Evidence map›Paper›PMID 30298073›Full record

ArticleFrontiers in immunology2018

Leptin Elicits LTC

Natália R T Amorim, Tatiana Luna-Gomes, Marcos Gama-Almeida, Glaucia Souza-Almeida, Claudio Canetti, Bruno L Diaz, Peter F Weller, Patricia Torres Bozza, Clarissa M Maya-Monteiro, Christianne Bandeira-Melo

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Leptin ElicitsFrontiers in endocrinology · 2020
    Article
  6. Article
  7. 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

10 authors at 4 institutions in 2 countries.

Natália R T AmorimLaboratório de Inflamação, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Tatiana Luna-GomesLaboratório de Inflamação, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Marcos Gama-AlmeidaLaboratório de Inflamação, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Glaucia Souza-AlmeidaLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz-IOC, FIOCRUZ, Rio de Janeiro, Brazil.
Claudio CanettiLaboratório de Inflamação, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Bruno L DiazLaboratório de Inflamação, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Peter F WellerDepartment of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA, United States.
Patricia Torres BozzaLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz-IOC, FIOCRUZ, Rio de Janeiro, Brazil.
Clarissa M Maya-MonteiroLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz-IOC, FIOCRUZ, Rio de Janeiro, Brazil.
Christianne Bandeira-MeloLaboratório de Inflamação, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Universidade Federal do Rio de Janeiro · BRFundação Oswaldo Cruz · BRBeth Israel Deaconess Medical Center · USUniversidade do Estado do Rio de Janeiro · BR

Funding

Human Eosinophils: Mechanisms of FunctioningR37AI020241 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WELLER, PETER F · 2010 to 2019
$4.5M
NIAID NIH HHS R37 AI020241
6 · The paper itself

Abstract

Leptin is a cytokine, produced mainly by mature adipocytes, that regulates the central nervous system, mainly to suppress appetite and stimulate energy expenditure. Leptin also regulates the immune response by controlling activation of immunomodulatory cells, including eosinophils. While emerging as immune regulatory cells with roles in adipose tissue homeostasis, eosinophils have a well-established ability to synthesize pro-inflammatory molecules such as lipid mediators, a key event in several inflammatory pathologies. Here, we investigated the impact and mechanisms involved in leptin-driven activation of eicosanoid-synthesizing machinery within eosinophils. Direct

Indexed as

AnimalsCells, CulturedChemokine CCL5EosinophilsFemaleHumansHydantoinsIntramolecular OxidoreductasesLeptinLeukotriene C4Lipid DropletsMaleMiceMice, Inbred BALB CPiperidinesPrimary Cell Culture4-benzhydryloxy-1-(3-(1H-tetrazol-5-yl-)-propyl)piperidineBW A868CCCL5 protein, humanCcl5 protein, mouseCCR3 protein, humanCcr3 protein, mouseChemokine CCL5HPGDS protein, humanHydantoinsIntramolecular OxidoreductasesLEP protein, humanLeptinLeukotriene C4PiperidinesProstaglandin D2prostaglandin D2 receptorReceptors, CCR3Receptors, ImmunologicReceptors, ProstaglandinRecombinant ProteinsCCL5CCR3eosinophilleptinleukotriene C4lipid bodylipid dropletprostaglandin D2

Identifiers

PMID30298073
PMCPMC6160734
OpenAlexW2889795652

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.