Table 1.
Biomaterial | MC type | Use of biomaterial | Outcome |
---|---|---|---|
Electrospun PDO, PCL, silk fibroin scaffolds76 | Murine: BMMCs | BMMCs, nonactivated and activated by IgE and IgE with dinitrophenol were seeded in vitro onto electrospun scaffolds. Cell adhesion, proliferation, and cytokine secretion were measured. | Nonactivated BMMCs were able to adhere to electrospun scaffolds other than silk. Activation increased adhesion, proliferation, and secretion of TNF-α, macrophage inflammatory protein-1α, and IL-13. |
PP mesh77 | Rat: in vivo | PP mesh was implanted on the surface of the thorax for up to 30 days. Quantities of cNOS+ and iNOS+ MCs were measured to quantify activation. | cNOS+ MC count peaked at day 1 while iNOS+ MC count was highest in day 5. On day 30, MC count was at control levels. |
Conjugated nanofiber matrix56 | Human: LAD2 cell line and ex vivo skin | The PAMP-12 motif, which is known to activate MCs, was conjugated to nanofiber matrices. These matrices were cultured with MCs in vitro and on human dermis ex vivo. | Matrices with PAMP-12 motif upregulated β-hexosaminidase release in a dose-dependent manner in LAD2s. On human ex vivo skin, tryptase mRNA transcripts were higher in dermis treated with matrices with PAMP-12 motif than nonconjugated matrices. |
pPE78 | Murine: in vivo | pPE was coated with murine microvascular fragments derived from adipose tissue or platelet-rich plasma. | While coated pPE promoted a prohealing phenotype in macrophages, there was no difference to uncoated controls in terms of MC number and adhesion. |
Nanosilver particles79 | Rat: in vivo | Commercial orthodontic brackets were coated with nanosilver particles and implanted subcutaneously for up to 60 days. | No difference to controls in terms of MC count, except at day 7 where MC count was lower in coated brackets than control brackets. |
Polystyrene film (honeycomb-like)80 | Murine: NCL-2 cell line | MCs were cultured in vitro on honeycomb structures made from polystyrene films. | More clustering and formation of multinucleated cells occurred on structures with larger pores. |
Ti discs81 | Rat: RBL-2H3 cell line | MCs were cultured in vitro on Ti discs with and without nanotopography. | Ti promoted faster adhesion than glass. However, there were no differences in β-hexosaminidase release and vinculin expression. MCs cultured on Ti discs with nanotopography exhibited increased growth and migration. |
PDO73 | Murine: BMMCs | PDO was electrospun into scaffolds with varying pore size and diameter. MCs were cultured on these scaffolds. | Stimulated MCs on PDO scaffolds of larger pore and fibers demonstrated downregulation of IL-6 and TNF-α, and upregulation of VEGF. |
Polyester fibers coated with masitinib-releasing poly(lactic-co-glycolic acid) microspheres82 | Murine: in vivo (MC-deficient model) | Masitinib-releasing fibers were subcutaneously implanted for up to 28 days in MC-deficient mice. Masitinib has been shown to inhibit MC proliferation. | There was no significant difference in FBR capsule formation of coated vs. noncoated implants in MC-deficient mice. However, MC-deficient mice experienced thicker fibrotic capsules around the coated implants than wild type mice. |
Commercial PP, PP with poliglecaprone, and polyester meshes83 | Murine: in vivo | Meshes were implanted subcutaneously for 14 days with or without daily cromolyn treatment (cromolyn is a known MC suppressant). | Inflammation and signs of FBR were seen in all 4 meshes, however, cromolyn treatment downregulated the FBR and inflammatory response. One exception was PP with poliglecaprone, where cromolyn treatment did not significantly downregulate inflammation compared to the saline control. |
ZnO nanoparticles55 | Rat: RBL-2H3 cell line, and Murine: BMMCs | NPs and bulk ZnO (particulates) were cultured in vitro with MCs. MC activation was assessed through histamine and β-hexosaminidase. | Histamine and β-hexosaminidase release were inhibited in a dose-dependent manner in response to ZnO NPs vs. bulk ZnO. |
BMMCs, bone marrow-derived MCs; cNOS, constitutive NOS; FBR, foreign body response; IgE, immunoglobulin E; IL-13, interleukin 13; iNOS, inducible NOS; MC, mast cell; NOS, nitric oxide synthase; NPs, nanoparticles; PCL, poly-ɛ-caprolactone; PDO, polydioxanone; PP, polypropylene; pPE, porous polyethylene; Ti, titanium; TNF-α, tumor necrosis factor-alpha; VEGF, vascular endothelial growth factor; ZnO, zinc oxide.