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

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 cyto...

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Autores principales: Sayan, Mutlay, Mossman, Brooke T.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5029018/
https://www.ncbi.nlm.nih.gov/pubmed/27650313
http://dx.doi.org/10.1186/s12989-016-0162-4
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author Sayan, Mutlay
Mossman, Brooke T.
author_facet Sayan, Mutlay
Mossman, Brooke T.
author_sort Sayan, Mutlay
collection PubMed
description 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.
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spelling pubmed-50290182016-09-27 The NLRP3 inflammasome in pathogenic particle and fibre-associated lung inflammation and diseases Sayan, Mutlay Mossman, Brooke T. Part Fibre Toxicol Review 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. BioMed Central 2016-09-20 /pmc/articles/PMC5029018/ /pubmed/27650313 http://dx.doi.org/10.1186/s12989-016-0162-4 Text en © The Author(s). 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Review
Sayan, Mutlay
Mossman, Brooke T.
The NLRP3 inflammasome in pathogenic particle and fibre-associated lung inflammation and diseases
title The NLRP3 inflammasome in pathogenic particle and fibre-associated lung inflammation and diseases
title_full The NLRP3 inflammasome in pathogenic particle and fibre-associated lung inflammation and diseases
title_fullStr The NLRP3 inflammasome in pathogenic particle and fibre-associated lung inflammation and diseases
title_full_unstemmed The NLRP3 inflammasome in pathogenic particle and fibre-associated lung inflammation and diseases
title_short The NLRP3 inflammasome in pathogenic particle and fibre-associated lung inflammation and diseases
title_sort nlrp3 inflammasome in pathogenic particle and fibre-associated lung inflammation and diseases
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5029018/
https://www.ncbi.nlm.nih.gov/pubmed/27650313
http://dx.doi.org/10.1186/s12989-016-0162-4
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