RRC ID 77692
Author Toita R, Kitamura M, Tsuchiya A, Kang JH, Kasahara S.
Title Releasable, Immune-Instructive, Bioinspired Multilayer Coating Resists Implant-Induced Fibrosis while Accelerating Tissue Repair.
Journal Adv Healthc Mater
Abstract Implantable biomaterials trigger foreign body reactions (FBRs), which reduces the functional life of medical devices and prevents effective tissue regeneration. Although existing therapeutic approaches can circumvent collagen-rich fibrotic encapsulation secondary to FBRs, they disrupt native tissue repair. Herein, we describe a new surface engineering strategy in which an apoptotic-mimetic, immunomodulatory, phosphatidylserine liposome (PSL) is released from an implant coating to induce the formation of a macrophage phenotype that mitigates FBRs and improves tissue healing. PSL-multilayers constructed on implant surfaces via the layer-by-layer method release PSLs over a 1-month period. In rat muscles, poly(etheretherketone), a nondegradable polymer implant model, induces FBRs with dense fibrotic scarring under an aberrant cellular profile that recruits high levels of inflammatory infiltrates, foreign body giant cells, scar-forming myofibroblasts, and inflammatory M1-like macrophages but negligible amounts of anti-inflammatory M2-like phenotypes. However, the PSL-multilayer coating markedly diminishes these detrimental signatures by shifting the macrophage phenotype. Unlike other therapeutics, PSL-multilayered coatings also stimulate muscle regeneration. This study demonstrates that PSL-multilayered coatings are effective in eliminating FBRs and promoting regeneration, hence offering potent and broad applications for implantable biomaterials. This article is protected by copyright. All rights reserved.
Pages e2302611
Published 2023-12-14
DOI 10.1002/adhm.202302611
PMID 38095751
PMC PMC11468989
MeSH Animals Biocompatible Materials* / pharmacology Fibrosis Foreign-Body Reaction / pathology Macrophages Prostheses and Implants* Rats
IF 7.367
Resource
Human and Animal Cells RAW 264(RCB0535) C2C12(RCB0987) NIH/3T3(RCB2767)