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New Insights Into Pathomechanisms and Treatment Possibilities for Lung Silicosis International Journal of Molecular Sciences Review New Insights into Pathomechanisms and Treatment Possibilities for Lung Silicosis Jana Adamcakova and Daniela Mokra * Department of Physiology, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, SK-03601 Martin, Slovakia; [email protected] * Correspondence: [email protected]; Tel.: +421-43-2633454 Abstract: Inhalation of silica particles is an environmental and occupational cause of silicosis, a type of pneumoconiosis. Development of the lung silicosis is a unique process in which the vicious cycle of ingestion of inhaled silica particles by alveolar macrophages and their release triggers inflammation, generation of nodular lesions, and irreversible fibrosis. The pathophysiology of silicosis is complex, and interactions between the pathomechanisms have not been completely understood. However, elucidation of silica-induced inflammation cascades and inflammation-fibrosis relations has uncovered several novel possibilities of therapeutic targeting. This article reviews new information on the pathophysiology of silicosis and points out several promising treatment approaches targeting silicosis-related pathways. Keywords: silica; silicosis; inflammation; oxidative stress; lung fibrosis Citation: Adamcakova, J.; Mokra, D. 1. Silica and Silicosis New Insights into Pathomechanisms Silica (silicon dioxide, SiO2, or quartz) naturally occurs in the earth´s crust and and Treatment Possibilities for Lung can be released in mining, sandblasting, quarrying, or fabrication of artificial stone [1,2]. Silicosis. Int. J. Mol. Sci. 2021, 22, 4162. Silica exists in several crystalline and amorphous forms with diverse physio-chemical https://doi.org/10.3390/ properties. Among them, crystalline silica with its polymerized tetrahedral framework ijms22084162 has the highest pathogenicity [2,3]. Professional exposure to crystalline silica may lead to: (1) chronic silicosis as a result of more than 10 years of low-moderate exposure dose; Academic Editor: Javier (2) accelerated silicosis, which occurs within 10 years of moderate-high exposure dose; Conde Aranda or (3) acute silicosis (or silicoproteinosis), which develops within 5 years of very high exposure dose [1,2]. Chronic silicosis is recognized in two forms. Simple (or nodular) Received: 31 March 2021 chronic silicosis is characterized by a development of small (<1 cm in size) and hard Accepted: 14 April 2021 Published: 17 April 2021 nodules in the upper lung lobes. These patients may be asymptomatic or may have dry cough or exertional dyspnoea [4]. The situation may become complicated when the silicotic nodules fuse to form conglomerate masses (>1 cm in size), which is characteristic Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in of the second form of chronic silicosis, progressive massive fibrosis. Clinical signs may published maps and institutional affil- be identical to simple silicosis or may be more serious, with the development of central iations. cavitation increasing the risk of mycobacterial infection, enlarged hilar or mediastinal lymphadenopathy, pleural thickening, higher risk of spontaneous pneumothorax, and weight loss [5]. Accelerated silicosis may initially have a similar pattern to simple chronic silicosis, but later the development of nodules and masses intensifies [6]. Acute silicosis may occur within several weeks or less than 5 years of high-intensity silica exposure, which Copyright: © 2021 by the authors. causes dyspnoea and a cough and rapidly progresses to respiratory failure. Acute silicosis Licensee MDPI, Basel, Switzerland. This article is an open access article is associated with hypertrophy of alveolar cells type II and production of excessive amounts distributed under the terms and of proteinaceous material, including surfactant proteins [3]. conditions of the Creative Commons 2. Pathomechanisms of Lung Silicosis Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ The background of pathological changes in silica-injured lungs is complex and not 4.0/). completely understood. Silica-induced lung injury presumably results from the combined Int. J. Mol. Sci. 2021, 22, 4162. https://doi.org/10.3390/ijms22084162 https://www.mdpi.com/journal/ijms Int. J. Mol. Sci. 2021, 22, x FOR PEER REVIEW 2 of 23 Int. J. Mol. Sci. 2021, 22, 4162 2. Pathomechanisms of Lung Silicosis 2 of 22 The background of pathological changes in silica-injured lungs is complex and not completely understood. Silica-induced lung injury presumably results from the combined action of several interactinginteracting pathomechanisms,pathomechanisms, such such as as the the direct direct cytotoxic cytotoxic effect effect of silicaof silica on onmacrophages, macrophages, activation activatio of macrophagen of macrophage surface receptors,surface receptors, lysosomal lysosomal rupture, production rupture, productionof reactive oxygen of reactive species oxygen (ROS), species activation (ROS of), inflammasome,activation of inflammasome, production of production cytokines and of cytokineschemokines, and cell chemokines, apoptosis/pyroptosis, cell apoptosis/pyroptosis, and lung fibrosis and [ 1lung,7–9 ]fibrosis (Figure [1,71). –9] (Figure 1). Figure 1.1.Scheme Scheme of of major major proposed proposed pathomechanisms pathomechanisms of pulmonary of pulmonary silicosis. silicosis. More details More about details the individualabout the pathomech-individual pathomechanismsanisms are provided are in theprovided following in the text. following Abbreviations: text. Abbreviations: ATP: adenosine ATP: triphosphate, adenosine DAMPs: triphosphate, danger-associated DAMPs: danger molecu-- associatedlar patterns, molecular HMGB1: patterns, high mobility HMGB1: group high box mobility 1 protein, group IL: interleukin, box 1 protein, K+: IL: potassium interleukin, cations, K+: potassium MAPK: mitogen-activated cations, MAPK: proteinmitogen kinase,-activated NF- proteinκB: nuclear kinase, factor NF- kappaκB: nuclear B, PAMPs: factor kappa pathogen-associated B, PAMPs: pathogen molecular-associated patterns, molecular PDGF: platelet-derivedpatterns, PDGF: plateletgrowth- factor,derived ROS: growth reactive factor, oxygen ROS: species, reactive SR: oxygen scavenger species, receptors, SR: scaven TGFβger: transforming receptors, TGFβ: growth transforming factor beta, growth TLR: Toll-like factor beta,receptor, TLR: TXNIP: Toll-like thioredoxin-interacting receptor, TXNIP: thioredoxin protein.-interacting protein. 2.1. Recognition Recognition of of Silica Silica by by Macrophage Macrophage Scavenger Receptors Silica particlesparticles are are recognized recognized by receptors by receptors localized localized on the surface on the of alveolarsurface macrophages.of alveolar macrophages.Among all classes Among of scavenger all classes receptors of scavenger (SR), receptors transmembrane (SR), transmembrane proteins SR-AI, proteins SR-AII andSR- AI,macrophage SR-AII and receptors macrophage with a receptor collagenouss with structure a collagenous (MARCO) structure are most (MARCO) associated are with most sil- associatedica binding with [10]. silica SR may binding play [10] a role. SR in may initiation play a of role apoptosis in initiation of alveolar of apoptosis macrophages of alveolar [11]. macrophagesHowever, other [11] pattern. However, recognition other pattern receptors, recognition e.g., the receptors, toll-like receptor e.g., the (TLR)4toll-like or receptor type 3 (TLR)4complement or type receptor, 3 complement may also receptor, participate may in silicaalso participate binding [7]. in silica binding [7]. 2.2. Direct Direct Cytotoxic Cytotoxic Effect Effect of Silica Particles on Macrophages Respirable silicasilica particlesparticles (<10 (<1µ0m), μm) which, which pass pass through through a mucociliary a mucociliary defence defence mecha- mechanismnism, may reach, may distalreach lungdistal compartments lung compartments where theywhere initiate they initiate a cascade a cascade of actions, of actions leading, leadingto the development to the development of lung silicosisof lung silicosis [12]. In the[12] terminal. In the terminal airways airways and alveoli, and thealveoli, inhaled the inhaledsilica is engulfedsilica is engulfed by alveolar by alveolar macrophages, macrophages which are, which primarily are primarily responsible responsible for clearing for clearingthe lung the from lung debris from [7 debris]. However, [7]. However, silica is extremelysilica is extremely toxic for toxic macrophages. for macrophages. If alveolar If alveolarmacrophages macrophages survive survive contact contact with silica, with theysilica, can they migrate can migrate out of out the of lung, the lung, or they or they can canmove move to the to lung the interstitium, lung interstitium where they, where change they into change activated in interstitialto activated macrophages, interstitial important for progression of silica-induced lung injury [13,14]. As discussed in a review by Hamilton et al. [7], the cytotoxicity of silica particles may be explained by several hypotheses. Crystalline silica (quartz, cristoballite, and some forms of tridymite) are in- herently piezoelectric, i.e., they generate opposite electric charges on opposite sides of Int. J. Mol. Sci. 2021, 22, 4162 3 of 22 the physical structure during the application of pressure. These piezoelectric properties of the crystals, particularly of those freshly fractured, trigger the generation of ROS. In addition, silanol (SiOH) groups present
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