Involvement of toll-like receptor 4 in the inflammatory reaction induced by hydroxyapatite particles

Grandjean-Laquerriere, Alexia; Tabary, Olivier; Jacquot, Jacky; Richard, Daniel; Frayssinet, Patrick; Guenounou, Moncef; Laurent-Maquin, Dominique; Laquerrière, Patrice; Gangloff, Sophie C.

doi:10.1016/j.biomaterials.2006.09.015

Cited by 106 publications

(56 citation statements)

References 22 publications

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“…Upregulation of TLR4 was consistent with the observation that the scaffold could activate macrophages, with or without fibroblasts [17]. In addition, macrophage activations are generally associated with phagocytosis of biomaterials [41][42][43]. Increased expression of TLR4 during scaffold degradation suggested its role in removing the debris of degraded scaffold through receptor-mediated phagocytosis.…”

Section: Receptors Involved In Scaffold Degradationsupporting

confidence: 83%

The biodegradability of electrospun Dextran/PLGA scaffold in a fibroblast/macrophage co-culture

2008

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Fibroblast and macrophage are two dominant cell types respond cooperatively to degrade implanted biomaterials. Using an electrospun Dextran/Poly-lactide-co-glycolide (PLGA) scaffold as a model, an in vitro fibroblast/macrophage co-culture system was developed to investigate the degradability of implantable biodegradable materials. SEM showed that both fibroblasts and macrophages were able to degrade the scaffold, separately or cooperatively. Under the synergistic coordination of macrophages and fibroblasts, scaffolds showed faster degradation rate than their counterparts incubated with a single type of cells as well as in PBS or cell culture medium. Lysozyme, non-specific esterase (NSE), gelatinase, hyaluronidase-1 and α-glucosidase were upregulated in the presence of the scaffold, suggesting their roles in the cell-mediated scaffold degradation. In addition, the expressions of cell surface receptors CD204 and Toll like receptor 4 (TLR4) were elevated one week after cell seeding, implying that these receptors might be involved in scaffold degradation. The results of in vivo subdermal implantation of the scaffold further confirmed the biodegradability of the Dextran/PLGA scaffold. The fibroblast/macrophage co-culture model adequately mimicked the in vivo environment and could be further developed into an in vitro tool for initial biomaterial evaluation.

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Section: Receptors Involved In Scaffold Degradationsupporting

confidence: 83%

The biodegradability of electrospun Dextran/PLGA scaffold in a fibroblast/macrophage co-culture

2008

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“…Similarly, Grandjean-Laquerriere et al [10] found that hydroxyapatite particles interacted with TLR4 to induce TNF-production by macrophages. However, Schematic representation of the inflammasome and the role of some innate immunity receptors in crystal-induced inflammation (CII).…”

Section: Role Of Myeloid Differentiation Factor 88 Interleukin-1 Recmentioning

confidence: 96%

Recent developments in crystal-induced inflammation pathogenesis and management

Lioté

Ea²

2007

Curr Rheumatol Rep

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Crystal-induced inflammation pathogenesis is undergoing a transition with respect to monosodium urate, calcium pyrophosphate dihydrate, and even basic calcium phosphate crystals. It is now recognized that innate immunity could be involved in the earlier pathogenic events and that the inflammasome, along with other signaling pathways, is activated and results in interleukin-1 processing and secretion, ultimately activating cells as a paracrine or autocrine cytokine. Management of acute and chronic monosodium urate crystal-induced inflammation, namely gout, has been critically reviewed by a dedicated European working group, and on the behalf of the European League against Rheumatism, 12 evidence-based recommendations have been reported. Calcium pyrophosphate dihydrate chronic inflammation could benefit from colchicine and from methotrexate as an anti-inflammatory agent.

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“…Moreover, it has recently been reported that human TLR4 can be activated by cobalt or nickel ions [88,110], both of which can be released by corrosion of cobaltchromium implants [39]. Functional studies have shown that deletion of TLR2 and/or TLR4 in murine systems substantially reduces the in vitro and in vivo responses to titanium [8,37], UHMWPE [40], cobalt-chromium [85], and hydroxyapatite [34] particles. Moreover, similar results have also been obtained for deletion of the myeloid differentiation primary response gene (MyD88) with both PMMA and cobalt-chromium particles [82,85].…”

Section: Toll-like Receptorsmentioning

confidence: 99%

Do Genetic Susceptibility, Toll-like Receptors, and Pathogen-associated Molecular Patterns Modulate the Effects of Wear?

Greenfield

2014

Clin Orthop Relat Res

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Background Overwhelming evidence supports the concept that wear particles are the primary initiator of aseptic loosening of orthopaedic implants. It is likely, however, that other factors modulate the biologic response to wear particles. This review focuses on three potential other factors: genetic susceptibility, Toll-like receptors (TLRs), and bacterial pathogen-associated molecular patterns (PAMPs). Where Are We Now? Considerable evidence is emerging that both genetic susceptibility and TLR activation are important factors that modulate the biologic response to wear particles, but it remains controversial whether bacterial PAMPs also do so. Where Do We Need to Go? Detailed understanding of the roles of these other factors may lead to identification of novel therapeutic targets for patients with aseptic loosening. How Do We Get There? Highest priority should be given to polymorphism replication studies with large numbers of patients and studies to replicate the reported correlation between bacterial biofilms and the severity of aseptic loosening.

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Involvement of toll-like receptor 4 in the inflammatory reaction induced by hydroxyapatite particles

Cited by 106 publications

References 22 publications

The biodegradability of electrospun Dextran/PLGA scaffold in a fibroblast/macrophage co-culture

The biodegradability of electrospun Dextran/PLGA scaffold in a fibroblast/macrophage co-culture

Recent developments in crystal-induced inflammation pathogenesis and management

Do Genetic Susceptibility, Toll-like Receptors, and Pathogen-associated Molecular Patterns Modulate the Effects of Wear?

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