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Pathology illustrates pathogenesis of indium lung diseases in rats induced by indium-tin oxide nanoparticles
Nan Liu1, Peng Wan1, Chenxiang Cao1
1School of Public Health, North China University of Science and Technology, Hebei Key Laboratory of Occupational Health and Safety for Coal Industry, Tangshan, Hebei, 063210, China.
Indium lung disease remains an ultra-rare interstitial lung disease with no initiative effective in changing the trial. It is related to excessive protein deposition, the development of interstitial inflammation, and subsequent pulmonary fibrosis. This is a "destructive" pulmonary disease. The pathogenesis of indium lung disease remains unclear because the disease progresses continuously, making early diagnosis difficult. This study aimed to identify the histopathological features of pulmonary injury during and after Nano-ITO intratracheal instillation. Male Sprague-Dawley rats were intratracheally instilled (single and multiple) with dispersed Nano-ITO at low (0.6 mg/kg) and high (6 mg/kg) doses and were sacrificed at 1, 4, 8 and 12 weeks after exposure to test inflammation, pulmonary alveolar proteinosis (PAP), and interstitial fibrosis in the lungs. The results demonstrated that even low-dose Nano-ITO exposure made the lungs susceptible to various types of lung injuries that may lead to PAP and disorders of lipid metabolism. The pro-inflammatory action of Nano-ITO-induced progressive interstitial fibrosis may promote this process by aggravating PAP, including the acute aggravation of foamed alveolar macrophages (AM) and lipid metabolism disorders. When inspecting the effects of these inflammatory responses, the current study uncovered the significance of prospective relationships between PAP, lipid metabolism disorders, and pulmonary fibrosis. Nano-ITO induces a large amount of reactive oxygen species production and mitochondrial damage to trigger redox imbalance, ultimately leading to indium lung disease. Nano-ITO causes pulmonary parenchymal lesions, and its pathological features mainly include: foam macrophage accumulation in respiratory bronchioles and alveolar cavities, fibrosis in alveolar septa (collagen deposition in alveolar septa), epithelial-mesenchymal transition (decreased expression of E-cadherin, increases expression of alpha smooth muscle actin and vimentin), intracytoplasmic lipid droplets (Oil Red-O-positive AM), and cholesterol clefts forming small nodules and granuloma. These findings suggest that intratracheal instillation of rats for 12 weeks is sufficient to observe progressive lung lesions caused by Nano-ITO and is an appropriate experimental scheme to evaluate the early stages of indium lung disease.
Indium lung disease remains an ultra-rare interstitial lung disease with no initiative effective in changing the trial. It is related to excessive protein deposition, the development of interstitial inflammation, and subsequent pulmonary fibrosis. This is a "destructive" pulmonary disease. The pathogenesis of indium lung disease remains unclear because the disease progresses continuously, making early diagnosis difficult. This study aimed to identify the histopathological features of pulmonary injury during and after Nano-ITO intratracheal instillation. Male Sprague-Dawley rats were intratracheally instilled (single and multiple) with dispersed Nano-ITO at low (0.6 mg/kg) and high (6 mg/kg) doses and were sacrificed at 1, 4, 8 and 12 weeks after exposure to test inflammation, pulmonary alveolar proteinosis (PAP), and interstitial fibrosis in the lungs. The results demonstrated that even low-dose Nano-ITO exposure made the lungs susceptible to various types of lung injuries that may lead to PAP and disorders of lipid metabolism. The pro-inflammatory action of Nano-ITO-induced progressive interstitial fibrosis may promote this process by aggravating PAP, including the acute aggravation of foamed alveolar macrophages (AM) and lipid metabolism disorders. When inspecting the effects of these inflammatory responses, the current study uncovered the significance of prospective relationships between PAP, lipid metabolism disorders, and pulmonary fibrosis. Nano-ITO induces a large amount of reactive oxygen species production and mitochondrial damage to trigger redox imbalance, ultimately leading to indium lung disease. Nano-ITO causes pulmonary parenchymal lesions, and its pathological features mainly include: foam macrophage accumulation in respiratory bronchioles and alveolar cavities, fibrosis in alveolar septa (collagen deposition in alveolar septa), epithelial-mesenchymal transition (decreased expression of E-cadherin, increases expression of alpha smooth muscle actin and vimentin), intracytoplasmic lipid droplets (Oil Red-O-positive AM), and cholesterol clefts forming small nodules and granuloma. These findings suggest that intratracheal instillation of rats for 12 weeks is sufficient to observe progressive lung lesions caused by Nano-ITO and is an appropriate experimental scheme to evaluate the early stages of indium lung disease.
