Evidence map›Paper›PMID 21170027›Full record

ArticleNature immunology2011

IL-1β-driven neutrophilia preserves antibacterial defense in the absence of the kinase IKKβ.

Li-Chung Hsu, Thomas Enzler, Jun Seita, Anjuli M Timmer, Chih-Yuan Lee, Ting-Yu Lai, Guann-Yi Yu, Liang-Chuan Lai, Vladislav Temkin, Ursula Sinzig and 4 more

Open access · greenAbstract read
In one paragraph

Article in Nature immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

78 citing papers in PubMed, 116 citations in OpenAlex.

  1. Article
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  8. Divergent functions of NLRP3 inflammasomes in cancer: a review.Cell communication and signaling : CCS · 2023
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18 more citing papers are in PubMed but not listed here.

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

14 authors at 4 institutions in 3 countries.

Li-Chung HsuInstitute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan. lichunghsu@ntu.edu.tw
Thomas Enzler
Jun Seita
Anjuli M Timmer
Chih-Yuan Lee
Ting-Yu Lai
Guann-Yi Yu
Liang-Chuan Lai
Vladislav Temkin
Ursula Sinzig
Thiha Aung
Victor Nizet
Irving L Weissman
Michael Karin
University of California, San Diego · USNational Taiwan University · TWStanford University · USUniversitätsmedizin Göttingen · DE

Funding

Interrogation of individual cells to identify progenitors and their nichesU01HL099999 · NHLBI · STANFORD UNIVERSITY · PI WEISSMAN, IRVING L. · 2009 to 2015
$7.8M
REGULATION OF NFKB AND IKK BY PROINFLAMMATORY STIMULIR01AI043477 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KARIN, MICHAEL · 1998 to 2017
$7.4M
Interrogation of individual cells to identify progenitor cells and their nichesU01HL099995 · NHLBI · STANFORD UNIVERSITY · PI KRASNOW, MARK A · 2009 to 2015
$7.0M
HSC Diversity: Regulation by Clonal Selection vs Epigenetic InductionR01CA086065 · NCI · STANFORD UNIVERSITY · PI WEISSMAN, IRVING L. · 2000 to 2017
$6.9M
NF-kappaB and Mitochondrial Signals as Positive and Negative Regulators of InflammationR37AI043477 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Michael Karin · 2018 to 2026
$6.0M
GAS Switch from Colonizing Bacterium to Invasive PathogenR01AI077780 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI NIZET, VICTOR · 2008 to 2019
$3.8M
NCI NIH HHS R01 CA086065NHLBI NIH HHS U01 HL099995NHLBI NIH HHS U01 HL099999NHLBI NIH HHS U01HL099999-02NIAID NIH HHS AI043477NIAID NIH HHS AI77780NIAID NIH HHS R01 AI043477NIAID NIH HHS R01 AI077780NIAID NIH HHS R37 AI043477
6 · The paper itself

Abstract

Transcription factor NF-κB and its activating kinase IKKβ are associated with inflammation and are believed to be critical for innate immunity. Despite the likelihood of immune suppression, pharmacological blockade of IKKβ-NF-κB has been considered as a therapeutic strategy. However, we found neutrophilia in mice with inducible deletion of IKKβ (Ikkβ(Δ) mice). These mice had hyperproliferative granulocyte-macrophage progenitors and pregranulocytes and a prolonged lifespan of mature neutrophils that correlated with the induction of genes encoding prosurvival molecules. Deletion of interleukin 1 receptor 1 (IL-1R1) in Ikkβ(Δ) mice normalized blood cellularity and prevented neutrophil-driven inflammation. However, Ikkβ(Δ)Il1r1(-/-) mice, unlike Ikkβ(Δ) mice, were highly susceptible to bacterial infection, which indicated that signaling via IKKβ-NF-κB or IL-1R1 can maintain antimicrobial defenses in each other's absence, whereas inactivation of both pathways severely compromises innate immunity.

Indexed as

AnimalsBacterial InfectionsCell CountCell Growth ProcessesCells, CulturedCell SurvivalDisease SusceptibilityGranulocyte-Macrophage Progenitor CellsI-kappa B KinaseImmunity, InnateInterleukin-1betaMiceMice, Inbred C57BLMice, KnockoutMicroarray AnalysisNeutrophilsI-kappa B KinaseIkbkb protein, mouseInterleukin-1betaReceptors, Interleukin-1 Type I

Identifiers

PMID21170027
PMCPMC3677078
OpenAlexW2125867335

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.