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Acute exposure to silica nanoparticles aggravate airway inflammation: different effects according to surface characteristics

Authors
 Hye Jung Park ; Jung-Ho Sohn ; Jae-Hyun Lee ; Jung-Won Park ; In-Hong Choi ; Kiju Um ; Hoon Choi ; Kangtaek Lee ; Kyung Hee Park ; Heejae Han ; Yoon Hee Park ; Yoon-Ju Kim 
Citation
 Experimental and Molecular Medicine, Vol.47 : e173, 2015 
Journal Title
 Experimental and Molecular Medicine 
ISSN
 1226-3613 
Issue Date
2015
Abstract
Silica nanoparticles (SNPs) are widely used in many scientific and industrial fields despite the lack of proper evaluation of their potential toxicity. This study examined the effects of acute exposure to SNPs, either alone or in conjunction with ovalbumin (OVA), by studying the respiratory systems in exposed mouse models. Three types of SNPs were used: spherical SNPs (S-SNPs), mesoporous SNPs (M-SNPs), and PEGylated SNPs (P-SNPs). In the acute SNP exposure model performed, 6-week-old BALB/c female mice were intranasally inoculated with SNPs for 3 consecutive days. In the OVA/SNPs asthma model, the mice were sensitized two times via the peritoneal route with OVA. Additionally, the mice endured OVA with or without SNP challenges intranasally. Acute SNP exposure induced significant airway inflammation and airway hyper-responsiveness, particularly in the S-SNP group. In OVA/SNPs asthma models, OVA with SNP-treated group showed significant airway inflammation, more than those treated with only OVA and without SNPs. In these models, the P-SNP group induced lower levels of inflammation on airways than both the S-SNP or M-SNP groups. Interleukin (IL)-5, IL-13, IL-1β and interferon-γ levels correlated with airway inflammation in the tested models, without statistical significance. In the mouse models studied, increased airway inflammation was associated with acute SNPs exposure, whether exposed solely to SNPs or SNPs in conjunction with OVA. P-SNPs appear to be relatively safer for clinical use than S-SNPs and M-SNPs, as determined by lower observed toxicity and airway system inflammation.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/140680
DOI
10.1038/emm.2015.50
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Yonsei Biomedical Research Center
1. 연구논문 > 1. College of Medicine > Dept. of Microbiology
1. 연구논문 > 1. College of Medicine > Dept. of Internal Medicine
Yonsei Authors
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