Abstract
Monocytes and macrophages are the first barrier of the innate immune system, which interact with abrasion and corrosion products, leading to the release of proinflammatory mediators and free reactive molecules. The aim of this study was to understand inflammation-relevant changes in monocytes and macrophages after exposure to corrosion products. To do this, the THP-1 cell line was used to analyze the effects of metal ions simultaneously in monocytes and differentiated macrophages. Cells were stimulated with several concentrations of metal salts (CoCl2, NiCl2, CrCl3 × 6H2O) to analyze viability, gene expression, protein release and ROS production. Untreated cells served as negative controls. While exposure to Cr(3+) did not influence cell viability in both cell types, the highest concentration (500 µM) of Co(2+) and Ni(2+) showed cytotoxic effects mirrored by significantly reduced metabolism, cell number and a concomitant increase of ROS. The release of IL-1β, IL-8, MCP-1 and M-CSF proteins was mainly affected in macrophages after metal ion exposure (100 µM), indicating a higher impact on pro-inflammatory activity. Our results prove that monocytes and macrophages react very sensitively to corrosion products. High concentrations of bivalent ions lead to cell death, while lower concentrations trigger the release of inflammatory mediators, mainly in macrophages.
Highlights
Degenerative joint diseases contribute to the decrease in quality of life during aging
Our results prove that monocytes and macrophages react very sensitively to corrosion products
THP-1 monocytes were cultivated in Roswell Park Memorial Institute (RPMI) 1640 medium supplemented with 20% fetal calf serum (FCS; Pan Biotech GmbH, Aidenbach, Germany), 2% L-Alanyl-L-Glutamin (Biochrom GmbH, Berlin, Germany), 1% amphotericin b and 1%
Summary
Degenerative joint diseases contribute to the decrease in quality of life during aging. Due to increased aging in the general population, therapeutic measures, including total joint replacement, progressively gain importance in tackling these diseases [1]. One major problem associated with total joint replacement is the necessity of revisions caused by the septic and aseptic loosening of the implant. According to Herberts et al, aseptic loosening accounts for more than 70% of knee prosthesis failures and 44% of hip prosthesis failures [2]. In order to improve the long-term outcome after total joint replacement, orthopedic research targets elevating the implant success rates and understanding the reasons for revision.
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