Evidence map›Paper›PMID 29390039›Full record

ArticlePloS one2018

Serum amyloid A3 is required for normal weight and immunometabolic function in mice.

Jennifer L Ather, Matthew E Poynter

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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.4field-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

27 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Serum amyloid A in HFpEF and cardiometabolic diseases.Basic research in cardiology · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Obese adipose tissue modulates proinflammatory responses of mouse airway epithelial cells.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Article
  12. Article
  13. Review
  14. Article
  15. The impact of obesity on immune function in pediatric asthma.Current opinion in allergy and clinical immunology · 2021
    Review
  16. Article
  17. Article
  18. Article
  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

2 authors at 1 institution in 1 country.

Jennifer L AtherVermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT, United States of America.
Matthew E PoynterVermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT, United States of America.ORCID 0000-0002-7578-4570
University of Vermont · US

Funding

VERMONT IMMUNOBIOLOIGY/ INFECTIOUS DISEASES CENTERP20RR021905 · NCRR · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI HILL, JACK · 2006 to 2011
$14.5M
Vermont Immunology/Infectious Diseases CenterP30GM118228 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BUDD, RALPH C · 2016 to 2021
$6.8M
Obese Allergic Asthma and the Impact of Weight Loss on Airway Epithelial FunctionR01HL133920 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI DIXON, ANNE E, POYNTER, MATTHEW E · 2016 to 2020
$3.9M
Ketone Body Supplementation in Obese AsthmaR01HL142081 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI POYNTER, MATTHEW E · 2018 to 2021
$1.8M
Serum Amyloid A3 in Allergic Asthma: An Endogenous Mediator of Disease SeverityR01HL107291 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI POYNTER, MATTHEW E · 2012 to 2015
$1.5M
NCRR NIH HHS P20 RR021905NHLBI NIH HHS R01 HL107291NHLBI NIH HHS R01 HL133920NHLBI NIH HHS R01 HL142081NIGMS NIH HHS P30 GM118228
6 · The paper itself

Abstract

Serum amyloid A (SAA) is an apolipoprotein that is robustly upregulated in numerous inflammatory diseases and has been implicated as a candidate pro-inflammatory mediator. However, studies comparing endogenous SAAs and recombinant forms of the acute phase protein have generated conflicting data on the function of SAA in immunity. We generated SAA3 knockout mice to evaluate the contribution of SAA3 to immune-mediated disease, and found that mice lacking SAA3 develop adult-onset obesity and metabolic dysfunction along with defects in innate immune development. Mice that lack SAA3 gain more weight, exhibit increased visceral adipose deposition, and develop hepatic steatosis compared to wild-type littermates. Leukocytes from the adipose tissue of SAA3-/- mice express a pro-inflammatory phenotype, and bone marrow derived dendritic cells from mice lacking SAA3 secrete increased levels of IL-1β, IL-6, IL-23, and TNFα in response to LPS compared to cells from wild-type mice. Finally, BMDC lacking SAA3 demonstrate an impaired endotoxin tolerance response and inhibited responses to retinoic acid. Our findings indicate that endogenous SAA3 modulates metabolic and immune homeostasis.

Indexed as

Body WeightAnimalsDendritic CellsDiet, High-FatHomeostasisImmune SystemInsulinIntra-Abdominal FatLipopolysaccharidesMiceMice, KnockoutObesitySerum Amyloid A ProteinInsulinLipopolysaccharidesSerum Amyloid A Protein

Identifiers

PMID29390039
PMCPMC5794179
OpenAlexW2786165615

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.