Evidence map›Paper›PMID 21913925›Full record

ArticleJournal of neurochemistry2011

Inflammasome activation and IL-1β/IL-18 processing are influenced by distinct pathways in microglia.

Richa Hanamsagar, Victor Torres, Tammy Kielian

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neurochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% 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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 157 citations in OpenAlex.

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  9. Hydrogen Sulfide (HAntioxidants (Basel, Switzerland) · 2025
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25 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

3 authors at 2 institutions in 1 country.

Richa HanamsagarDepartment of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska 68198, USA.
Victor Torres
Tammy Kielian
University of Nebraska Medical Center · USNew York University · US

Funding

Receptors Involved in Microglial Responses to S. aureusR01NS055385 · NINDS · UNIV OF ARKANSAS FOR MED SCIS · PI KIELIAN, TAMMY L · 2007 to 2010
$1.1M
NINDS NIH HHS 2R01 NS055385NINDS NIH HHS R01 NS055385
6 · The paper itself

Abstract

Microglia are important innate immune effectors against invading CNS pathogens, such as Staphylococcus aureus (S. aureus), a common etiological agent of brain abscesses typified by widespread inflammation and necrosis. The NLRP3 inflammasome is a protein complex involved in IL-1β and IL-18 processing following exposure to both pathogen- and danger-associated molecular patterns. Although previous studies from our laboratory have established that IL-1β is a major cytokine product of S. aureus-activated microglia and is pivotal for eliciting protective anti-bacterial immunity during brain abscess development, the molecular machinery responsible for cytokine release remains to be determined. Therefore, the functional role of the NLRP3 inflammasome and its adaptor protein apoptosis-associated speck-like protein (ASC) in eliciting IL-1β and IL-18 release was examined in primary microglia. Interestingly, we found that IL-1β, but not IL-18 production, was significantly attenuated in both NLRP3 and ASC knockout microglia following exposure to live S. aureus. NLRP3 inflammasome activation was partially dependent on autocrine/paracrine ATP release and α- and γ-hemolysins produced by live bacteria. A cathepsin B inhibitor attenuated IL-β release from NLRP3 and ASC knockout microglia, demonstrating the existence of alternative inflammasome-independent mechanisms for IL-1β processing. In contrast, microglial IL-18 secretion occurred independently of cathepsin B and inflammasome action. Collectively, these results demonstrate that microglial IL-1β processing is regulated by multiple pathways and diverges from mechanisms utilized for IL-18 cleavage. Understanding the molecular events that regulate IL-1β production is important for modulating this potent proinflammatory cytokine during CNS disease.

Indexed as

Adenosine TriphosphateAnimalsAnimals, NewbornApoptosis Regulatory ProteinsBacterial ProteinsBacterial ToxinsCARD Signaling Adaptor ProteinsCarrier ProteinsCells, CulturedCell SurvivalCerebral CortexCytoskeletal ProteinsDose-Response Relationship, DrugDrug InteractionsEnzyme InhibitorsEnzyme-Linked Immunosorbent AssayAdenosine TriphosphateApoptosis Regulatory ProteinsAZ 11645373Bacterial ProteinsBacterial ToxinsCARD Signaling Adaptor ProteinsCarrier ProteinsCytoskeletal ProteinsEnzyme Inhibitorsgamma-hemolysin, Staphylococcus aureusHemolysin ProteinsInterleukin-18Interleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousePurinergic P2 Receptor AntagonistsPycard protein, mousestaphylococcal alpha-toxinThiazoles

Identifiers

PMID21913925
PMCPMC3202981
OpenAlexW1502842924

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.