Macrophage behavior on surface-modified polyurethanes

Abstract

Adherent macrophages and foreign body giant cells (FBGCs) are known to release degradative molecules that can be detrimental to the long-term biostability of polyurethanes. The modification of polyurethanes using surface modifying endgroups (SMEs) and/or the incorporation of silicone into the polyurethane soft segments may alter macrophage adhesion, fusion and apoptosis resulting in improved long-term biostability. An in vitro study of macrophage adhesion, fusion and apoptosis was performed on polyurethanes modified with fluorocarbon SMEs, polyethylene oxide (PEO) SMEs, or poly(dimethylsiloxane) (PDMS) co-soft segment and SMEs. The fluorocarbon SME and PEO SME modifications were shown to have no effect on macrophage adhesion and activity, while silicone modification had varied effects. Macrophages were capable of adapting to the surface and adhering in a similar manner to the silicone-modified and unmodified polyurethanes. In the absence of IL-4, macrophage fusion was comparable on the modified and unmodified polyurethanes, while macrophage apoptosis was promoted on the silicone modified surfaces. In contrast, when exposed to IL-4, a cytokine known to induce FBGC formation, silicone modification resulted in more macrophage fusion to form foreign body giant cells. In conclusion, fluorocarbon SME and PEO SME modification does not affect macrophage adhesion, fusion and apoptosis, while silicone modification is capable of mediating macrophage fusion and apoptosis. Silicone modification may be utilized to direct the fate of adherent macrophages towards FBGC formation or cell death through apoptosis.

Surface chemistry mediates adhesive structure, cytoskeletal organization, and fusion of macrophages

“…23,24 In our previous study, we investigated the effect of PDMS in the soft segment and SME of the polyurethanes on macrophage adhesion and activity. 25 We reported that silicone modification did not affect monocyte/macrophage adhesion on modified and unmodified polyurethanes. However, silicone modification promoted macrophage fusion and apoptosis on modified materials.…”

Foreign body reaction to biomaterials

“…[30] Biomaterial surface chemistry influences apoptosis of adherent macrophages both in vitro and in vivo. [12,[53][54][55] Caspase-3, a protein involved in apoptosis signaling, is activated by neutrophils under shear stress and leads to detachment from biomaterials. [56] Caspases are involved in cleaving gelsolin, a protein involved in regulating actin polymerization, and this in turn disrupts adhesion.…”

“…The surface needs to support fusion. Macrophage fusion on biomaterial surfaces is material dependent [55] indicating that surfaces must have an appropriate array of absorbed proteins in order for adherent cells to undergo the necessary phenotype to fuse into foreign body giant cells. After culturing human monocytes on polystyrene coated with different protein substrates (i.e.…”

Cytokine induction of sol–gel-derived TiO₂ and SiO₂ coatings on metallic substrates after implantation to rat femur

“…biomaterial features, the most important are the material size, surface topology and chemistry, mechanical forces, and the release of degradation products from the implant. 3,[8][9][10]20,21 Hence, the interactions between the implant and bone are mostly determined by the biomaterial surface. Therefore, altering the surface and its features is a way to improve implant -tissue interaction.…”