Nanotopographical Coatings Induce an Early Phenotype-Specific Response of Primary Material-Resident M1 and M2 Macrophages.

Tobias Schmitz,Heike Walles,Jürgen Groll,Claus Moseke,Tobias Weigel,Uwe Gbureck,Jan Hansmann,Maren Jannasch

doi:10.3390/ma13051142

Abstract

Implants elicit an immunological response after implantation that results in the worst case in a complete implant rejection. This biomaterial-induced inflammation is modulated by macrophages and can be influenced by nanotopographical surface structures such as titania nanotubes or fractal titanium nitride (TiN) surfaces. However, their specific impact on a distinct macrophage phenotype has not been identified. By using two different levels of nanostructures and smooth samples as controls, the influence of tubular TiO2 and fractal TiN nanostructures on primary human macrophages with M1 or M2-phenotype was investigated. Therefore, nanotopographical coatings were either, directly generated by physical vapor deposition (PVD) or by electrochemical anodization of titanium PVD coatings. The cellular response of macrophages was quantitatively assessed to demonstrate a difference in biocompatibility of nanotubes in respect to human M1 and M2-macrophages. Depending on the tube diameter of the nanotubular surfaces, low cell numbers and impaired cellular activity, was detected for M2-macrophages, whereas the impact of nanotubes on M1-polarized macrophages was negligible. Importantly, we could confirm this phenotypic response on the fractal TiN surfaces. The results indicate that the investigated topographies specifically impact the macrophage M2-subtype that modulates the formation of the fibrotic capsule and the long-term response to an implant.

Highlights

Any medical device, prosthesis or biomaterial creates a trauma following implantation, whereby the presence of the implant subsequently effects the healing of the trauma site
SEM revealed that a 4 h coating of the glass substrates produced a the control experiment (Ti) coating with a dense surface (Figure 2a)
Macrophages originate from monocytes that rapidly differentiate when recruited in the context of inflammation [39,40]

Summary

Introduction

Prosthesis or biomaterial creates a trauma following implantation, whereby the presence of the implant subsequently effects the healing of the trauma site. The altered healing process is known as the foreign body reaction (FBR) and results in the worst case in a complete implant rejection [1]. The FBR is a key factor in the long-term survival and function of an implanted biomaterial [2]. During the FBR, macrophages play a major role [3,4]. Materials 2020, 13, 1142 population of short-lived pro-inflammatory M1 macrophages is replaced by long-vitae M2 macrophages. The chronic accumulation and fusion of these M2 macrophages in the proximity of the implant induces the production of a dense fibrous capsule by fibroblasts, isolating the foreign body from the native tissue [4]

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