Evidence map›Paper›PMID 24146912›Full record

ArticlePloS one2013

Organization and biology of the porcine serum amyloid A (SAA) gene cluster: isoform specific responses to bacterial infection.

Helle G Olsen, Kerstin Skovgaard, Ole L Nielsen, Páll S Leifsson, Henrik E Jensen, Tine Iburg, Peter M H Heegaard

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
5.1field-weighted citation impact, top 5% 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

15 citing papers in PubMed, 32 citations in OpenAlex.

  1. SAA4: An Underdog Within the Serum Amyloid a Superfamily?International journal of molecular sciences · 2026
    Review
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  13. Transcriptome profiling of the cancer and adjacent nontumor tissues from cervical squamous cell carcinoma patients by RNA sequencing.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  14. Acute-phase protein serum amyloid A3 is a novel paracrine coupling factor that controls bone homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Article
  15. Protein profiling of isolated uterine AA amyloidosis causing fetal death in goats.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    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

7 authors at 2 institutions in 1 country.

Helle G OlsenDepartment of Veterinary Disease Biology, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg, Denmark.
Kerstin Skovgaard
Ole L Nielsen
Páll S Leifsson
Henrik E Jensen
Tine Iburg
Peter M H Heegaard
University of Copenhagen · DKTechnical University of Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Serum amyloid A (SAA) is a prominent acute phase protein. Although its biological functions are debated, the wide species distribution of highly homologous SAA proteins and their uniform behavior in response to injury or inflammation in itself suggests a significant role for this protein. The pig is increasingly being used as a model for the study of inflammatory reactions, yet only little is known about how specific SAA genes are regulated in the pig during acute phase responses and other responses induced by pro-inflammatory host mediators. We designed SAA gene specific primers and quantified the gene expression of porcine SAA1, SAA2, SAA3, and SAA4 by reverse transcriptase quantitative polymerase chain reaction (RT-qPCR) in liver, spleen, and lung tissue from pigs experimentally infected with the Gram-negative swine specific bacterium Actinobacillus pleuropneumoniae, as well as from pigs experimentally infected with the Gram-positive bacterium Staphylococcus aureus. Our results show that: 1) SAA1 may be a pseudogene in pigs; 2) we were able to detect two previously uncharacterized SAA transcripts, namely SAA2 and SAA4, of which the SAA2 transcript is primarily induced in the liver during acute infection and presumably contributes to circulating SAA in pigs; 3) Porcine SAA3 transcription is induced both hepatically and extrahepatically during acute infection, and may be correlated to local organ affection; 4) Hepatic transcription of SAA4 is markedly induced in pigs infected with A. pleuropneumoniae, but only weakly in pigs infected with S. aureus. These results for the first time establish the infection response patterns of the four porcine SAA genes which will be of importance for the use of the pig as a model for human inflammatory responses, e.g. within sepsis, cancer, and obesity research.

Indexed as

Multigene FamilyActinobacillusAnimalsBacterial InfectionsGene Expression ProfilingGene Expression RegulationHumansOrgan SpecificityProtein IsoformsSerum Amyloid A ProteinStaphylococcus aureusSus scrofaProtein IsoformsSerum Amyloid A Protein

Identifiers

PMID24146912
PMCPMC3795699
OpenAlexW2076681619

What OpenQuestion holds

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LicenceCC BY
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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.