Foreign body response (FBR) (FBR)

The foreign body response (FBR) is a complex biological process that occurs at the interface between a host tissue and an implanted biomaterial or medical device (Source 1.1.1). It is characterized by the immediate adsorption of host proteins onto the material surface, followed by the recruitment and adhesion of monocytes and macrophages (Source 1.1.2). These macrophages can subsequently fuse to form multinucleated foreign body giant cells (FBGCs), which attempt to degrade the material through the release of reactive oxygen species and enzymes (Source 1.1.4). The process typically culminates in the formation of a dense, relatively avascular fibrous capsule that can impair the function and longevity of the implant (Source 1.1.1). While not a single molecular target, the FBR is mediated by key receptors such as Integrin alpha-M beta-2 (Mac-1) and signaling pathways involving cytokines like IL-4 and TGF-beta, which are often targeted in the design of 'immuno-informed' biomaterials to improve biocompatibility (Source 1.1.3, 1.1.5). Pharmacological interventions often involve the use of corticosteroids like dexamethasone or anti-proliferative agents like sirolimus to suppress the inflammatory cascade and prevent excessive fibrosis (Source 1.1.1, 1.1.2). Experimental strategies also target specific adhesion molecules like CD11b or fusion-related proteins like CD44 to mitigate the response without systemic immunosuppression (Source 1.1.3, 1.1.4).

Other names

Macrophage adhesion and foreign body response at the tissue–material interfaceForeign body reactionBiomaterial-associated inflammationFibrous encapsulationMacrophage-mediated biomaterial response

Inhibition of macrophage recruitment, suppression of pro-inflammatory cytokine release, and prevention of macrophage fusion into giant cells.