4th Annual Mountain West
Biomedical Engineering Conference
September 5-6, 2008
Abstract Details
Presented By: | Chamberlain, Lisa |
Affiliated with: | University of Utah, Pharmaceutical Chemistry |
Authors: | Lisa M. Chamberlain, David Higgins, Mercedes Gonzales-Juarrero, David Grainger |
From: | Separate institution names with commas |
Title
Abstract
Implanted biomaterials cause chronic and acute host inflammatory response followed by atypical fibrosis at the wound site. This process, known as the foreign body response (FBR), is often responsible for device failure and its importance increases as the use of medical implants continues to rise. Host reactions that produce the FBR are poorly understood, but are correlated with macrophage attachment to the biomaterial surface and subsequent release of inflammatory cytokines. To further investigate the role of the macrophage in the FBR in vivo, model biomaterials (Nylon mesh, Teflon-AF® and PLLA) were implanted into C57/BL-6 mice for a period of 21 days. Excised tissue samples from early (days 1, 3, and 7) and late (day 21) time points were analyzed for cytokine production and cellular markers using immunohistochemistry. Dynamics of macrophage infiltration (using F4/80 as a marker), and cytokine expression (MCP-1, IL-6, IL-4, TNF, and TGF-B) show clear differences from surface to surface, giving insight to the mechanisms of the FBR in vivo.
We report faster macrophage infiltration and higher IL-6 positive cells in wound sites containing biodegradable (PLLA) materials compared to Teflon-AF® or nylon materials. Additionally, IL-4 positive cells were seen in higher numbers for PLLA and Teflon-AF® than nylon implants. Higher numbers of TGF-B positive cells were found with Teflon-AF® implants, and TNF expression was significantly higher with lab-prepared materials (Teflon-AF® and PLLA) than with commercially available implants (nylon mesh).