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T, Alsulaimani F. Bacteria induce osteoclastogenesis via an osteoblast-independent pathway. Infect Immun 2002; 70: 3143 8
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This article cites 30 articles, 10 of which can be accessed free
expression by short interfering RNA attenuates
"... Down-regulation of Toll-like receptor 4 gene ..."
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BioMed Central
, 2009
"... Research article Plasmodium chabaudi limits early Nippostrongylus brasiliensis-induced pulmonary immune activation and Th2 polarization in co-infected mice ..."
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Research article Plasmodium chabaudi limits early Nippostrongylus brasiliensis-induced pulmonary immune activation and Th2 polarization in co-infected mice
Edinburgh Research Explorer
"... Macrophages exposed continuously to lipopolysaccharide and other agonists that act via toll-like receptors exhibit a sustained and additive activation state Citation for published version: ..."
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Macrophages exposed continuously to lipopolysaccharide and other agonists that act via toll-like receptors exhibit a sustained and additive activation state Citation for published version:
Review Article The Role of TLR and Chemokine in Wear Particle-Induced Aseptic Loosening
, 2012
"... which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Wear particle-induced periprosthetic osteolysis remains the principal cause of aseptic loosening of orthopaedic implants. Monocytes/macrophages phagocytose wear particles and r ..."
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which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Wear particle-induced periprosthetic osteolysis remains the principal cause of aseptic loosening of orthopaedic implants. Monocytes/macrophages phagocytose wear particles and release cytokines that induce inflammatory response. This response promotes osteoclast differentiation and osteolysis. The precise mechanisms by which wear particles are recognized and induce the accumulation of inflammatory cells in the periprosthetic tissue have not been fully elucidated. Recent studies have shown that toll-like receptors (TLRs) contribute to the cellular interaction with wear particles. Wear particles are recognized by monocytes/macrophages through TLRs coupled with the adaptor protein MyD88. After the initial interaction, wear particles induce both local and systemic migration of monocytes/macrophages to the periprosthetic region. The cellular migration is mediated through chemokines including interleukin-8, macrophage chemotactic protein-1, and macrophage inhibitory protein-1 in the periprosthetic tissues. Interfering with chemokine-receptor axis can inhibit cellular migration and inflammatory response. This paper highlights recent advances in TLR, and chemokine participated in the pathogenesis of aseptic loosening. A comprehensive understanding of the recognition and migration mechanism is critical to the development of measures that prevent wear particle-induced aseptic loosening of orthopaedic implants. 1.
CONTENT ALERTS
, 2009
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