Evidence map›Paper›PMID 22751446›Full record

ArticleInnate immunity2013

Deletion of scavenger receptor A gene in mice resulted in protection from septic shock and modulation of TLR4 signaling in isolated peritoneal macrophages.

Robert Drummond, David M Cauvi, Dennis Hawisher, Donghuan Song, Diego F Niño, Raul Coimbra, Stephen Bickler, Antonio De Maio

Open access · bronzeAbstract read
In one paragraph

Article in Innate immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Scavenger receptor A1 participates in uptake ofEmerging microbes & infections · 2021
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Critical regulation of inflammation via class A scavenger receptor.International journal of chronic obstructive pulmonary disease
    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

8 authors at 2 institutions in 1 country.

Robert DrummondMSTP program Johns Hopkins University, School of Medicine, Baltimore, MD, USA.
David M Cauvi
Dennis Hawisher
Donghuan Song
Diego F Niño
Raul Coimbra
Stephen Bickler
Antonio De Maio
University of California, San Diego · USJohns Hopkins Medicine · US

Funding

Mentoring Young Minds to Increase Diversity in the Biomedical ResearchR25GM083275 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DE MAIO, ANTONIO, LAWSON, MARK ANDREW · 2008 to 2022
$9.9M
Modifier genes of sepsisR01GM073825 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DE MAIO, ANTONIO · 2006 to 2009
$1.5M
CD14: Biosynthesis, Trafficking and SecretionF31GM090681 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI NINO, DIEGO FERNANDO · 2010 to 2013
$126k
NIGMS NIH HHS F31 GM090681NIGMS NIH HHS GM073825NIGMS NIH HHS R01 GM073825NIGMS NIH HHS R25 GM083275
6 · The paper itself

Abstract

Scavenger receptor A (Sra), also known as macrophage scavenger receptor 1 (Msr1), is a surface glycoprotein preferentially present in macrophages that plays a primary role in innate immunity. Previous studies have shown that Sra is a modifier gene for the response to bacterial LPS in mice at the level of IL-10 production, in particular. In the present study, we found that Sra(-/-) mice are more resistant to septic shock induced by cecal ligation and puncture than wild-type C57BL/6 J (B6) mice. In addition, Sra(-/-) mice displayed initial elevated high density lipoprotein (HDL) circulating levels. Naïve peritoneal macrophages (PMs) were isolated from Sra(-/-) mice to understand the possible protective mechanism. Incubation of these cells with LPS was found to modulate TLR4 signaling, leading to a reduction in IL-10 and IL-6 mRNA levels, but not TNF-α expression, at low concentrations of LPS in comparison with PMs isolated from B6 mice. No differences were found in LPS binding between PMs derived from Sra(-/-) or B6 mice. The lack of Sra binding to LPS was confirmed after transfection of Chinese hamster ovary (CHO) cells with the Sra gene. The contribution of Sra to the outcome of sepsis may be a combination of changes in TLR4 signaling pathway and elevated levels of HDL in circulation, but also LPS toxicity.

Indexed as

AnimalsCHO CellsCricetinaeCytokinesLipopolysaccharidesMacrophages, PeritonealMaleMiceMice, Inbred C57BLMice, KnockoutScavenger Receptors, Class AShock, SepticSignal TransductionToll-Like Receptor 4CytokinesLipopolysaccharidesScavenger Receptors, Class AToll-Like Receptor 4

Identifiers

PMID22751446
PMCPMC4349423
OpenAlexW2129376521

What OpenQuestion holds

Textmetadata
LicenceTDM
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.