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Silicosis: Pathogenesis and Changklan Muang Chiang Mai 50100 Thailand; Tel: 66 53 276364; Fax: 66 53 273590; E-Mail Central Annals of Clinical Pathology Bringing Excellence in Open Access Review Article *Corresponding author Attapon Cheepsattayakorn, 10th Zonal Tuberculosis and Chest Disease Center, 143 Sridornchai Road Silicosis: Pathogenesis and Changklan Muang Chiang Mai 50100 Thailand; Tel: 66 53 276364; Fax: 66 53 273590; E-mail: Biomarkers Submitted: 04 October 2018 Accepted: 31 October 2018 1,2 3 Attapon Cheepsattayakorn * and Ruangrong Cheepsattayakorn Published: 31 October 2018 1 10 Zonal Tuberculosis and Chest Disease Center, Chiang Mai, Thailand ISSN: 2373-9282 2 Department of Disease Control, Ministry of Public Health, Thailand Copyright 3 Department of Pathology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand © 2018 Cheepsattayakorn et al. OPEN ACCESS Abstract Ramazzini first described this disease, namely “Pneumonoultramicroscopicsilicovolcanokoniosis” Keywords and then was changed according to the types of exposed dust. No reliable figures on the silica- • Silicosis inhalation exposed individuals are officially documented. How silica particles stimulate pulmonary • Biomarkers response and the exact path physiology of silicosis are still not known and urgently require further • Pathogenesis research. Nevertheless, many researchers hypothesized that pulmonary alveolar macrophages play a major role by secreting fibroblast-stimulating factor and re-ingesting these ingested silica particles by the pulmonary alveolar macrophage with progressive magnification. Finally, ending up of the death of the pulmonary alveolar macrophages and the development of pulmonary fibrosis appear. Various mediators, such as CTGF, FBRS, FGF2/bFGF, and TNFα play a major role in the development of silica-induced pulmonary fibrosis. A hypothesis of silicosis-associated abnormal immunoglobulins has been postulated. In conclusion, novel studies on pathogenesis and biomarkers of silicosis are urgently needed for precise prevention and control of this silently threaten disease of the world. ABBREVIATIONS - lation of lymphocytes and alveolar macrophages, and thickening ACE: Angiotensin Converting Enzyme; ANCA: Anti- acterized by hyalinized and fibrotic pulmonary nodules, accumu Neutrophil Cytoplasmic Antibody; ANF: Anti-Nuclear Antibody; continuous inhalation of the silica dust (crystalline silica, SiO BAL Bronchoalveolar Lavage; CSF Colony-Stimulating Factor; of pulmonary alveolar interstitium [4]. The diseaseis caused by 2 DCs: Dendritic Cells; DNA: Deoxyribonucleic Acid; FasL: Fas - Ligand; FEV1: Forced Expiratory Volume in one second; FGF (Silicon dioxide)) with marked inflammation and irreversible Fibroblast Growth Factor; FSF: Fibroblast-Stimulating Factor; IL: scarring of the lungs with nodules in the upper lobes [5,6] Oxy Interleukin; L-BAL: Bronchoalveolar Lavage Lymphocyte; mRNA gen and silicon, together amount for 74.32 % weight and 83.77 under% of crustal the conditions rocks are of the increased two most pressure occurring and common heat that elements exists in Protein; MCP: Monocyte Chemotactic Factor; NALP3: (or NLRP3) amorphouson the surface and of crystalline the earth (quartz,[7]. Silicon a typical dioxide component or silica is of formed rocks) messenger Ribonucleic Acid; MIP: Macrophage Inflammatory Nucleotide-binding oligomerization domain-Like Receptor form. The risk of developing silicosis is closely associated with containing Pyrin domain 3; RA: Receptor Antagonist; RF: the accumulated exposure of a person to respirable crystalline Rheumatoid Factor; SSc: Systemic Sclerosis; SLE: Systemic Lupus silica during his or her working lifetime. The intensity of accumu- Erythematosus; Th 17: T helper 17; TNF: Tumor Necrosis Factor; lated respirable silica exposure can be calculated as the following VC: Vital Capacity; WNT: Wingless Type - OBJECTIVE OF THE STUDY age of free silica in mg/m3 SilicosisAccumulated is the silica most dosefrequently = fraction occurring of respirable pneumoconiosis dust X percent due to The objective of this study is to review the new ideas of wide prevalence in the atmosphere X number and of more years common of exposure than [8].the pathogenesis of silicosis and possibly practical novel biomarkers for silicosis. world, silicosis is an occupational hazard with greater risk for INTRODUCTION workersother types engaged of dust in [1,9,10].stone crushing, Both in stone Developing cutting, and cement developed indus- tries, glass manufacturing, mining, agriculture, and construction. The name of this disease “Pneumonoultramicroscopicsilicov- PATHOGENESIS - olcanokoniosis ”, first description by Ramazzini [1] was changed ures on the silica-inhalation exposed populations. Nevertheless, inspired into the lungs, these particles get embedded into the due to the types of exposed dust [2]. There are no reliable fig When the silica particles of 0.5 to 5 microns in diameter are - and scarring damage the pulmonary alveolar sacs, prevent gas in 2000, the CAREX registry recorded 3.2 million silica-exposed alveolar sacs and ducts and cause inflammation. The inflammation people in the European Union [3]. Silicosis is histologically char Cite this article: Cheepsattayakorn A, Cheepsattayakorn R (2018) Silicosis: Pathogenesis and Biomarkers. Ann Clin Pathol 6(5): 1147. Cheepsattayakorn et al. (2018) Email: [email protected] Central Bringing Excellence in Open Access exchange in the lungs, and contribute to abnormal breathing. The damage to the lung tissue leads to reduction of oxygen supply to the blood. Silicosis isan irreversible medical condition [12]. NALP3 (or NLRP3) inflammasome-driven IL-1β mediates without cure. Degree of silica-dust exposure is directly associated releasethe inflammatory of cathepsin response B with production following of exposurte reactive oxygen to crystalline species with occurrence of silicosis. Through the process of inhalation, (ROS),silica [15]. potassium Following effux, uptake and lysosomalof silica by rupture, scavenger the receptors,activation different size of the silica particles deposit in the different parts et al demonstrated in their study results that anti-deoxyribonucleic acid (anti-DNA), in size particles reach up to upper respiratory tract causing antimitochondrialof inflammasome occurantibody, [15-18]. antinuclear Castro factor (ANF), anti- of the human respiratory system. For examples, 10-5 microns smooth muscle antibody, antithyroglobulin antibody, rheumatoid the mid-respiratory system and may cause tracheaitis, bronchitis factor (RF) or latex agglutination test, thyroid antimicrosomal andrhinitis bronchiolitis, and laryngitis, and 3-15-3 microns in size particles directlyreach up are to antibody, and Waaler-Rose test revealed the percentages of deposited in the alveoli causing asthma, chronic obstructive pulmonary disease, and other pulmonary interstitial diseases lesionspositive are in microscopicallythe studied subjects characterized of 20.6 %, by 1.7 aggregation %, 20.6 %, of 1.7 dust- %, response and the precise pathophysiology of silicosis are still laden1.7 %, macrophages3.4 %, 3.4 %, and that 3.4 surround %, respectively a collagenous [19]. Early central pulmonary region researchincluding silicosisquestions. [11]. Nevertheless, How silica particlesstimulate several studies pulmonary indicated interactions between respirable silica particles and pulmonary collagen distinctly becomes whorled and reveals decreasing alveolar macrophages and this interaction plays major role in to develop nodular to stellate lesions [20]. Then the central the development of the silicosis disease. The intensity of the pulmonary nodules, called “ mixed dust pneumoconiosis ” that causednumber by of ainflammatory combination cellsof silica around plus theanother periphery dust are[20]. likely The the pulmonary alveolar response that provides explanation to to persist their stellate feature with less whorled arrangement someinhaled silicosis silica extensionparticles influencewhy rock drillerson the andnature sandblasters and extent who of are intensively exposed to freshy fractured silica dust develop silica or cristobalite can enhance the immune response, trigger, promote,in ordinary or silicosisaccelerate [20]. the Silicadevelopment particle, of particularly autoimmune crystalline diseases Several studies revealed that silica promote macrophage silicosis disease [12]. particles by lysozymal enzymes and damaging silica-particle- ingested[13,21]. According pulmonary to inabilityalveolar to macrophages break down thewith crystalline its repeated silica mediators and chemotactic factors that trigger cellular responses activation. The affected macrophages release inflammatory process, this phenomenon results in spreading immune activity of the leukocytes and lymphocytes and then release the fibroblast demonstrated that crystallinity does not indicate the mechanisms and pulmonary fibrosis [13]. Nevertheless, recent studies have stimulating factor (Figure 1). Hyalinization and collagen deposition are promoted by the fibroblast stimulating factor (FSF) Many silica-exposed patients with altered immune functions are pulmonary nodular lesion.This pulmonary nodule composes of a of silica pathogenicity, whereas silanols play the major role [22]. centraland resulting acellular in zoneactivation with freeof fibroblast silica and [13] surrounding and pathologically spirals of likely to develop autoimmune disorders and pulmonary fibrosis immunological[23]. Nevertheless, status, approximately whereas some 20 patients % to reveal25 % acceleratedof patients factor.collagen Then and macrophages
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