Evidence map›Paper›PMID 30052667›Full record

ArticlePloS one2018

The protective role of human ghrelin in sepsis: Restoration of CD4 T cell proliferation.

Mian Zhou, Monowar Aziz, Manhendar Ochani, Weng-Lang Yang, Archna Sharma, Ping Wang

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 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. The Immunomodulatory Activity ofJournal of immunology research · 2023
    Article
  3. Review
  4. Targeting of G-protein coupled receptors in sepsis.Pharmacology & therapeutics · 2020
    Review
  5. Bioinformatics Analysis for Multiple Gene Expression Profiles in Sepsis.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  6. Physiological Effect of Ghrelin on Body Systems.International journal of endocrinology · 2020
    Review
  7. Article
  8. Ghrelin as an Anti-Sepsis Peptide: Review.Frontiers in immunology · 2020
    Review
  9. 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

6 authors at 1 institution in 1 country.

Mian ZhouCenter for Immunology and Inflammation, The Feinstein Institute for Medical Research, Manhasset, New York, United State of America.
Monowar AzizCenter for Immunology and Inflammation, The Feinstein Institute for Medical Research, Manhasset, New York, United State of America.
Manhendar OchaniCenter for Immunology and Inflammation, The Feinstein Institute for Medical Research, Manhasset, New York, United State of America.
Weng-Lang YangCenter for Immunology and Inflammation, The Feinstein Institute for Medical Research, Manhasset, New York, United State of America.
Archna SharmaCenter for Immunology and Inflammation, The Feinstein Institute for Medical Research, Manhasset, New York, United State of America.ORCID 0000-0003-4745-0220
Ping WangCenter for Immunology and Inflammation, The Feinstein Institute for Medical Research, Manhasset, New York, United State of America.ORCID 0000-0002-8195-4505
Feinstein Institute for Medical Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Decrease of CD4 T cell numbers causes immunosuppression in sepsis. We previously showed the beneficial role of ghrelin in sepsis. We hypothesize that the protective outcome of ghrelin in sepsis is mediated partially through the restoration of CD4 T cells' proliferation. Sepsis was induced in mice by cecal ligation and puncture (CLP). The percentage of CD4 T cells in spleen was assessed by flow cytometry and their proliferation was determined by carboxyfluorescein succinimidyl ester (CSFE). Compared to sham mice, the percentages of splenic CD4 T cells were reduced by 20%, 21%, and 29% at day 1, 2 and 3 after CLP, respectively. Human ghrelin was given to 3 day septic mice by s.c. injection at 5 and 24 h after CLP. Treatment with ghrelin restored the loss of CD4 T cells by increasing their proliferation in septic mice. The expression of cyclin D1 and B1 was significantly increased, while the expression of p57 was decreased in ghrelin-treated mice compared to vehicle-treated mice in sepsis. Treatment with human ghrelin significantly increased the p-AKT levels in the spleen compared to vehicle-treated septic mice. Human ghrelin plays an important role in reestablishing the proliferation of CD4 T cells and serves as a promising therapeutic agent in sepsis.

Indexed as

AnimalsApoptosisCD4-Positive T-LymphocytesCell CycleCell ProliferationCells, CulturedDisease Models, AnimalGhrelinHomeostasisHumansMaleMice, Inbred C57BLProtective AgentsProto-Oncogene Proteins c-aktSepsisSpleenGhrelinProtective AgentsProto-Oncogene Proteins c-akt

Identifiers

PMID30052667
PMCPMC6063405
OpenAlexW2884886828

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.