NDLI: Wear particles promote endotoxin tolerance in macrophages by inducing interleukin-1 receptor-associated kinase-M expression.

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Wear particles promote endotoxin tolerance in macrophages by inducing interleukin-1 receptor-associated kinase-M expression.

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Wear particles promote endotoxin tolerance in macrophages by inducing interleukin-1 receptor-associated kinase-M expression.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhang, Yangchun Yu, Shiming Xiao, Jianhong Hou, Changhe Li, Ziqing Zhang, Ziji Zhai, Qiyi Lehto, Matti Konttinen, Yrjö T. Sheng, Puyi
Description	Country affiliation: China Author Affiliation: Zhang Y ( Huangpu Joint Centre, First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510700, China.)
Abstract	Toll-like receptors (TLRs) recognizing pathogen-associated molecular patterns (PAMP) play a role in local immunity and participate in implant-associated loosening. TLRs-mediated signaling is regulated by interleukin-1 receptor-associated kinase-M (IRAK-M). Our previous studies have proved that IRAK-M is induced by wear particles in macrophages from periprosthetic tissues. In this study, the IRAK-M-related mechanisms were further explored by lipopolysaccharide (LPS) and/or titanium (Ti) particles stimulations and small interfering RNAs (siRNAs). The protein level of IRAK-M was studied using western blotting and tumor necrosis factor- (TNF- ), and interleukin-1ß (IL-1ß) levels were measured using ELISA. Results showed that in RAW264.7 cells stimulated by LPS after Ti particle pre-exposure, IRAK-M was slightly changed, compared with LPS stimulation. And levels of TNF- and IL-1ß in cultures stimulated by LPS first after Ti particle pre-exposure were lower than in the other two groups which were stimulated by LPS with or without Ti particles (p < 0.001), whereas there were no statistic differences between the later two (p > 0.05). The cytokines were lowest in Ti particles alone stimulation. After siRNAs silenced, IRAK-M-deficient cells exhibited increased expression of the cytokines in LPS stimulation after Ti particle pre-exposure and when stimulated with Ti particles alone. Our findings suggest that debris-induced IRAK-M decreases foreign body reactions, but at the same time, the over-expression of IRAK-M may also be detrimental on local intrusion of PAMPs or bacteria, negatively regulates the LPS-induced and TLRs-mediated inflammation and results in immunosuppression in periprosthetic tissue, which may predispose to implant-associated infections.
File Format	HTM / HTML
ISSN	15493296
Issue Number	3
Volume Number	101
e-ISSN	15524965
Journal	Journal of Biomedical Materials Research Part A
Language	English
Publisher	Wiley
Publisher Date	2013-03-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Research Support, Non-u.s. Gov't Toxicity Biosynthesis Macrophages Journal Article Lipopolysaccharides Immunology Foreign-body Reaction Titanium Genetics Cell Line Adverse Effects Gene Expression Regulation Gene Silencing Immune Tolerance Interleukin-1beta Metabolism Drug Effects Tumor Necrosis Factor-alpha Discipline Biomedical Engineering Pathology Animals Interleukin-1 Receptor-associated Kinases Mice Prostheses And Implants
Content Type	Text
Resource Type	Article
Subject	Ceramics and Composites Metals and Alloys Biomaterials Biomedical Engineering

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