Gene expression analyses of human macrophage phagocytizing sub-μ titanium particles by allergy DNA chip (GenopalTM)
Issue title: Selected papers presented at the International Symposium on Nanotoxicity Assessment and Biomedical Environmental Application of Fine Particles and Nanotubes, Hokkaido, Japan, 16–17 June 2008, Part 1
Affiliations: Department of Dental Materials Science and Technology, Iwate Medical University School of Dentistry, Morioka, Japan | Department of Oral Microbiology, Iwate Medical University School of Dentistry, Morioka, Japan | Department of Oral Anatomy II, Iwate Medical University School of Dentistry, Morioka, Japan | Department of Materials Processing, Graduate School of Engineering, Tohoku University, Sendai, Japan
Note: [] Address for correspondence: Masayuki Taira, PhD, Department of Dental Materials Science and Technology, Iwate Medical University School of Dentistry, 1-3-27 Chuo-dori Morioka, 020-8505, Japan. Tel.: +81 19 651 5111, Ext. 4217; Fax: +81 19 651 8407; E-mail: mtaira@iwate-med.ac.jp.
Abstract: The purpose of this study was to examine gene expressions of macrophage phagocytizing sub-μ Ti particles by a DNA chip. Human monocytic cell line THP-1 was differentiated into macrophages by culturing for two days in medium supplemented with 200 nM phorbol ester (PMA). The macrophages were then cultured in four media: medium without PMA (control); medium with suspended sub-μ Ti particles (0.5 wt%); medium with 1.0 μg/ml lipopolysaccharide (LPS); and medium with LPS and Ti particles. After 6 hours' culture, total RNA were extracted and gene expressions were evaluated by DNA allergy chip with 205 allergy and inflammation related gene spots. We found that phagocytosis of sub-μ Ti particles and LPS independently and synergistically up-regulated 17 inflammation-related genes more than two-fold. The extensive expressions of four genes (CCL1, IL1B, IL6 and IL8) were further confirmed by real-time quantitative PCR. It turned out that dual stimulation of LPS and Ti particles most up-regulated three genes (IL1B, IL6 and IL8), followed by LPS while Ti particles moderately but least increased, suggesting that phagocytosis of sub-μ Ti particles induces moderate inflammation with its degree less than LPS, but phagocytosis of sub-μ Ti particles has the potential to worsen inflammation caused by LPS-stimulated macrophages.
