Evidence map›Paper›PMID 27594529›Full record

ArticleToxicology and applied pharmacology2016

Autophagy deficiency in macrophages enhances NLRP3 inflammasome activity and chronic lung disease following silica exposure.

Forrest Jessop, Raymond F Hamilton, Joseph F Rhoderick, Pamela K Shaw, Andrij Holian

Abstract read
In one paragraph

Article in Toxicology and applied pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 103 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. NLRP3 inflammasome in health and disease (Review).International journal of molecular medicine · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Neutrophil extracellular traps and pulmonary fibrosis: an update.Journal of inflammation (London, England) · 2023
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Autophagy in major human diseases.The EMBO journal · 2021
    Review
  19. Review
  20. Review
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.

Forrest JessopCenter for Environmental Health Sciences, University of Montana, Missoula, Montana, United States.
Raymond F HamiltonCenter for Environmental Health Sciences, University of Montana, Missoula, Montana, United States.
Joseph F RhoderickCenter for Environmental Health Sciences, University of Montana, Missoula, Montana, United States.
Pamela K ShawCenter for Environmental Health Sciences, University of Montana, Missoula, Montana, United States.
Andrij HolianCenter for Environmental Health Sciences, University of Montana, Missoula, Montana, United States. Electronic address: andrij.holian@umontana.edu.
University of Montana · USCenter for Environmental Health · US

Funding

THE ROLE OF PULMONARY SUBPOPULATIONS AND TH2 IMMUNITY IN BALB/C SILICOSIS MODELP20RR017670 · NCRR · UNIVERSITY OF MONTANA · PI ROBERTS, KEVAN · 2002 to 2011
$22.0M
Molecular Histology and Fluorescent ImagingP30GM103338 · NIGMS · UNIVERSITY OF MONTANA · PI HOLIAN, ANDRIJ · 2013 to 2017
$5.6M
Dietary DHA attenuation of nanoparticle inflammationR01ES023209 · NIEHS · UNIVERSITY OF MONTANA · PI HOLIAN, ANDRIJ · 2014 to 2018
$2.8M
Upgrade of current CompuCyte LSC??? to the CompuCyte iCys??? Laser Scanning CytomS10RR026325 · NCRR · UNIVERSITY OF MONTANA · PI ROBERTS, KEVAN · 2010 to 2010
$306k
NCRR NIH HHS P20 RR017670NCRR NIH HHS S10 RR026325NIEHS NIH HHS R01 ES023209NIGMS NIH HHS P30 GM103338
6 · The paper itself

Abstract

Autophagy is an important metabolic mechanism that can promote cellular survival following injury. The specific contribution of autophagy to silica-induced inflammation and disease is not known. The objective of these studies was to determine the effects of silica exposure on the autophagic pathway in macrophages, as well as the general contribution of autophagy in macrophages to inflammation and disease. Silica exposure enhanced autophagic activity in vitro in Bone Marrow derived Macrophages and in vivo in Alveolar Macrophages isolated from silica-exposed mice. Impairment of autophagy in myeloid cells in vivo using Atg5(fl/fl)LysM-Cre(+) mice resulted in enhanced cytotoxicity and inflammation after silica exposure compared to littermate controls, including elevated IL-18 and the alarmin HMGB1 in the whole lavage fluid. Autophagy deficiency caused some spontaneous inflammation and disease. Greater silica-induced acute inflammation in Atg5(fl/fl)LysM-Cre(+) mice correlated with increased fibrosis and chronic lung disease. These studies demonstrate a critical role for autophagy in suppressing silica-induced cytotoxicity and inflammation in disease development. Furthermore, this data highlights the importance of basal autophagy in macrophages and other myeloid cells in maintaining lung homeostasis.

Indexed as

AutophagyAnimalsFemaleHMGB1 ProteinLungMacrophages, AlveolarMaleMiceMice, TransgenicNLR Family, Pyrin Domain-Containing 3 ProteinSilicon DioxideHMGB1 ProteinHMGB1 protein, mouseNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanSilicon DioxideAtg5AutophagyHMGB1IL-18NLRP3 InflammasomeSilicosis

Identifiers

PMID27594529
PMCPMC5054752
OpenAlexW2508286724

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.