Evidence map›Paper›PMID 22169929›Full record

ArticleJournal of cellular physiology2012

NALP-3 inflammasome silencing attenuates ceramide-induced transepithelial permeability.

Narasaiah Kolliputi, Lakshmi Galam, Prasanna Tamarapu Parthasarathy, Srinivas M Tipparaju, Richard F Lockey

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
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  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. The Role of NLRP3 Inflammasome in Radiation-Induced Cardiovascular Injury.Frontiers in cell and developmental biology · 2020
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Deficiency of the Purinergic Receptor 2XOxidative medicine and cellular longevity · 2017
    Article
  19. Article
  20. CORM-2 inhibits TXNIP/NLRP3 inflammasome pathway in LPS-induced acute lung injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016
    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

5 authors at 2 institutions in 1 country.

Narasaiah KolliputiDivision of Allergy and Immunology, Department of Internal Medicine, College of Medicine, University of South Florida, Tampa, Florida 33612, USA. nkollipu@health.usf.edu
Lakshmi Galam
Prasanna Tamarapu Parthasarathy
Srinivas M Tipparaju
Richard F Lockey
University of South Florida · USUniversity of Tampa · US

Funding

Molecular Mechanisms of Hyperoxic Lung InjuryR01HL105932 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI KOLLIPUTI, NARASAIAH · 2011 to 2019
$2.9M
NHLBI NIH HHS R01 HL105932
6 · The paper itself

Abstract

The hallmark of acute lung injury (ALI) is the influx of proinflammatory cytokines into lung tissue and alveolar permeability that ultimately leads to pulmonary edema. However, the mechanisms involved in inflammatory cytokine production and alveolar permeability are unclear. Recent studies suggest that excessive production of ceramide has clinical relevance as a mediator of pulmonary edema and ALI. Our earlier studies indicate that the activation of inflammasome promotes the processing and secretion of proinflammatory cytokines and causes alveolar permeability in ALI. However, the role of ceramide in inflammasome activation and the underlying mechanism in relation to alveolar permeability is not known. We hypothesized that ceramide activates the inflammasome and causes inflammatory cytokine production and alveolar epithelial permeability. To test this hypothesis, we analyzed the lung ceramide levels during hyperoxic ALI in mice. The effect of ceramide on activation of inflammasome and production of inflammatory cytokine was assessed in primary mouse alveolar macrophages and THP-1 cells. Alveolar transepithelial permeability was determined in alveolar epithelial type-II cells (AT-II) and THP-1 co-cultures. Our results reveal that ceramide causes inflammasome activation, induction of caspase-1, IL-1β cleavage, and release of proinflammatory cytokines. In addition, ceramide further induces alveolar epithelial permeability. Short-hairpin RNA silencing of inflammasome components abrogated ceramide-induced secretion of proinflammatory cytokines in vitro. Inflammasome silencing abolishes ceramide-induced alveolar epithelial permeability in AT-II. Collectively, our results demonstrate for the first time that ceramide-induced secretion of proinflammatory cytokines and alveolar epithelial permeability occurs though inflammasome activation.

Indexed as

Acute Lung InjuryAnimalsCarrier ProteinsCells, CulturedCeramidesCytokinesDose-Response Relationship, DrugEpithelial CellsGene Expression RegulationHyperoxiaInflammationMacrophages, AlveolarMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinOxygenCarrier ProteinsCeramidesCytokinesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanOxygenRNA, Small Interfering

Identifiers

PMID22169929
PMCPMC3323724
OpenAlexW1999680418

What OpenQuestion holds

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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.