Titanium dioxide nanoparticles induce emphysema-like lung injury in mice
Journal
FASEB Journal
Journal Volume
20
Journal Issue
13
Pages
E1732-E1741
Date Issued
2006
Author(s)
Abstract
Titanium dioxide nanoparticles (nano-TiO2) have been widely used as a photocatalyst in air and water cleaning. However, these nanoparticles inhalation can induce pulmonary toxicity and its mechanism is not fully understood. In this study we investigated the pulmonary toxicity of nanoTiO 2 and its molecular pathogenesis. The adult male ICR mice were exposed to intratracheal single dose of 0.1 or 0.5 mg nanoTiO2 (19-21 nm) and lung tissues were collected at 3rd day, 1st wk, and 2nd wk for morphometric, microarray gene expression, and pathway analyses. NanoTiO 2 can induce pulmonary emphysema, macrophages accumulation, extensive disruption of alveolar septa, type II pneumocyte hyperplasia, and epithelial cell apoptosis. NanoTiO2 induced differential expression of hundreds of genes include activation of pathways involved in cell cycle, apoptosis, chemokines, and complement cascades. In particular, nanoTiO2 up-regulates placenta growth factor (PlGF) and other chemokines (CXCL1, CXCL5, and CCL3) expressions that may cause pulmonary emphysema and alveolar epithelial cell apoptosis. Cultured human THP-1 cell-derived macrophages treated with nanoTiO2 in vitro also resulted in upregulations of PlGF, CXCL1, CXCL5, and CCL3. These results indicated that nanoTiO2 can induce severe pulmonary emphysema, which may be caused by activation of PlGF and related inflammatory pathways. ? FASEB.
SDGs
Other Subjects
CXCL1 chemokine; epithelial derived neutrophil activating factor 78; macrophage inflammatory protein 1alpha; nanoparticle; placental growth factor; titanium dioxide; nanoparticle; titanium; titanium dioxide; animal experiment; animal model; animal tissue; apoptosis; article; cell culture; cell cycle; cell hyperplasia; cell infiltration; cell proliferation; complement factor; controlled study; DNA microarray; epithelium cell; gene activation; gene expression; genetic transcription; human; human cell; in vitro study; lung alveolus cell type 2; lung alveolus epithelium; lung alveolus wall; lung emphysema; lung injury; lung parenchyma; lung toxicity; macrophage; male; microarray analysis; morphometrics; mouse; nonhuman; nucleotide sequence; pathogenesis; priority journal; protein expression; upregulation; animal; cell differentiation; cell line; cell survival; chemically induced disorder; cytology; drug effect; emphysema; Institute for Cancer Research mouse; monocyte; nanotechnology; pathology; Animals; Cell Differentiation; Cell Line; Cell Survival; Emphysema; Humans; Macrophages; Male; Mice; Mice, Inbred ICR; Monocytes; Nanoparticles; Nanotechnology; Titanium
Type
journal article