Evidence map›Paper›PMID 24915862›Full record

ArticleParticle and fibre toxicology2014

Inflammasome activation in airway epithelial cells after multi-walled carbon nanotube exposure mediates a profibrotic response in lung fibroblasts.

Salik Hussain, Stacey Sangtian, Shamika M Anderson, Ryan J Snyder, Jamie D Marshburn, Annette B Rice, James C Bonner, Stavros Garantziotis

Open access · goldAbstract read
In one paragraph

Article in Particle and fibre toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

62 citing papers in PubMed, 133 citations in OpenAlex.

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  8. Nanomaterial-induced pyroptosis: a cell type-specific perspective.Frontiers in cell and developmental biology · 2023
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  10. The role of lysosome in regulated necrosis.Acta pharmaceutica Sinica. B · 2020
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  18. Increased HIF-1Oxidative medicine and cellular longevity · 2019
    Article
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2 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

8 authors at 3 institutions in 1 country.

Salik HussainClinical Research Unit, National Institute of Environmental Health Sciences (NIEHS)/National Institute of Health (NIH), Research Triangle Park, Durham, NC, USA. salik.hussain@nih.gov.
Stacey Sangtian
Shamika M Anderson
Ryan J Snyder
Jamie D Marshburn
Annette B Rice
James C Bonner
Stavros Garantziotis
National Institutes of Health · USNational Institute of Environmental Health Sciences · USNorth Carolina State University · US

Funding

Program in Clinical Research, Clinical Support Services and Clinical TrainingZIDES102465 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI KIRSCHNER, LAWRENCE · 2009 to 2025
$84.7M
The Role of Hyaluronan And Inter-Alpha-Trypsin Inhibitor in Tissue InjuryZIAES102605 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI GARANTZIOTIS, STAVROS · 2009 to 2025
$22.6M
Genetic Susceptibility to Nanoparticle-Induced Respiratory DiseaseR01ES020897 · NIEHS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI BONNER, JAMES CHRISTOPHER · 2012 to 2017
$1.7M
Intramural NIH HHSNIEHS NIH HHS R01 ES020897NIEHS NIH HHS R01-ES020897
6 · The paper itself

Abstract

backgroundIn vivo studies have demonstrated the ability of multi-walled carbon nanotubes (MWCNT) to induce airway remodeling, a key feature of chronic respiratory diseases like asthma and chronic obstructive pulmonary disease. However, the mechanism leading to remodeling is poorly understood. Particularly, there is limited insight about the role of airway epithelial injury in these changes.

objectivesWe investigated the mechanism of MWCNT-induced primary human bronchial epithelial (HBE) cell injury and its contribution in inducing a profibrotic response.

methodsPrimary HBE cells were exposed to thoroughly characterized MWCNTs (1.5-24 μg/mL equivalent to 0.37-6.0 μg/cm2) and MRC-5 human lung fibroblasts were exposed to 1:4 diluted conditioned medium from these cells. Flow cytometry, ELISA, immunostainings/immunoblots and PCR analyses were employed to study cellular mechanisms.

resultsMWCNT induced NLRP3 inflammasome dependent pyroptosis in HBE cells in a time- and dose-dependent manner. Cell death and cytokine production were significantly reduced by antioxidants, siRNA to NLRP3, a caspase-1 inhibitor (z-WEHD-FMK) or a cathepsin B inhibitor (CA-074Me). Conditioned medium from MWCNT-treated HBE cells induced significant increase in mRNA expression of pro-fibrotic markers (TIMP-1, Tenascin-C, Procollagen 1, and Osteopontin) in human lung fibroblasts, without a concomitant change in expression of TGF-beta. Induction of pro-fibrotic markers was significantly reduced when IL-1β, IL-18 and IL-8 neutralizing antibodies were added to the conditioned medium or when conditioned medium from NLRP3 siRNA transfected HBE cells was used.

conclusionsTaken together these results demonstrate induction of a NLRP3 inflammasome dependent but TGF-beta independent pro-fibrotic response after MWCNT exposure.

Indexed as

AntioxidantsApoptosisCulture Media, ConditionedEnzyme-Linked Immunosorbent AssayEpithelial CellsFibroblastsFlow CytometryHumansImmunohistochemistryInflammationNanotubes, CarbonPulmonary FibrosisReactive Oxygen SpeciesRNA, MessengerSuspensionsAntioxidantsCulture Media, ConditionedNanotubes, CarbonReactive Oxygen SpeciesRNA, MessengerSuspensions

Identifiers

PMID24915862
PMCPMC4067690
OpenAlexW2119035575

What OpenQuestion holds

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LicenceCC BY
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.