The recognition of biomaterials: Pattern recognition of medical polymers and their adsorbed biomolecules

Abstract

All biomedical materials are recognized as foreign entities by the host immune system despite the substantial range of different materials that have been developed by material scientists and engineers. Hydrophobic biomaterials, hydrogels, biomaterials with low protein binding surfaces, and those that readily adsorb a protein layer all seem to incite similar host responses in vivo that may differ in magnitude, but ultimately result in encapsulation by fibrotic tissue. The recognition of medical materials by the host is explained by the very intricate pattern recognition system made up of integrins, toll-like receptors, scavenger receptors, and other surface proteins that enable leukocytes to perceive almost any foreign body. In this review, we describe the various pattern recognition receptors and processes that occur on biomedical material surfaces that permit detection of a range of materials within the host.

Macrophage responses to implants: prospects for personalized medicine

“…play a major role in implant recognition and initiation of FBR [48]. These proteins are recognized by several macrophage integrins, including macrophage-1 antigen (CD11b/CD18) and arginine-glycine-aspartic acid-binding integrins avb3, avb5, and a5b1 [58,59]. Integrins are not only involved in the initial adhesion to biomaterials but also mediate inflammatory responses and regulate the extent of fibrotic encapsulation [58].…”

“…Another study that uses TLR4 knockout mice suggested that monocyte/macrophage adhesion on the surface of PET implants is inhibited in the absence of TLR4 [62]. TLRs are able to recognize certain types of biomaterial directly [59]. However, accumulation of endogenous DAMPs on the surface of biomaterials and their subsequent recognition by TLRs upon initial tissue injury are another proposed mechanism [59].…”

“…TLRs are able to recognize certain types of biomaterial directly [59]. However, accumulation of endogenous DAMPs on the surface of biomaterials and their subsequent recognition by TLRs upon initial tissue injury are another proposed mechanism [59]. Overall, a central pathway implicated in the release of multiple proinflammatory factors upon biomaterial contact involves activation of NF-kB downstream of TLR and integrin stimulation by biomaterial surfaces coated with pathogenassociated molecular patterns and DAMPs.…”

Polymer scaffold architecture is a key determinant in mast cell inflammatory and angiogenic responses

“…Yet, implantation can prompt unresolved inflammation, frustrated phagocytosis, and macrophage fusion to form foreign body giant cells . This is true with polymeric materials due to how immune cells can recognize polymers with their pattern recognition receptors (PRR; e.g., toll‐like receptors or scavenger receptors) . This sustained PRR signaling can lead to fibrotic encapsulation of the biomaterial, contributing to implant failure, and persistent pain .…”

Transparent Substrates Prepared From Different Amorphous Polymers Can Directly Modulate Primary Human B cell functions

“…Free physical valences can also lead to adsorption of certain molecules, such as soluble factors used to activate cells, from cell culture medium. For example, immunoglobulins or PAMP, which are frequently used to specifically activate B cell surface receptors such as the BCR or TLR, can adsorb to polymeric surfaces with a high number of free valences …”