The early onset and persistent worsening pulmonary alveolar proteinosis in rats by indium oxide nanoparticles

Kim, Sung-Hyun; Jeon, Soyeon; Lee, Dong-Keun; Lee, Seonghan; Jeong, Jinho; Kim, Jong Sung; Cho, Wan‐Seob

doi:10.1080/17435390.2019.1694184

Cited by 18 publications

(14 citation statements)

References 43 publications

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“…The IL‐1β, IL‐6, and TNF‐α concentrations were dramatically decreased along with the increase of exposure dose compared with the control group. The changing trend of the relationship between the cytokines concentration and the CNPs exposure dose was contrary to that reported previously by others (Guo et al, 2019; Kim et al, 2019). Previous literature has shown that pulmonary fibrosis is described as an endpoint following inhaled nanoparticle deposition in the lung (Lu, Zhu, Chen, & Liu, 2014).…”

Section: Resultscontrasting

confidence: 98%

Assessment of pulmonary toxicity of potential antioxidant drug PEGylated nanoceria after intratracheal instillation in rats

Qian

Zhang

Chen

et al. 2020

J of Applied Toxicology

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Cerium oxide (CeO2) nanoparticles have unique redox properties and exert excellent antioxidant effects in the biological environment. In recent years, many researchers have focused on the CeO2 nanoparticles as an effective antioxidant drug in the prevention and treatment of various diseases. However, the toxicity of CeO2 nanoparticles in vivo remains controversial and still needs intensive research. Therefore, the objective of this study is to investigate the pulmonary and systemic toxicity in rats after 14 days of exposure to the PEGylated CeO2 nanoparticles (abbreviated as CNPs; exposure dose of 2, 10, or 20 mg/kg) through a single intratracheal instillation (IT). We assessed the indicators of lung injury and the pathological damage degree of lung tissue. The bronchoalveolar lavage fluid (BALF) analysis and lung histopathology revealed the occurrence of slight pulmonary inflammation in the 20‐mg/kg experimental group rats. However, the inflammation factors in the lung tissue of every group rats did not significantly increase, and the levels of superoxide dismutase (SOD) and glutathione (GSH) in lung tissue homogenate rose considerably in the experimental groups. Collectively, these results indicated that pulmonary exposure by the high dose of CNPs could induce mild pulmonary inflammation but did not cause severe systemic toxicity. Moreover, we speculate that the mechanism of pulmonary toxicity of CNPs in rats was due to the autophagic death of healthy lung epithelial cells mediated by endoplasmic reticulum stress. Our results implicate that CNPs can be safely used as an antioxidant drug for the oxidative stress pulmonary diseases.

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Section: Resultscontrasting

confidence: 98%

Assessment of pulmonary toxicity of potential antioxidant drug PEGylated nanoceria after intratracheal instillation in rats

Qian

Zhang

Chen

et al. 2020

J of Applied Toxicology

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“…[ 4–6 ] While larger particles, deposited in airways, can be efficiently cleared from the bronchial region by the mucociliary escalator, [ 7 ] nanomaterials, the term used here for both submicron‐sized particles (at least two dimensions below 1 µm) and nanoparticles (at least one dimension below 100 nm), can reach the alveolar region. [ 7,8 ] Due to the persistency of most nanomaterials, stemming from ineffective alveolar clearance, [ 9 ] even a single exposure can trigger chronic adverse conditions such as inflammation, [ 10–15 ] leading to lethal diseases, for example lung cancer, heart disease, and brain damage with accelerated cognitive decline. [ 16,17 ]…”

Section: Figurementioning

confidence: 99%

Prediction of Chronic Inflammation for Inhaled Particles: the Impact of Material Cycling and Quarantining in the Lung Epithelium

Kokot

Sebastijanović

et al. 2020

Advanced Materials

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While new exciting applications arise from rapid development of new advanced materials, their lifecycle, from production, processing, to degradation or even combustion, may inevitably result in the release of particulate matter into the environment. [1-3] According to the Organisation for Economic Cooperation and Development (OECD) and the World Health Organization (WHO), inhalation of particulate matter, predominantly of anthropogenic origin, is associated with several million human deaths globally every year. [4-6] While larger particles, deposited in airways, can be efficiently cleared from the bronchial region by the mucociliary escalator, [7] nanomaterials, the term used here for both submicron-sized particles (at least two dimensions below 1 µm) and nanoparticles (at least one dimension below 100 nm), can reach the alveolar region. [7,8] Due to the persistency On a daily basis, people are exposed to a multitude of health-hazardous airborne particulate matter with notable deposition in the fragile alveolar region of the lungs. Hence, there is a great need for identification and prediction of material-associated diseases, currently hindered due to the lack of in-depth understanding of causal relationships, in particular between acute exposures and chronic symptoms. By applying advanced microscopies and omics to in vitro and in vivo systems, together with in silico molecular modeling, it is determined herein that the long-lasting response to a single exposure can originate from the interplay between the newly discovered nanomaterial quarantining and nanomaterial cycling between different lung cell types. This new insight finally allows prediction of the spectrum of lung inflammation associated with materials of interest using only in vitro measurements and in silico modeling, potentially relating outcomes to material properties for a large number of materials, and thus boosting safe-by-design-based material development. Because of its profound implications for animal-free predictive toxicology, this work paves the way to a more efficient and hazard-free introduction of numerous new advanced materials into our lives.

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“…Exceptionally long-lasting inflammatory responses, reflected in prolonged accumulation of infiltrated leukocytes in the lungs, have been shown to follow both single [13][14][15][16][17][18] and repetitive exposure [19][20][21] to some nanomaterials. The insolubility and bio-persistency of the particles have been associated with continuous release of pro-inflammatory mediators from irritated resident cells or dying immune cells, frequently co-observed with chronic dysregulated lipid metabolism [22][23][24][25][26][27] .…”

Section: Introduction -Mechanism Of Persistent Inflammation Unknownmentioning

confidence: 99%

“…Mice were exposed to18,54 or 162 µg of TiO2 nanotubes per mouse and lungs were harvested on 1 st and 28 th day post exposure for transcriptomic analysis to evaluate overlapping sets of genes differentially expressed in the in vivo and in vitro experimental data. The goal of the analysis is to determine and compare alterations in lipid metabolism, immune response in terms of proinflammatory signalling and cholesterol metabolism between two experimental systems.…”

mentioning

confidence: 99%

From the Roundabout of Molecular Events to Nanomaterial-Induced Chronic Inflammation Prediction

Majaron

Kokot

Sebastijanović

et al. 2020

Preprint

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Many chronic diseases manifest in prolonged inflammation and often ignored dysregulated lipid metabolism. When associated with inhalation of nanomaterials, limited information is available on the relevant molecular events and their causal connections. This prevents reliable prediction of outcomes by efficient testing strategies. To unravel how acute nanomaterial exposure leads to chronic conditions, we employed advanced microscopy and omics in vitro and in vivo together with in silico modelling.For selected metal-oxide nanomaterials, we show that lung epithelial cells survive the exposure by excreting internalized nanomaterials and passivating them on the surface, employing elevated lipid synthesis. Macrophages, on the contrary, lose their integrity whilst degrading the passivized bio-nano agglomerates, releasing the nanomaterials, which are taken up again by the epithelial cells. Constant proinflammatory signalling recruits new phagocytes that feed the vicious cycle of events, resulting in a long-lasting response to a single exposure. The proposed mechanism explains the nanomaterialassociated in vivo chronic outcomes and allows its prediction based on in vitro measurements. Similar mechanisms may trigger other chronic diseases affecting millions of lives worldwide.

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The early onset and persistent worsening pulmonary alveolar proteinosis in rats by indium oxide nanoparticles

Cited by 18 publications

References 43 publications

Assessment of pulmonary toxicity of potential antioxidant drug PEGylated nanoceria after intratracheal instillation in rats

Assessment of pulmonary toxicity of potential antioxidant drug PEGylated nanoceria after intratracheal instillation in rats

Prediction of Chronic Inflammation for Inhaled Particles: the Impact of Material Cycling and Quarantining in the Lung Epithelium

From the Roundabout of Molecular Events to Nanomaterial-Induced Chronic Inflammation Prediction

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