergy at Shenzhen University, Shenzhen, 518060, China.
Ruijin WuDepartment of Gastroenterology, The Shanghai Tenth People's Hospital of Tongji University, Shanghai, 200072, China.
Jiang-Qi LiuBrain Body Institute, McMaster University, Hamilton, ON, Canada L8N 4A6.
Huan-Ping ZhangBrain Body Institute, McMaster University, Hamilton, ON, Canada L8N 4A6.
Zhigang LiuShenzhen Key Laboratory of Allergy &Immunology, Shenzhen University School of Medicine and State Key Laboratory of Respiratory Disease for Allergy at Shenzhen University, Shenzhen, 518060, China.
Zhanju LiuDepartment of Gastroenterology, The Shanghai Tenth People's Hospital of Tongji University, Shanghai, 200072, China.
Ping-Chang Yang1] Shenzhen Key Laboratory of Allergy &Immunology, Shenzhen University School of Medicine and State Key Laboratory of Respiratory Disease for Allergy at Shenzhen University, Shenzhen, 518060, China [2] Brain Body Institute, McMaster University, Hamilton, ON, Canada L8N 4A6.
McMaster University · CAShanghai Tenth People's Hospital · CNTongji University · CNShenzhen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis of some chronic inflammation such as inflammatory bowel disease is unclear. Insulin-like growth factor-1 (IGF1) has active immune regulatory capability. This study aims to investigate into the mechanism by which IGF1 modulates the monocyte (Mo) properties to inhibit immune inflammation in the intestine. In this study, the production of IGF1 by intestinal epithelial cells was evaluated by real time RT-PCR and Western blotting. Mos were analyzed by flow cytometry. A mouse colitis model was created with trinitrobenzene sulfonic acid. The results showed that mouse IECs produced IGF1, which could be up regulated by exposure to CpG-ODN (CpG-oligodeoxynueleotides) in the culture. Culture the CpG-ODN-primed IEC cells and Mos or exposure of Mos to IGF1 in the culture induced the Mos to express IL-10. The IGF1-primed Mos showed the immune suppressive effect on inhibiting the immune inflammation in the mouse colon. In conclusion, the IGF1-primed Mos are capable of suppressing immune inflammation in the intestine.

Indexed as

Immunosuppression TherapyAnimalsCell LineCell SeparationColitisEpithelial CellsInflammationInsulin-Like Growth Factor IInterleukin-10IntestinesLipopolysaccharide ReceptorsMice, Inbred BALB CMonocytesOligodeoxyribonucleotidesPhenotypeReceptor, IGF Type 1CPG-oligonucleotideInsulin-Like Growth Factor IInterleukin-10Lipopolysaccharide ReceptorsOligodeoxyribonucleotidesReceptor, IGF Type 1Trinitrobenzenesulfonic Acid

Identifiers

PMID25588622
PMCPMC4295102
OpenAlexW1978723007

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.