Evidence map›Paper›PMID 27650313›Full record

ReviewParticle and fibre toxicology2016

The NLRP3 inflammasome in pathogenic particle and fibre-associated lung inflammation and diseases.

Mutlay Sayan, Brooke T Mossman

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Particle and fibre toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed, 1 pooled it
6.8field-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

141 citing papers in PubMed, 1 synthesis or guideline pooled it, 294 citations in OpenAlex.

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81 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

2 authors at 1 institution in 1 country.

Mutlay SayanDepartment of Medicine, University of Vermont College of Medicine, 111 Colchester Avenue, Burlington, 05401, VT, USA.
Brooke T MossmanDepartment of Pathology and Laboratory Medicine, University of Vermont College of Medicine, 89 Beaumont Avenue, Burlington, 05405, VT, USA. brooke.mossman@uvm.edu.
University of Vermont · US

Funding

SIGNALING IN EPITHELIAL INJURY, PROLIFERATION &FIBROSISP01HL067004 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI MOSSMAN, BROOKE TAYLOR · 2001 to 2005
$7.6M
ENVIRONMENTAL PATHOLOGY TRAINING PROGRAMT32ES007122 · NIEHS · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI VAN DER VLIET, ALBERT · 1985 to 2012
$4.2M
NHLBI NIH HHS P01 HL067004NIEHS NIH HHS T32 ES007122
6 · The paper itself

Abstract

The concept of the inflammasome, a macromolecular complex sensing cell stress or danger signals and initiating inflammation, was first introduced approximately a decade ago. Priming and activation of these intracellular protein platforms trigger the maturation of pro-inflammatory chemokines and cytokines, most notably, interleukin-1β (IL-1β) and IL-18, to promulgate innate immune defenses. Although classically studied in models of gout, Type II diabetes, Alzheimer's disease, and multiple sclerosis, the importance and mechanisms of action of inflammasome priming and activation have recently been elucidated in cells of the respiratory tract where they modulate the responses to a number of inhaled pathogenic particles and fibres. Most notably, inflammasome activation appears to regulate the balance between tissue repair and inflammation after inhalation of pathogenic pollutants such as asbestos, crystalline silica (CS), and airborne particulate matter (PM). Different types of fibres and particles may have distinct mechanisms of inflammasome interaction and outcome. This review summarizes the structure and function of inflammasomes, the interplay between various chemokines and cytokines and cell types of the lung and pleura after inflammasome activation, and the events leading to the development of non-malignant (allergic airway disease and chronic obstructive pulmonary disease (COPD), asbestosis, silicosis) and malignant (mesothelioma, lung cancer) diseases by pathogenic particulates. In addition, it emphasizes the importance of communication between cells of the immune system, target cells of these diseases, and components of the extracellular matrix (ECM) in regulation of inflammasome-mediated events.

Indexed as

AnimalsHumansInflammasomesLung DiseasesNLR Family, Pyrin Domain-Containing 3 ProteinParticulate MatterPneumoniaSilicon DioxideInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinParticulate MatterSilicon DioxideAirborne particulate matterAllergic airway diseaseAsbestosFibrosisInflammationLung cancerMesotheliomaNanotubesSilica

Identifiers

PMID27650313
PMCPMC5029018
OpenAlexW2521751481

What OpenQuestion holds

Textmetadata
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.