Evidence map›Paper›PMID 30126923›Full record

ArticleEMBO reports2018

Serum amyloid A promotes LPS clearance and suppresses LPS-induced inflammation and tissue injury.

Ni Cheng, Yurong Liang, Xiaoping Du, Richard D Ye

Open access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

69 citing papers in PubMed, 119 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Serum Amyloid A: A Double-Edged Sword in Health and Disease.International journal of molecular sciences · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Flagellin in blood andiScience · 2025
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

9 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 2 countries.

Ni ChengDepartment of Pharmacology and Center for Lung and Vascular Biology, College of Medicine, University of Illinois, Chicago, IL, USA.ORCID 0000-0002-9013-690X
Yurong LiangDepartment of Pharmacology and Center for Lung and Vascular Biology, College of Medicine, University of Illinois, Chicago, IL, USA.
Xiaoping DuDepartment of Pharmacology and Center for Lung and Vascular Biology, College of Medicine, University of Illinois, Chicago, IL, USA.
Richard D YeDepartment of Pharmacology and Center for Lung and Vascular Biology, College of Medicine, University of Illinois, Chicago, IL, USA richardye@umac.mo.ORCID 0000-0002-2164-5620
University of Illinois Urbana-Champaign · US

Funding

Role of SAA in Inflammation and ImmunityR56AI040176 · NIAID · UNIVERSITY OF ILLINOIS AT CHICAGO · PI YE, RICHARD D · 2010 to 2010
$406k
NIAID NIH HHS R56 AI040176
6 · The paper itself

Abstract

Lipopolysaccharide (LPS) is a major microbial mediator for tissue injury and sepsis resulting from Gram-negative bacterial infection. LPS is an external factor that induces robust expression of serum amyloid A (SAA), a major constituent of the acute-phase proteins, but the relationship between SAA expression and LPS-induced tissue injury remains unclear. Here, we report that mice with inducible transgenic expression of human SAA1 are partially protected against inflammatory response and lung injury caused by LPS and cecal ligation and puncture (CLP). In comparison, transgenic SAA1 does not attenuate TNFα-induced lung inflammation and injury. The SAA1 expression level correlates inversely with the endotoxin concentrations in serum and lung tissues since SAA1 binds directly to LPS to form a complex that promotes LPS uptake by macrophages. Disruption of the SAA1-LPS interaction with a SAA1-derived peptide partially reduces the protective effect and exacerbates inflammation. These findings demonstrate that acute-phase SAA provides innate feedback protection against LPS-induced inflammation and tissue injury.

Indexed as

AnimalsAnimals, Genetically ModifiedGene Expression RegulationGram-Negative BacteriaGram-Negative Bacterial InfectionsHumansImmunity, InnateInflammationLipopolysaccharidesLung InjuryMacrophagesMiceMice, TransgenicSepsisSerum Amyloid A ProteinTumor Necrosis Factor-alphaLipopolysaccharidesSAA1 protein, humanSerum Amyloid A ProteinTumor Necrosis Factor-alphaacute‐phase responseinflammationinnate immunitylipopolysaccharideserum amyloid A

Identifiers

PMID30126923
PMCPMC6172460
OpenAlexW2887347048

What OpenQuestion holds

Textmetadata
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.