{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T06:21:53Z","timestamp":1789971713835,"version":"4.0.1"},"reference-count":51,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2006,1,3]],"date-time":"2006-01-03T00:00:00Z","timestamp":1136246400000},"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":[[2006,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Particulate wear debris induces the expression of pro\u2010inflammatory cytokine and chemokine genes in various cell types of the periprosthetic region. We have previously reported that titanium particles stimulate the selective induction of interleukin\u20108 (IL\u20108) and monocyte chemoattractant protein\u20101 (MCP\u20101) chemokines in human osteoblast\u2010like osteosarcoma cells. In this study, we characterize the human bone marrow\u2010derived osteoblast chemokine response to titanium particles. We demonstrate that titanium particles result in enhanced IL\u20108 and MCP\u20101 protein secretion as well as differential chemokine gene activation. Osteoblast chemokine expression was regulated at the level of gene transcription, with a time\u2010dependent induction of NF\u2010\u03baB activation. Inhibition studies with <jats:italic>N<\/jats:italic>\u2010acetyl\u2010<jats:sc>L<\/jats:sc>\u2010cysteine (Nac) and MG\u2010132 suggest that titanium particle activation of NF\u2010\u03baB activity and IL\u20108 chemokine exression involves oxidant signaling and I\u03baB\u03b1\u2010proteasomal degradation. Activation of the NF\u2010\u03baB transcription factor, as well as the IL\u20108 gene, are redox\u2010regulated. We also demonstrate that while cytochalasin D, a potent inhibitor of phagocytosis, suppressed the titanium particle effect on IL\u20108 protein release in human bone marrow\u2010derived osteoblasts, the inhibitor had no effect on IL\u20108 expression in MG\u201063 osteoblast\u2010like cells. Collectively, these results provide insight into the potential mechanisms responsible for the particulate activation of osteoblast chemokine expression and suggest an important role for the osteoblast in the pathogenesis of periprosthetic osteolysis. \u00a9 2005 Wiley Periodicals, Inc. 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