Evidence map›Paper›PMID 30410021›Full record

ArticleScientific reports2018

Serum Amyloid A3 is required for normal lung development and survival following influenza infection.

Jennifer L Ather, Oliver Dienz, Jonathan E Boyson, Vikas Anathy, Eyal Amiel, Matthew E Poynter

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. 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
1.0field-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, 24 citations in OpenAlex.

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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.

Jennifer L AtherVermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT, 05405, USA.
Oliver DienzDepartment of Surgery, University of Vermont, Burlington, VT, 05405, USA.
Jonathan E BoysonDepartment of Surgery, University of Vermont, Burlington, VT, 05405, USA.
Vikas AnathyDepartment of Pathology and Laboratory Medicine, University of Vermont, Burlington, VT, 05405, USA.
Eyal AmielDepartment of Biomedical and Health Sciences, University of Vermont, Burlington, VT, 05405, USA.
Matthew E PoynterVermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT, 05405, USA. Matthew.Poynter@uvm.edu.ORCID http://orcid.org/0000-0002-7578-4570
University of Vermont · US

Funding

VERMONT IMMUNOBIOLOIGY/ INFECTIOUS DISEASES CENTERP20RR021905 · NCRR · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BUDD, RALPH C · 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
A host genetic locus that regulates susceptibility to influenza infection.R21AI119974 · NIAID · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BOYSON, JONATHAN E · 2015 to 2016
$423k
NCRR NIH HHS P20 RR021905NHLBI NIH HHS R01 HL107291NHLBI NIH HHS R01 HL133920NHLBI NIH HHS R01 HL142081NIAID NIH HHS R21 AI119974NIGMS NIH HHS P30 GM118228
6 · The paper itself

Abstract

Serum amyloid A (SAA) proteins are a family of acute phase apolipoproteins implicated to directly modulate innate and adaptive immune responses. However, new studies comparing endogenous SAAs and recombinant forms of these proteins have questioned the function of SAA in inflammation and immunity. We generated SAA3 knockout mice to evaluate the contribution of SAA3 to lung development and immune-mediated lung disease. While SAA3 deficiency does not affect the generation of house dust mite-induced allergic asthma, mice lacking SAA3 develop adult-onset obesity, intrinsic airway hyperresponsiveness, increased inflammatory and fibrotic gene expression in the lung, and elevated levels of lung citrullinated proteins. Polyclonally stimulated CD4

Indexed as

AnimalsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesGene Knockout TechniquesInfluenza A Virus, H1N1 SubtypeLipopolysaccharidesLungLung DiseasesMiceOrthomyxoviridae InfectionsPyroglyphidaeRespiratory HypersensitivitySerum Amyloid A ProteinSurvival AnalysisLipopolysaccharidesSaa3 protein, mouseSerum Amyloid A Protein

Identifiers

PMID30410021
PMCPMC6224415
OpenAlexW2898746327

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.