Evidence map›Paper›PMID 10377115›Full record

ArticleInfection and immunity1999

Deacylation of purified lipopolysaccharides by cellular and extracellular components of a sterile rabbit peritoneal inflammatory exudate.

Y Weinrauch, S S Katz, R S Munford, P Elsbach, J Weiss

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

13 citing papers in PubMed, 32 citations in OpenAlex.

  1. Endotoxins and Biological Implications-Review.Public health challenges · 2026
    Review
  2. Review
  3. Review
  4. Article
  5. Endotoxemia-menace, marker, or mistake?Journal of leukocyte biology · 2016
    Review
  6. Article
  7. Review
  8. Review
  9. The bactericidal/permeability-increasing protein (BPI) in infection and inflammatory disease.Clinica chimica acta; international journal of clinical chemistry · 2007
    Review
  10. Review
  11. Article
  12. Article
  13. 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

5 authors at 3 institutions in 1 country.

Y WeinrauchDepartments of Microbiology, New York University School of Medicine, New York, New York 10016, USA.
S S Katz
R S Munford
P Elsbach
J Weiss
New York University · USThe University of Texas Southwestern Medical Center · USUniversity of Iowa · US

Funding

MEDICAL SCIENTIST TRAININGT32GM007308 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI PHILIPS, MARK REID · 1985 to 2019
$23.2M
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
MICROBICIDAL ACTIVITY OF LEUKOCYTES: ACTIVE FACTORSR37DK005472 · NIDDK · NEW YORK UNIVERSITY · PI ELSBACH, PETER · 1987 to 1994
–
NIAID NIH HHS AI 18188NIAID NIH HHS R01 AI018188NIAID NIH HHS R37 AI018188NIAID NIH HHS R56 AI018188NIDDK NIH HHS R37 DK 05472NIGMS NIH HHS 5T32GM07308NIGMS NIH HHS T32 GM007308
6 · The paper itself

Abstract

The extent to which the mammalian host is capable of enzymatic degradation and detoxification of bacterial lipopolysaccharides (LPS) is still unknown. Partial deacylation of LPS by the enzyme acyloxyacyl hydrolase (AOAH) provides such a mechanism, but its participation in the disposal of LPS under physiological conditions has not been established. In this study, deacylation of isolated radiolabeled LPS by both cellular and extracellular components of a sterile inflammatory peritoneal exudate elicited in rabbits was examined ex vivo. AOAH-like activity, tested under artificial conditions (pH 5.4, 0.1% Triton X-100), was evident in all components of the exudate (mononuclear cells [MNC] > polymorphonuclear leukocytes [PMN] > inflammatory [ascitic] fluid [AF]). Under more physiological conditions, in a defined medium containing purified LPS-binding protein, the LPS-deacylating activity of MNC greatly exceeded that of PMN. In AF, MNC (but not PMN) also produced rapid and extensive CD14-dependent LPS deacylation. Under these conditions, almost all MNC-associated LPS underwent deacylation within 1 h, a rate greatly exceeding that previously found in any cell type. The remaining extracellular LPS was more slowly subject to CD14-independent deacylation in AF. Quantitative analysis showed a comparable release of laurate and myristate but no release of 3-hydroxymyristate, consistent with an AOAH-like activity. These findings suggest a major role for CD14(+) MNC and a secondary role for AF in the deacylation of cell-free LPS at extravascular inflammatory sites.

Indexed as

Peritoneal CavityAcylationAnimalsAscitic FluidBiodegradation, EnvironmentalInflammationLipopolysaccharidesRabbitsLipopolysaccharides

Identifiers

PMID10377115
PMCPMC116520
OpenAlexW1780456323

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.