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      International Journal of Nanomedicine (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on the application of nanotechnology in diagnostics, therapeutics, and drug delivery systems throughout the biomedical field. Sign up for email alerts here.

      105,621 Monthly downloads/views I 7.033 Impact Factor I 10.9 CiteScore I 1.22 Source Normalized Impact per Paper (SNIP) I 1.032 Scimago Journal & Country Rank (SJR)

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      Pathological Comparison of Rat Pulmonary Models Induced by Silica Nanoparticles and Indium-Tin Oxide Nanoparticles

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          Abstract

          Purpose

          The objective of this study was to evaluate and compare the histopathological implications of silica nanoparticles (Nano-SiO 2) and indium-tin oxide nanoparticles (Nano-ITO), in vivo.

          Methods

          Male Sprague-Dawley rats were exposed to Nano-SiO 2 (50 mg/kg) and Nano-ITO (6 mg/kg) by a single intratracheal instillation, respectively. Broncho-alveolar lavage fluid (BALF) and lung tissue were obtained at 7, 14, 28, and 56 days post exposure for analysis of BALF inflammatory factors, total protein, and for lung tissue pathology. Histopathological and ultrastructural change in lungs were investigated by hematoxylin and eosin, Masson’s trichrome, sirius red staining, periodic acid Schiff stain, and transmission electron microscopy. The expression of SP-A, collagen type I and III in lung tissue was determined by immunohistochemistry and ELISA.

          Results

          The rats in both models exhibited obvious collagen fibrosis and the severity of the lung injury increased with time after exposure to respective dosage increased. Several parameters of pulmonary inflammation and fibrosis significantly increased in both groups, which was reflected by increased LDH activity, total proteins, TNF-α, and IL-6 levels in BALF, and confirmed by histopathological examination. The results also showed that the two models exhibited different features. Exposure to Nano-ITO caused persistent chronic lung inflammation, illustrated by the infiltration of a large amount of enlarged and foamy macrophages and neutrophils into the lung parenchyma. In Nano-SiO 2 exposed rat lung tissue, granulomatous inflammation was most prominent followed by progressive and massive fibrotic nodules. Compared with the Nano-SiO 2 rats, Nano-ITO exposed rats exhibited significantly severe pulmonary alveolar proteinosis (PAP) pathological changes, lower fibrosis, and higher levels of inflammatory biomarkers. However, Nano-SiO 2 exposed rats had greater fibrosis pathological changes and more severe granulomas than Nano-ITO exposed rats.

          Conclusion

          This study suggests that the Nano-SiO 2-induced model has greater value in research into granulomas and fibrosis, while the Nano-ITO-induced model has greater repeatability in area of PAP.

          Most cited references19

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          Silica binding and toxicity in alveolar macrophages.

          Raymond F Hamilton, Sheetal A Thakur, Andrij Holian (2008)
          Inhalation of the crystalline form of silica is associated with a variety of pathologies, from acute lung inflammation to silicosis, in addition to autoimmune disorders and cancer. Basic science investigators looking at the mechanisms involved with the earliest initiators of disease are focused on how the alveolar macrophage interacts with the inhaled silica particle and the consequences of silica-induced toxicity on the cellular level. Based on experimental results, several rationales have been developed for exactly how crystalline silica particles are toxic to the macrophage cell that is functionally responsible for clearance of the foreign particle. For example, silica is capable of producing reactive oxygen species (ROS) either directly (on the particle surface) or indirectly (produced by the cell as a response to silica), triggering cell-signaling pathways initiating cytokine release and apoptosis. With murine macrophages, reactive nitrogen species are produced in the initial respiratory burst in addition to ROS. An alternative explanation for silica toxicity includes lysosomal permeability, by which silica disrupts the normal internalization process leading to cytokine release and cell death. Still other research has focused on the cell surface receptors (collectively known as scavenger receptors) involved in silica binding and internalization. The silica-induced cytokine release and apoptosis are described as the function of receptor-mediated signaling rather than free radical damage. Current research ideas on silica toxicity and binding in the alveolar macrophage are reviewed and discussed.
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            Pulmonary alveolar proteinosis in workers at an indium processing facility.

            Kristin J Cummings, Walter E Donat, David B Ettensohn … (2010)
            Two cases of pulmonary alveolar proteinosis, including one death, occurred in workers at a facility producing indium-tin oxide (ITO), a compound used in recent years to make flat panel displays. Both workers were exposed to airborne ITO dust and had indium in lung tissue specimens. One worker was tested for autoantibodies to granulocytemacrophage-colonystimulating factor (GM-CSF) and found to have an elevated level. These cases suggest that inhalational exposure to ITO causes pulmonary alveolar proteinosis, which may occur via an autoimmune mechanism.
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              The molecular basis of pulmonary alveolar proteinosis.

              Brenna Carey, Bruce C Trapnell (2010)
              Pulmonary alveolar proteinosis (PAP) comprises a heterogenous group of diseases characterized by abnormal surfactant accumulation resulting in respiratory insufficiency, and defects in alveolar macrophage- and neutrophil-mediated host defense. Basic, clinical and translational research over the past two decades have raised PAP from obscurity, identifying the molecular pathogenesis in over 90% of cases as a spectrum of diseases involving the disruption of GM-CSF signaling. Autoimmune PAP represents the vast majority of cases and is caused by neutralizing GM-CSF autoantibodies. Genetic mutations that disrupt GM-CSF receptor signaling comprise a rare form of hereditary PAP. In both autoimmune and hereditary PAP, loss of GM-CSF signaling blocks the terminal differentiation of alveolar macrophages in the lungs impairing the ability of alveolar macrophages to catabolize surfactant and to perform many host defense functions. Secondary PAP occurs in a variety of clinical diseases that presumedly cause the syndrome by reducing the numbers or functions of alveolar macrophages, thereby impairing alveolar macrophage-mediated pulmonary surfactant clearance. A similar phenotype occurs in mice deficient in the production of GM-CSF or GM-CSF receptors. PAP and related research has uncovered a critical and emerging role for GM-CSF in the regulation of pulmonary surfactant homeostasis, lung host defense, and systemic immunity. Copyright 2010 Elsevier Inc. All rights reserved.
              Article 0 comments Cited 27 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Nanomedicine
                Journal ID (iso-abbrev): Int J Nanomedicine
                Journal ID (publisher-id): ijn
                Title: International Journal of Nanomedicine
                Publisher: Dove
                ISSN (Print): 1176-9114
                ISSN (Electronic): 1178-2013
                Publication date (Electronic): 15 September 2022
                Publication date Collection: 2022
                Volume: 17
                Pages: 4277-4292
                Affiliations
                [1 ]School of Public Health, North China University of Science and Technology , Tangshan, People’s Republic of China
                [2 ]School of Public Health, Xinxiang Medical University , Xinxiang, People’s Republic of China
                Author notes
                Correspondence: Sanqiao Yao, Email sanqiaoyao@xxmu.edu.cn
                Article
                Publisher ID: 380259
                DOI: 10.2147/IJN.S380259
                PMC ID: 9484578
                PubMed ID: 36134200
                SO-VID: 5c0a4b95-47ee-474b-a960-1d743d582f1c
                Copyright © © 2022 Guan et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 16 July 2022
                Date accepted : 11 September 2022
                Page count
                Figures: 8, References: 19, Pages: 16
                Funding
                Funded by: the Basic Scientific Research Funds for Provincial Universities of North China University of Science and Technology;
                Funded by: the National Natural Science Foundation of China;
                Funded by: Graduate Innovation Project;
                This research was funded by the Basic Scientific Research Funds for Provincial Universities of North China University of Science and Technology [JQN2020013], grants from the National Natural Science Foundation of China ([U21A20334], and Graduate Innovation Project (No. 2019B17).
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Molecular medicine
                Keywords: silica nanoparticles,indium-tin oxide nanoparticles,silicosis,indium lung disease,pulmonary alveolar proteinosis
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: silica nanoparticles, indium-tin oxide nanoparticles, silicosis, indium lung disease, pulmonary alveolar proteinosis

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