Document Detail


The effect of surface modification of amorphous silica particles on NLRP3 inflammasome mediated IL-1beta production, ROS production and endosomal rupture.
MedLine Citation:
PMID:  20561679     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Although amorphous silica particles (SPs) are widely used in cosmetics, foods and medicinal products, it has gradually become evident that SPs can induce substantial inflammation accompanied by interleukin-1beta (IL-1beta) production. Here, to develop safe forms of SPs, we examined the mechanisms of SP-induced inflammation and the relationship between particle characteristics and biological responses. We compared IL-1beta production levels in THP-1 human macrophage like cells in response to unmodified SP of various diameters (30- to 1000-nm) and demonstrated that unmodified microsized 1000-nm SP (mSP1000) induced higher levels of IL-1beta production than did smaller unmodified SPs. Furthermore, we found that unmodified mSP1000-induced IL-1beta production was depended on the sequence of reactive oxygen species (ROS) production, endosomal rupture, and subsequent activation of pro-inflammatory complex NLRP3 inflammasome. In addition, we compared IL-1beta production levels in THP-1 cells treated with mSP1000s modified with a functional group (-COOH, -NH(2), -SO(3)H, -CHO). Although unmodified and surface-modified mSP1000s were taken up with similar frequencies equally into the THP-1 cells, surface modification of mSP1000 dramatically suppressed IL-1beta production by reducing ROS production. Our results reveal a part of NLRP3 activation pathway and provide basic information that should help to create safe and effective forms of SPs.
Authors:
Tomohiro Morishige; Yasuo Yoshioka; Hiroshi Inakura; Aya Tanabe; Xinglei Yao; Shogo Narimatsu; Youko Monobe; Takayoshi Imazawa; Shin-ichi Tsunoda; Yasuo Tsutsumi; Yohei Mukai; Naoki Okada; Shinsaku Nakagawa
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-06-18
Journal Detail:
Title:  Biomaterials     Volume:  31     ISSN:  1878-5905     ISO Abbreviation:  Biomaterials     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-07-12     Completed Date:  2010-10-20     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8100316     Medline TA:  Biomaterials     Country:  England    
Other Details:
Languages:  eng     Pagination:  6833-42     Citation Subset:  IM    
Copyright Information:
Copyright 2010 Elsevier Ltd. All rights reserved.
Affiliation:
Laboratory of Biotechnology and Therapeutics, Graduate School of Pharmaceutical Sciences, Osaka University, 1-6 Yamadaoka, Suita, Osaka 565-0871, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Carrier Proteins / metabolism*
Caspase 1 / metabolism
Cathepsin B / metabolism
Cell Death / drug effects
Cell Line
Endosomes / drug effects,  enzymology,  pathology*
Enzyme Activation / drug effects
Female
Humans
Inflammation / metabolism*,  pathology
Interleukin-1beta / biosynthesis*
Mice
Mice, Inbred C57BL
Monocytes / drug effects,  enzymology,  pathology,  ultrastructure
Particle Size
Phagocytosis / drug effects
Reactive Oxygen Species / metabolism*
Silicon Dioxide / chemistry*,  pharmacology*
Surface Properties / drug effects
Chemical
Reg. No./Substance:
0/Carrier Proteins; 0/Interleukin-1beta; 0/NLRP3 protein, human; 0/Reactive Oxygen Species; 7631-86-9/Silicon Dioxide; EC 3.4.22.1/Cathepsin B; EC 3.4.22.36/Caspase 1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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