Title of article :
The role of titanium surface topography on J774A.1 macrophage inflammatory cytokines and nitric oxide production
Author/Authors :
Kai Soo Tan، نويسنده , , Li Qian، نويسنده , , Roy Rosado، نويسنده , , Patrick M. Flood، نويسنده , , Lyndon F. Cooper، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2006
Pages :
8
From page :
5170
To page :
5177
Abstract :
A role for monocyte/macrophage modulation of wound healing at endosseous implants is proposed. The modification of the endosseous implant surface topography can alter cell adhesion and resultant cell behavior. The aim of this study was to define the effect of increased cpTitanium surface topography on adherent J744A.1 macrophage phenotype in culture. The J744A.1 cells were cultured on 20 mm diameter cpTitanium disks prepared with smooth and grit-blasted/acid rough surface topographies for 24–72 h. Following culture in growth media with or without lipopolysaccharide (LPS), total RNA was isolated and real-time polymerase chain reaction (PCR) was used to measure the steady-state levels of the pro-inflammatory cytokines interleukin 1-beta (IL-1β) and interleukin 6 (IL-6) and the anti-inflammatory cytokine interleukin-10 (IL-10). Additional evidence of pro-inflammatory signaling was sought by measurement of cellular nitric oxide (NO) production. In the absence of LPS, IL-1β levels were increased on grit-blasted/acid rough surfaces during the first 48 h. In contrast, IL-6 levels were reduced on the grit-blasted/acid rough surfaces. When cultures were treated with LPS, high levels of IL-1β and IL-6 expression were measured, irrespective of surface topography. The responses of J744A.1 cells to surface and superimposed LPS stimulation suggest only modest effects of the modeled endosseous implant surface on adherent cell pro-inflammatory cytokine expression and NO signaling.
Keywords :
nitric oxide , interleukins , surface topography , macrophage
Journal title :
Biomaterials
Serial Year :
2006
Journal title :
Biomaterials
Record number :
547177
Link To Document :
بازگشت