TABLE 1.
Biomaterial choice | Material type |
In vitro: Decreased dentritic cell maturation (decreased levels of CD40,CD80, and CD86, HLA-DQ HLA-DR, CD83); increased secretion of TNF–a (295,296) In vitro: Decreased natural killer cell activity, decreased T- and B-cell proliferation85 |
Surface property modulation |
Surface treatments | |
Hydrophilic surface |
In vitro: Increased apoptosis of adherent primary human macrophages; increased levels of anti-inflammatory cytokine IL-10 and decreased levels of inflammation-associated chemokine IL-8297,298 |
|
Anti-fouling coating |
In vitro: Decreased passive cell attachment and cell activation (i.e., non-specific cell-material interaction)299, 300 |
|
Surface topography | ||
Aligned structures |
In vitro: Decreased initial monocyte adhesion In vivo: Increased cell infiltration; decreased fibrous capsule88 |
|
Micro/Nano structures |
In vitro: Increased pro-inflammatory cytokines IL-1, IL-6, TNF-a301 In vivo: Decreased/ thinner fibrous capsule302 |
|
Bioactive molecule incorporation |
Providing integrins adhesion sites |
In vitro and in vivo: RGD and PHSRN domains increased formation of FBGC303,304 |
Coupling of anti- inflammatory drugs to biomaterials |
In vivo: Decreased anti-inflammatory cytokines, prostaglandins, proteolytic enzymes, free oxygen radicals and nitric oxide; Decreased T helper (Th)1-directed immunity305,306 |
|
Delivery of growth factors/bioactive molecules |
In vivo: Increase macrophage chemotaxis and activation307 In vivo: Decreased capsule formation308 |
|
Artificial ECM | Hydrogels |
In vivo: host response dependent on species of origin, tissue of origin, processing materials, method of terminal sterilization309 |
Artificial ECM coatings for synthetic implants |
In vitro and in vivo: Increased cell adhesion and proliferation310,311 |