Centrality of Myeloid-Lineage Phagocytes in Particle-Triggered Inflammation and Autoimmunity

Exposure to exogenous particles found as airborne contaminants or endogenous particles that form by crystallization of certain nutrients can activate inflammatory pathways and potentially accelerate autoimmunity onset and progression in genetically predisposed individuals. The first line of innate i...

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Autores principales:	Olivia K. Favor, James J. Pestka, Melissa A. Bates, Kin Sing Stephen Lee
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	endogenous and exogenous particles inflammation autoimmunity myeloid-lineage phagocytes inflammasome activity immunogenic cell death Toxicology. Poisons RA1190-1270
Acceso en línea:	https://doaj.org/article/55e5c7e59e9f484fa950481215ed62a6
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spelling	oai:doaj.org-article:55e5c7e59e9f484fa950481215ed62a62021-11-04T08:03:46ZCentrality of Myeloid-Lineage Phagocytes in Particle-Triggered Inflammation and Autoimmunity2673-308010.3389/ftox.2021.777768https://doaj.org/article/55e5c7e59e9f484fa950481215ed62a62021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/ftox.2021.777768/fullhttps://doaj.org/toc/2673-3080Exposure to exogenous particles found as airborne contaminants or endogenous particles that form by crystallization of certain nutrients can activate inflammatory pathways and potentially accelerate autoimmunity onset and progression in genetically predisposed individuals. The first line of innate immunological defense against particles are myeloid-lineage phagocytes, namely macrophages and neutrophils, which recognize/internalize the particles, release inflammatory mediators, undergo programmed/unprogrammed death, and recruit/activate other leukocytes to clear the particles and resolve inflammation. However, immunogenic cell death and release of damage-associated molecules, collectively referred to as “danger signals,” coupled with failure to efficiently clear dead/dying cells, can elicit unresolved inflammation, accumulation of self-antigens, and adaptive leukocyte recruitment/activation. Collectively, these events can promote loss of immunological self-tolerance and onset/progression of autoimmunity. This review discusses critical molecular mechanisms by which exogenous particles (i.e., silica, asbestos, carbon nanotubes, titanium dioxide, aluminum-containing salts) and endogenous particles (i.e., monosodium urate, cholesterol crystals, calcium-containing salts) may promote unresolved inflammation and autoimmunity by inducing toxic responses in myeloid-lineage phagocytes with emphases on inflammasome activation and necrotic and programmed cell death pathways. A prototypical example is occupational exposure to respirable crystalline silica, which is etiologically linked to systemic lupus erythematosus (SLE) and other human autoimmune diseases. Importantly, airway instillation of SLE-prone mice with crystalline silica elicits severe pulmonary pathology involving accumulation of particle-laden alveolar macrophages, dying and dead cells, nuclear and cytoplasmic debris, and neutrophilic inflammation that drive cytokine, chemokine, and interferon-regulated gene expression. Silica-induced immunogenic cell death and danger signal release triggers accumulation of T and B cells, along with IgG-secreting plasma cells, indicative of ectopic lymphoid tissue neogenesis, and broad-spectrum autoantibody production in the lung. These events drive early autoimmunity onset and accelerate end-stage autoimmune glomerulonephritis. Intriguingly, dietary supplementation with ω-3 fatty acids have been demonstrated to be an intervention against silica-triggered murine autoimmunity. Taken together, further insight into how particles drive immunogenic cell death and danger signaling in myeloid-lineage phagocytes and how these responses are influenced by the genome will be essential for identification of novel interventions for preventing and treating inflammatory and autoimmune diseases associated with these agents.Olivia K. FavorOlivia K. FavorJames J. PestkaJames J. PestkaJames J. PestkaMelissa A. BatesMelissa A. BatesKin Sing Stephen LeeKin Sing Stephen LeeKin Sing Stephen LeeFrontiers Media S.A.articleendogenous and exogenous particlesinflammationautoimmunitymyeloid-lineage phagocytesinflammasome activityimmunogenic cell deathToxicology. PoisonsRA1190-1270ENFrontiers in Toxicology, Vol 3 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	endogenous and exogenous particles inflammation autoimmunity myeloid-lineage phagocytes inflammasome activity immunogenic cell death Toxicology. Poisons RA1190-1270
spellingShingle	endogenous and exogenous particles inflammation autoimmunity myeloid-lineage phagocytes inflammasome activity immunogenic cell death Toxicology. Poisons RA1190-1270 Olivia K. Favor Olivia K. Favor James J. Pestka James J. Pestka James J. Pestka Melissa A. Bates Melissa A. Bates Kin Sing Stephen Lee Kin Sing Stephen Lee Kin Sing Stephen Lee Centrality of Myeloid-Lineage Phagocytes in Particle-Triggered Inflammation and Autoimmunity
description	Exposure to exogenous particles found as airborne contaminants or endogenous particles that form by crystallization of certain nutrients can activate inflammatory pathways and potentially accelerate autoimmunity onset and progression in genetically predisposed individuals. The first line of innate immunological defense against particles are myeloid-lineage phagocytes, namely macrophages and neutrophils, which recognize/internalize the particles, release inflammatory mediators, undergo programmed/unprogrammed death, and recruit/activate other leukocytes to clear the particles and resolve inflammation. However, immunogenic cell death and release of damage-associated molecules, collectively referred to as “danger signals,” coupled with failure to efficiently clear dead/dying cells, can elicit unresolved inflammation, accumulation of self-antigens, and adaptive leukocyte recruitment/activation. Collectively, these events can promote loss of immunological self-tolerance and onset/progression of autoimmunity. This review discusses critical molecular mechanisms by which exogenous particles (i.e., silica, asbestos, carbon nanotubes, titanium dioxide, aluminum-containing salts) and endogenous particles (i.e., monosodium urate, cholesterol crystals, calcium-containing salts) may promote unresolved inflammation and autoimmunity by inducing toxic responses in myeloid-lineage phagocytes with emphases on inflammasome activation and necrotic and programmed cell death pathways. A prototypical example is occupational exposure to respirable crystalline silica, which is etiologically linked to systemic lupus erythematosus (SLE) and other human autoimmune diseases. Importantly, airway instillation of SLE-prone mice with crystalline silica elicits severe pulmonary pathology involving accumulation of particle-laden alveolar macrophages, dying and dead cells, nuclear and cytoplasmic debris, and neutrophilic inflammation that drive cytokine, chemokine, and interferon-regulated gene expression. Silica-induced immunogenic cell death and danger signal release triggers accumulation of T and B cells, along with IgG-secreting plasma cells, indicative of ectopic lymphoid tissue neogenesis, and broad-spectrum autoantibody production in the lung. These events drive early autoimmunity onset and accelerate end-stage autoimmune glomerulonephritis. Intriguingly, dietary supplementation with ω-3 fatty acids have been demonstrated to be an intervention against silica-triggered murine autoimmunity. Taken together, further insight into how particles drive immunogenic cell death and danger signaling in myeloid-lineage phagocytes and how these responses are influenced by the genome will be essential for identification of novel interventions for preventing and treating inflammatory and autoimmune diseases associated with these agents.
format	article
author	Olivia K. Favor Olivia K. Favor James J. Pestka James J. Pestka James J. Pestka Melissa A. Bates Melissa A. Bates Kin Sing Stephen Lee Kin Sing Stephen Lee Kin Sing Stephen Lee
author_facet	Olivia K. Favor Olivia K. Favor James J. Pestka James J. Pestka James J. Pestka Melissa A. Bates Melissa A. Bates Kin Sing Stephen Lee Kin Sing Stephen Lee Kin Sing Stephen Lee
author_sort	Olivia K. Favor
title	Centrality of Myeloid-Lineage Phagocytes in Particle-Triggered Inflammation and Autoimmunity
title_short	Centrality of Myeloid-Lineage Phagocytes in Particle-Triggered Inflammation and Autoimmunity
title_full	Centrality of Myeloid-Lineage Phagocytes in Particle-Triggered Inflammation and Autoimmunity
title_fullStr	Centrality of Myeloid-Lineage Phagocytes in Particle-Triggered Inflammation and Autoimmunity
title_full_unstemmed	Centrality of Myeloid-Lineage Phagocytes in Particle-Triggered Inflammation and Autoimmunity
title_sort	centrality of myeloid-lineage phagocytes in particle-triggered inflammation and autoimmunity
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/55e5c7e59e9f484fa950481215ed62a6
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Centrality of Myeloid-Lineage Phagocytes in Particle-Triggered Inflammation and Autoimmunity

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