Attenuating Immune Response of Macrophage by Enhancing Hydrophilicity of Ti Surface. (3rd May 2015)

• Record Type: Journal Article
• Authors: Dai, Xiaohan; Wei, Yan; Zhang, Xuehui; Meng, Song; Mo, Xiaoju; Liu, Xing; Deng, Xuliang; Zhang, Li; Deng, Xuming
• Other Names: Liu Dawei Academic Editor.
• Is Part Of: Journal of nanomaterials. Volume 2015(2015)
• Publication Date: 2015-05-03
• Subjects: Nanostructured materials -- Periodicals; Nanotechnology -- Periodicals; Nanomatériaux; Nanostructured materials; Nanotechnology; Nanostructures; Nanotechnology; Periodicals; Fulltext; Internet Resources; Periodicals; 620.115
• DOI: 10.1155/2015/712810
• Languages: English
• ISSNs: 1687-4110

Abstract

Abstract : Immune responses can determine the in vivo fate of implanted materials. The strategy for developing implants has shifted towards using materials with immunomodulatory activity. However, the immunoregulatory effect of hydrophilicity of titanium surface on the macrophage behavior and its underlying mechanism remain poorly understood. Here, the Ti surface hydrophilicity-dependent behavior of murine RAW264.7 macrophages was investigated in vitro . Two laboratory models with significantly different surface hydrophilicity and similar roughness were established with Ti-polished and Ti-H2 O2 surfaces. The results of cell morphology observation showed that the Ti-H2 O2 surface yielded enhanced cell adhesion and less multinucleated cell formation. CCK-8 assay indicated that the growth rate of macrophage on Ti-H2 O2 surface is higher than that of Ti-polished. ELISA assay result revealed lower level of proinflammatory factor TNF- α and higher level of anti-inflammatory factor IL-10 on the Ti-H2 O2 surface compared to Ti-polished. Subsequently, immunofluorescence and western blotting analysis showed that activation of the NF- κ B-TNF- α pathway might be involved in the modulation of the immune response by surface hydrophilicity. Together, these results suggested that relative high hydrophilic Ti surface might attenuate the immune response of macrophage by activating NF- κ B signaling. These findings could provide new insights into designing implant devices for orthopedic applications.