Evidence map›Paper›PMID 19860560›Full record

ArticleThe Journal of infectious diseases2009

Overproduction of acyloxyacyl hydrolase by macrophages and dendritic cells prevents prolonged reactions to bacterial lipopolysaccharide in vivo.

Noredia Ojogun, Tang-Yong Kuang, Baomei Shao, David R Greaves, Robert S Munford, Alan W Varley

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.6field-weighted citation impact, top 26% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Acyloxyacyl hydrolase modulates pelvic pain severity.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
  11. Crystal structure of the mammalian lipopolysaccharide detoxifier.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Genetics of chronic rhinosinusitis: state of the field and directions forward.The Journal of allergy and clinical immunology · 2013
    Review
  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

6 authors at 2 institutions in 2 countries.

Noredia OjogunDepartment of Internal Medicine, University of Texas Southwestern Medical School, Dallas, TX, USA.
Tang-Yong Kuang
Baomei Shao
David R Greaves
Robert S Munford
Alan W Varley
The University of Texas Southwestern Medical Center · USUniversity of Oxford · GB

Funding

INTERACTIONS OF ENDOTOXIN WITH PLASMA AND CELLSR01AI018188 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI VARLEY, ALAN WAYNE · 1985 to 2011
$3.9M
INTERACTIONS OF ENDOTOXIN WITH PLASMA AND CELLSR37AI018188 · NIAID · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI MUNFORD, ROBERT S · 1992 to 2001
$729k
Interactions of Endotoxin with Plasma and CellsR56AI018188 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI MUNFORD, ROBERT S · 2007 to 2007
$523k
NIAID NIH HHS AI18188NIAID NIH HHS R01 AI018188NIAID NIH HHS R37 AI018188NIAID NIH HHS R56 AI018188
6 · The paper itself

Abstract

Although recognition of lipopolysaccharide (LPS) by the myeloid differentiation factor 2-Toll-like receptor 4 complex is important for triggering protective inflammatory responses in animals, terminating many of these responses requires LPS inactivation by a host lipase, acyloxyacyl hydrolase (AOAH). To test whether endogenously produced recombinant AOAH can modulate responses to LPS and gram-negative bacteria, we engineered transgenic mice that overexpress AOAH in dendritic cells and macrophages, cell types that normally produce it. Transgenic mice deacylated LPS more rapidly than did wild-type controls. They also were protected from LPS-induced hepatosplenomegaly, recovered more quickly from LPS-induced weight loss, and were more likely to survive when challenged with live Escherichia coli. Constitutive overexpression of AOAH in vivo hastened recovery from LPS exposure without interfering with the normal acute inflammatory response to this important microbial signal molecule. Our results suggest that the extent to which macrophages and dendritic cells produce AOAH may influence the outcome of many gram-negative bacterial diseases.

Indexed as

AnimalsAntibodies, MonoclonalAntigens, CDAntigens, Differentiation, MyelomonocyticCarboxylic Ester HydrolasesCD68 MoleculeDendritic CellsEnzyme InductionGram-Negative Bacterial InfectionsHepatomegalyLipopolysaccharidesLiverMacrophages, PeritonealMiceMice, Inbred C57BLMice, Transgenicacyloxyacyl hydrolaseAntibodies, MonoclonalAntigens, CDAntigens, Differentiation, MyelomonocyticCarboxylic Ester HydrolasesCD68 antigen, humanCD68 MoleculeCD68 protein, mouseLipopolysaccharidesRNA, Messenger

Identifiers

PMID19860560
PMCPMC2783937
OpenAlexW2147461100

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.