Evidence map›Paper›PMID 11254563›Full record

ArticleInfection and immunity2001

Critical role of CD14 for production of proinflammatory cytokines and cytokine inhibitors during sepsis with failure to alter morbidity or mortality.

S J Ebong, S M Goyert, J A Nemzek, J Kim, G L Bolgos, D G Remick

Abstract read
In one paragraph

Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

20 citing papers in PubMed, 47 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
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  5. Article
  6. CD14 signaling mediates lung immunopathology and mice mortality induced by Achromobacter xylosoxidans.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Article
  7. Article
  8. Article
  9. Perspectives for Monocyte/Macrophage-Based Diagnostics of Chronic Inflammation.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2016
    Review
  10. Article
  11. Review
  12. Protein kinase G oxidation is a major cause of injury during sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  13. Article
  14. Interleukin 5 is protective during sepsis in an eosinophil-independent manner.American journal of respiratory and critical care medicine · 2012
    Article
  15. Article
  16. Article
  17. Sepsis, apoptosis and complement.Biochemical pharmacology · 2008
    Review
  18. Article
  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 1 country.

S J EbongDepartment of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48109-0602, USA.
S M Goyert
J A Nemzek
J Kim
G L Bolgos
D G Remick
University of Michigan–Ann Arbor · USNorth Shore University Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We investigated the immunopathophysiologic responses during sepsis induced by cecal ligation and puncture (CLP) in CD4-deficient (CD14 knockout [CD14KO]) mice. Our studies were designed to specifically test the role of CD14 in the inflammatory response to sepsis and to ascertain if alterations would improve morbidity or mortality. Sepsis was induced using the CLP model with appropriate antibiotic treatment. The severity of sepsis increased in the CD14KO mice with increasing puncture size (18 gauge [18G], 21G, and 25G). Following CLP, body temperature (at 12 h) and gross motor activity levels of the sham and 25G CLP groups recovered to normal, while the 21G and 18G CLP groups exhibited severe hypothermia coupled with decreased gross motor activity and body weight. There were no significant differences in survival, temperature, body weight, or activity levels between CD14KO and control mice after 21G CLP. However, CD14KO mice expressed two- to fourfold less pro-inflammatory (interleukin-1beta [IL-1beta], tumor necrosis factor [TNF], and IL-6) and anti-inflammatory (IL-10, IL-1 receptor antagonist, and TNF receptors I and II) cytokines in the blood after 21G CLP. Plasma levels of the chemokines macrophage inflammatory protein 2alpha and KC were similarly reduced in CD14KO mice. A similar trend of decreased cytokine and cytokine inhibitor levels was observed in the peritoneal cavity of CD14KO mice. Our results indicate that the CD14 pathway of activation plays a critical role in the production of both pro-inflammatory cytokines and cytokine inhibitors but has minimal impact on the morbidity or mortality induced by the CLP model of sepsis.

Indexed as

AnimalsBody TemperatureChemokinesCytokinesInterleukin 1 Receptor Antagonist ProteinLipopolysaccharide ReceptorsMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMotor ActivityReceptors, Tumor Necrosis FactorSepsisSialoglycoproteinsChemokinesCytokinesIl1rn protein, mouseInterleukin 1 Receptor Antagonist ProteinLipopolysaccharide ReceptorsReceptors, Tumor Necrosis FactorSialoglycoproteins

Identifiers

PMID11254563
PMCPMC98135
OpenAlexW2063398521

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.