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. 2018 May 28:9:1157.
doi: 10.3389/fimmu.2018.01157. eCollection 2018.

Systematic Overview of Solid Particles and Their Host Responses

Fei Shu  1   2 , Yan Shi  1   3
Affiliations

Systematic Overview of Solid Particles and Their Host Responses

Fei Shu et al. Front Immunol. .

Abstract

Crystalline/particulate substances trigger a plethora of signaling events in host cells. The most prominent consequence is the inflammatory reactions that underlie crystal arthropathies, such as gout and pseudogout. However, their impact on our health was underestimated. Recent work on the role of cholesterol crystal in the development of atherosclerosis and the harm of environmental particulates has set up new frontiers in our defense against their detrimental effects. On the other hand, in the last 100 years, crystalline/particulate substances have been used with increasing frequencies in our daily lives as a part of new industrial manufacturing and engineering. Importantly, they have become a tool in modern medicine, used as vaccine adjuvants and drug delivery vehicles. Their biological effects are also being dissected in great detail, particularly with regard to their inflammatory signaling pathways. Solid structure interaction with host cells is far from being uniform, with outcomes dependent on cell types and chemical/physical properties of the particles involved. In this review, we offer a systematic and broad outlook of this landscape and a sage analysis of the complex nature of this topic.

Keywords: adjuvant; biological crystal; cell death; host response; solid particle.

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Figures

Figure 1
Figure 1
Overview of reactive oxygen species (ROS) implicated in solid particle-induced cell death and NACHT, LRR, PYD domains-containing protein 3 (NLRP3) inflammasome activation. Solid particle treatment causes mitochondrial stress and ROS production. The oxidative stress mediates the damage of DNA, proteins, and lipids, which may be an important cause of cytotoxicity. ROS production also induces NLRP3 inflammasome activation by dissociating thioredoxin-interacting protein (TXNIP) from thioredoxin then allows its binding to NLRP3, which leads to NLRP3 activation.
Figure 2
Figure 2
Overview of three major hypotheses of solid particle-induced cell death. In addition to cell death related to reactive oxygen species production, there are three major proposals on solid particle-induced cell death. The first is through receptor-interacting serine/threonine-protein kinase 1/3 (RIPK1/RIPK3)-mixed lineage kinase domain-like (MLKL)-driven necroptosis, which was found in calcium oxalate, monosodium urate (MSU), calcium pyrophosphate dihydrate (CPPD), cystine, TiO2, and calcium phosphate-treated epithelial cells and neutrophils. The second is through K+ efflux-activated NACHT, LRR, PYD domains-containing protein 3 (NLRP3)-dependent pyroptosis, which was found in silica, asbestos, carbon nanoparticles-treated macrophages and dendritic cells (DCs). The third is through lysosome rupture-released multiple redundant cathepsins after Syk-dependent phagocytosis, which was found in silica, alum, MSU, and nanoparticle-treated neutrophils, basophils, eosinophils, macrophages, and mast cells. GSDMD, gasdermin D.
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