Evidence map›Paper›PMID 35481682›Full record

ArticleJournal of leukocyte biology2022

T-Cell Activation and LPS: A Dangerous Duo for Organ Dysfunction.

Austin W Kerr, Philip A Efron, Shawn D Larson, Jaimar C Rincon

Open access · greenAbstract readEditorialComment
In one paragraph

Article in Journal of leukocyte biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.0field-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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Austin W KerrSepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, FL.
Philip A EfronSepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, FL.
Shawn D LarsonSepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, FL.
Jaimar C RinconSepsis and Critical Illness Research Center, Department of Surgery, University of Florida College of Medicine, Gainesville, FL.
University of Florida · USFlorida College · US

Funding

Molecular Biology in Burns and TraumaT32GM008721 · NIGMS · UNIVERSITY OF FLORIDA · PI Philip A Efron · 1999 to 2026
$5.0M
Novel Mechanisms and Approaches to Treat Neonatal SepsisR01GM097531 · NIGMS · UNIVERSITY OF FLORIDA · PI LARSON, SHAWN DAVID, MOLDAWER, LYLE L · 2011 to 2018
$2.3M
Prevention of Neonatal Sepsis by Therapeutic Targeting of MDSCsR01GM143143 · NIGMS · UNIVERSITY OF FLORIDA · PI LARSON, SHAWN DAVID · 2022 to 2025
$1.5M
NIGMS NIH HHS R01 GM097531NIGMS NIH HHS R01 GM143143NIGMS NIH HHS T32 GM008721
6 · The paper itself

Abstract

Lipopolysaccharide (LPS), one of the main components of cell membranes in gram-negative bacteria, is commonly used to promote inflammation-induced organ dysfunction. In the TLR4/LPS pathway, LPS binding protein and CD14 enable lipid A of LPS to be recognized by the TLR4-MD2 receptor complex. The intracellular domain of the TLR4/LPS complex stimulates MyD88-dependent/independent and TRIF-dependent pathways, which in turn activate NF-B and IRF3, leading to subsequent production of pro-inflammatory mediators. LPS has been demonstrated to induce microcirculatory disturbances via promotion of leukocyte adhesion to the vascular endothelium and the release of reactive oxygen species (ROS), damaging the vessels and causing vascular dysfunction. Thus, LPS is frequently used as a systemic model of inflammation as LPS administration increases circulating pro-inflammatory mediators, which triggers leukocyte adhesion and leads to multi-organ failure and death.

Indexed as

LipopolysaccharidesToll-Like Receptor 4HumansInflammationInflammation MediatorsMicrocirculationMultiple Organ FailureMyeloid Differentiation Factor 88Signal TransductionT-LymphocytesInflammation MediatorsLipopolysaccharidesMyeloid Differentiation Factor 88Toll-Like Receptor 4

Identifiers

PMID35481682
PMCPMC12500235
OpenAlexW4225004714

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.