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. 2018 Sep 3;23(9):2247.
doi: 10.3390/molecules23092247.

Silicon Dioxide Nanoparticles Enhance Endotoxin-Induced Lung Injury in Mice

Affiliations

Silicon Dioxide Nanoparticles Enhance Endotoxin-Induced Lung Injury in Mice

Je-Won Ko et al. Molecules. .

Abstract

Silicon dioxide nanoparticles (SiONPs), which are metal oxide nanoparticles, have been used in a wide variety of applications. In this study, acute pulmonary responses were examined after the intranasal instillation of SiONPs in mice primed with or without lipopolysaccharide (LPS, intranasal, 5 µg/mouse). The exposure to SiONPs increased the inflammatory cell counts and proinflammatory cytokines in the bronchoalveolar lavage fluid. SiONPs induced airway inflammation with increases in the phosphorylation of mitogen-activated protein kinases (MAPKs). The ratios of the inflammatory responses induced by the SiONPs were increased in the acute pulmonary disease model primed by LPS. Taken together, SiONPs exhibited toxicity to the respiratory system, which was associated with MAPK phosphorylation. In addition, the exposure to SiONPs exacerbated any existing inflammatory pulmonary diseases. These data showed the additive, as well as synergistic, interaction effects of SiONPs and LPS. We conclude that the exposure to SiONPs causes potential toxicity in humans, especially those with respiratory diseases.

Keywords: inflammation; mitogen-activated protein kinase; respiratory tract; silicon dioxide nanoparticles.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Morphology of SiONPs. (A,B) TEM images of SiONPs. (C,D) SEM images of SiONPs.
Figure 2
Figure 2
Effects of SiONPs exposure on inflammatory cell counts in BALF. (A) Representative images of inflammatory cells of each group. (B) Neutrophils in BALF of each group. (C) Lymphocytes in BALF of each group. (D) Macrophages in BALF of each group. (E) Eosinophils in BALF of each group. (F) Total cells in BALF of each group. Data represent the means ± SD (n = 5 per group). * p < 0.05 and ** p < 0.01 vs. vehicle control. ## p < 0.01 vs. LPS.
Figure 3
Figure 3
Effect of SiONPs exposure on proinflammatory cytokines in BALF. Levels of (A) IL-1β and (B) TNF-α. Data represent the means ± SD (n = 5 per group). ** p < 0.01 vs. vehicle control. # p < 0.01 and ## p < 0.05 vs. LPS.
Figure 4
Figure 4
Effect of SiONPs exposure on inflammatory responses in lung tissues of each group. (A) Representative images of inflammatory responses in lung tissue of each group. (B) Quantitative analysis of inflammatory responses in lung tissue of each group. (C) Quantitative analysis of Ki-67 expression in lung tissue of each group. Data represent the means ± SD (n = 5 per group). * and p < 0.05 and ** p < 0.01 vs. vehicle control. ## p < 0.01 vs. LPS.
Figure 5
Figure 5
Effect of SiONPs exposure on ERK and JNK phosphorylation in lung tissues of each group. (A) ERK and JNK expression on gels. (B) Densitometric value of ERK phosphorylation. (C) Densitometric value of JNK phosphorylation. Data represent the means ± SD (n = 5 per group). ** p < 0.01 vs. vehicle control. ## p < 0.01 vs. LPS.

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