Dermal fillers do not induce upregulation of NLRP3 inflammasomes or expression of inflammatory cytokines in granulomas

Background Filling materials have increasingly been used in aesthetics over the last decades. Understanding the pathophysiology of granuloma formation as a very relevant unwanted side effect of filler application may be essential to help avoid these adverse events. Aims Our aim was to investigate the role of the inflammasome in the formation of filler granuloma, as a central column of the innate immune response. Methods RPMI 1640 medium was used for growth of THP-1 cells and the induction of THP-1 macrophages. Sonication was applied in order to crush the acrylic particles of the filler. ELISA was the method of analysis for the specific cytokines. Biopsy specimens of filler granuloma were analyzed by various immunohistochemical methods. GraphPad Prism 5 software was used for the statistical data analysis. Results Neither was the sensor NALP3 overexpressed, nor could an elevated expression of cleaved IL-1 beta, IL-18, or IFN-gamma be detected. Furthermore, no increased expression of IL-8 or IL-1 beta was detectable in vitro. Conclusion No increased inflammasome activation could be observed; however, filler granulomas were infiltrated with granulocytes and macrophages. Therefore, we speculate that an unspecific immune response might be the key player in the formation of filler granuloma.