Any material that is implanted within the body is going to elicit a foreign body response. This process is characterized by protein deposition followed by macrophage and monocyte recruitment, macrophage fusion to form foreign body giant cells, then deposition of a dense collagen matrix by macrophages and fibroblasts. These responses can result in the destruction of the device or render it non-functional while causing damage to surrounding tissue. Much research has focused on the role of macrophages in this response; however, detail is still missing regarding how our body recognizes these materials as foreign. We identified a class of proteins that are adsorbed to the surface of implanted materials that is also present during injury. If we implanted materials in mouse that lacked these proteins, there was a strong and significant decrease in the number of macrophages recruited to the material, and more importantly the amount of fibrosis around the material also decreased. If we implant a device that slowly releases small molecule inhibitors of these proteins, we are able to manage and inhibit fibrosis in wild type mice. These studies have described a bottom-up approach to understand the basic biology behind immune responses to biomaterials, identifying putative therapeutic targets, and subsequently developing a modified material to mitigate fibrosis.

Molecular mechanisms of the foreign body response: From scars on our skin to the foreign body capsule

Macromolecular Chemistry: The Second Century

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ACS Spring 2020 National Meeting & Expo

The official archive and repository for all ACS Meetings & Expositions abstracts and select posters or presentations.