Tumor necrosis factor primes and metal particles activate the NLRP3 inflammasome in human primary macrophages.

ABSTRACT: Aseptic loosening of total joint replacements is driven by a macrophage-mediated inflammatory reaction to implant-derived wear particles. Phagocytosis of implant debris has been suggested to activate the NLRP3 inflammasome leading to secretion of interleukin (IL)-1β. However, factors and molecular mechanisms driving the particle-induced inflammasome activation are yet to be fully elucidated. In this study, we investigated the inflammasome response of human primary macrophages to titanium, chromium, and molybdenum particles in vitro. We observed that particles alone were not sufficient to induce IL-1β secretion, but an additional priming signal-such as bacterial lipopolysaccharide (LPS)-was required to license the inflammasome activation. By using specific inhibitors against the inflammasom

SUBMITTER: Jamsen E 

PROVIDER: S-EPMC7729209 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature