Evidence map›Paper›PMID 22364946›Full record

ArticleMolecular immunology2012

Reduced oxidative tissue damage during endotoxemia in IRAK-1 deficient mice.

Neeraj Singh, Liwu Li

Open access · greenAbstract read
In one paragraph

Article in Molecular immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

  1. Deciphering the Inflammatory Network in Pediatric Recurrent Tonsillitis: The Role of TRAF6, IRAK1, and miR-146a-5p.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2026
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  8. PIM1 inhibition attenuated endotoxin-induced acute lung injury through modulating ELK3/ICAM1 axis on pulmonary microvascular endothelial cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Article
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  10. Advances in the Study of the Potential Hepatotoxic Components and Mechanism ofEvidence-based complementary and alternative medicine : eCAM · 2020
    Review
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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

2 authors at 1 institution in 1 country.

Neeraj SinghDepartment of Biomedical Sciences & Pathobiology, Virginia Tech, Blacksburg, VA 24061, United States.
Liwu Li
Virginia Tech · US

Funding

The novel role and regulation of IRAK in innate immunityR01AI064414 · NIAID · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LI, LIWU · 2005 to 2010
$1.9M
Regulation of signaling events in septic leukocytesR01AI050089 · NIAID · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LI, LIWU · 2002 to 2006
$1.5M
NIAID NIH HHS R01 AI050089NIAID NIH HHS R01 AI064414
6 · The paper itself

Abstract

The generation of reactive oxygen species (ROS) triggered by bacterial endotoxin lipopolysaccharide (LPS) plays a key role during the pathogenesis of sepsis. Given the key role that the interleukin-1 receptor associated kinase-1 (IRAK-1) plays in LPS-mediated Toll-like-receptor 4 (TLR4) pathway, we herein tested whether deletion of IRAK-1 gene in mice may render protection from LPS-induced oxidative tissue damage. In this report, we studied the levels of oxidative stress in vital organs including liver, kidney, and brain from wild type (WT) and IRAK-1 deficient mice injected with a lethal dose of LPS (25mg/kg), a TLR4-specific agonist. We demonstrated that LPS challenge induced marked elevation of lipid peroxidation and nitrite levels in the plasma and tissues of WT mice, as well as elevated pro-inflammatory mediators. In contrast, IRAK-1 deficient mice had significantly lower lipid peroxidation and nitrite levels, as well as lower levels of pro-inflammatory mediators. Mechanistically, LPS triggered higher levels of iNOS activity and elevated membrane translocation of p47(phox), a key component of NADPH oxidase in immune cell derived from WT mice compared to IRAK-1 deficient mice. Additionally, tissues harvested from WT mice injected with LPS exhibited reduced activities of anti-oxidant enzymes including glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD). In contrast, LPS challenge failed to reduce the activities of GPx and SOD in IRAK-1 deficient tissues. As a consequence, LPS caused significantly pronounced damage to liver and kidney tissues in WT mice as compared to IRAK-1 deficient mice.

Indexed as

AnimalsEndotoxemiaInterleukin-1 Receptor-Associated KinasesLipid PeroxidationMiceMice, Inbred C57BLMice, KnockoutOxidative StressReactive Oxygen SpeciesReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionInterleukin-1 Receptor-Associated KinasesReactive Oxygen Species

Identifiers

PMID22364946
PMCPMC4440666
OpenAlexW1994112020

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.