When non-biological materials are implanted in the body the innate immune system responds by surrounding the material with dense fibrous collagen and persistent inflammation at the surface of the material. This response, deemed the foreign body response (FBR), prevents biomaterials from interacting with the body long-term and contributes to implant failure. Studies have shown that Prostaglandin E2 has opposing roles depending on which one of the four cell surface receptors it binds: receptor subtypes EP1 & EP3 potentiate inflammation while receptor subtypes EP2 & EP4 inhibit inflammation. Our prior in vitro studies pointed to EP2 as be the receptor that attenuates inflammation in macrophages, which are the immune cells responsible for the FBR. Thus, we hypothesize that specifically targeting EP2 can prevent fibrosis in the FBR. We aim to test this hypothesis by identifying the roles of both EP2 and EP4 receptors in the FBR through a transgenic mouse model and developing a biomaterial strategy that activates the EP2 receptor to assess its ability to suppress the FBR in vivo. Four commonly used biomaterials that span a wide range of material properties will be used throughout this project.
The student should have some knowledge of biology and a strong interest in biomaterials.