Effects of surface-coupled polyethylene oxide on human macrophage adhesionand foreign body giant cell formation in vitro

Citation
Cr. Jenney et Jm. Anderson, Effects of surface-coupled polyethylene oxide on human macrophage adhesionand foreign body giant cell formation in vitro, J BIOMED MR, 44(2), 1999, pp. 206-216
Citations number
52
Categorie Soggetti
Multidisciplinary
Journal title
JOURNAL OF BIOMEDICAL MATERIALS RESEARCH
ISSN journal
00219304 → ACNP
Volume
44
Issue
2
Year of publication
1999
Pages
206 - 216
Database
ISI
SICI code
0021-9304(199902)44:2<206:EOSPOO>2.0.ZU;2-F
Abstract
Surface immobilized polyethylene oxide (PEG) has been shown to efficiently reduce protein adsorption and cellular adhesion, resulting in a biologicall y passive surface. To explore the in vitro effects of surface immobilized P EO on the human inflammatory cells, macrophages, and foreign body giant cel ls (FBGCs), we developed a diisocyanate-based method for coupling PEG to am ine-modified glass, a surface previously shown to enhance macrophage adhesi on and FBGC formation. Contact angle analysis and X-ray photoelectron spect roscopy confirmed the presence of PEG molecules bound to the surface and re vealed that PEG molecular weight significantly influenced the efficiency of PEO coupling. We used a 10-day human monocyte culture protocol to demonstr ate that the presence of surface coupled PEG molecules does not significant ly decrease initial monocyte density or monocyte-derived macrophage density after 3 days. However, PEG-coupled surfaces significantly reduced long-ter m monocyte-derived macrophage density and virtually eliminated interleukin- 4-induced FBGC formation observed at day 10. The cellular response to these PEG-coupled surfaces was related to the molecular weight of the PEG chains , which was varied between 200 Da and 18.5 kDa. These results suggest that an optimized PEG surface treatment may be effective in reducing inflammator y cell adhesion and possible degradation during the inflammatory response t o an implanted biomedical device. (C) 1999 John Wiley & Sons, Inc.