{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T09:22:12Z","timestamp":1789204932859,"version":"build-2803163510"},"reference-count":31,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2009,4,7]],"date-time":"2009-04-07T00:00:00Z","timestamp":1239062400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Biomedical Materials Res"],"published-print":{"date-parts":[[2010,3,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The biological response to orthopaedic wear debris is central to peri\u2010prosthetic tissue inflammation and osteolysis, through mechanisms that include local inflammatory cytokine production. In particular, interleukin\u20101 \u03b2 (IL\u20101\u03b2) and tumor necrosis factor\u2010\u03b1 (TNF\u2010\u03b1|) are generated in high quantities following monocyte accumulation in periprosthetic inflammatory tissue, and these cytokine combine with other inflammatory mediators to trigger osteolysis. Since the precise mechanisms involved in debris\u2010associated inflammation remain unclear, it is important to understand how wear debris particles initially interact with inflammatory cells. We have previously demonstrated that the severity of the inflammation response is influenced by the size, shape, and quantity of particles accumulated in tissues. The current <jats:italic>in vitro<\/jats:italic> and <jats:italic>in vivo<\/jats:italic> results indicate that heat\u2010shock protein (Hsp) expression is elevated when monocytes are exposed to wear debris particles. We have also addressed the mechanisms by which heat\u2010shock protein 60 (Hsp60) positively modulates inflammatory cytokines via Toll\u2010like receptor\u20104 (TLR4) signal transduction pathway on mononuclear cells. Furthermore, down\u2010regulation of TLR4 expression using antisense oligonucleotides targeted to TLR4 mRNA suppressed cytokine production in both exogenous Hsp60 and particles stimulated cultures. Collectively, these data indicate that monocytic Hsp60 is an additional inducible immunoregulatory mediator in response to particle\u2010induced cell stress. \u00a9 2009 Wiley Periodicals, Inc. 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