The roles of monocytic heat shock protein 60 and Toll-like receptors in the regional inflammation response to wear debris particles
| Autor: | Lawrence G. Morawa, Sam Nasser, Bingrong Zheng, Michael Latteier, Weiping Ren, Paul H. Wooley, Hsiao-Nan Hao |
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| Rok vydání: | 2009 |
| Předmět: |
Adult
Materials science medicine.medical_treatment Joint Prosthesis Interleukin-1beta Biomedical Engineering Inflammation Monocytes Proinflammatory cytokine Biomaterials Mice Heat Shock Transcription Factors Heat shock protein medicine Animals Humans Particle Size Cells Cultured Heat-Shock Proteins Mice Inbred BALB C Tumor Necrosis Factor-alpha Monocyte Toll-Like Receptors Metals and Alloys Chaperonin 60 Oligonucleotides Antisense Cell biology Prosthesis Failure DNA-Binding Proteins medicine.anatomical_structure Cytokine Immunology Ceramics and Composites TLR4 Tumor necrosis factor alpha Signal transduction medicine.symptom Inflammation Mediators Polyethylenes Transcription Factors |
| Zdroj: | Journal of biomedical materials research. Part A. 92(4) |
| ISSN: | 1552-4965 |
| Popis: | The biological response to orthopaedic wear debris is central to peri-prosthetic tissue inflammation and osteolysis, through mechanisms that include local inflammatory cytokine production. In particular, interleukin-1 beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha|) 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-associated 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 in vitro and in vivo results indicate that heat-shock protein (Hsp) expression is elevated when monocytes are exposed to wear debris particles. We have also addressed the mechanisms by which heat-shock protein 60 (Hsp60) positively modulates inflammatory cytokines via Toll-like receptor-4 (TLR4) signal transduction pathway on mononuclear cells. Furthermore, down-regulation 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-induced cell stress. |
| Databáze: | OpenAIRE |
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