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Immune System Imaging
Published in Margarida M. Barroso, Xavier Intes, In Vivo, 2020
Michael J. Hickey, M. Ursula Norman
Monocyte release from the bone marrow is mediated by different mechanisms from those used by neutrophils, with CCR2 being central to this response (Serbina and Pamer, 2006). To examine monocyte behavior in the bone marrow, various myeloid cell reporter mice have been examined. Cx3Cr1gfp/+ mice express GFP in monocytes, macrophages and other myeloid lineages. GFP-labeled cells in the bone marrow of these mice adopt both spherical and dendritic morphologies, consistent with GFP labeling monocytes and their progenitors, as well as macrophages and dendritic cells (DCs) (Evrard et al., 2015). To detect monocyte progenitors/immature monocytes more selectively, MacBlue mice (expressing cyan fluorescent protein/CFP in monocytes) have been used (Jacquelin et al., 2013). In these mice, CFP is more monocyte-restricted than GFP is in Cx3Cr1gfp/+ mice, and CFP+ cells in the bone marrow are predominantly spherical in nature and, therefore, more likely to represent immature monocytes. In 2PM imaging studies of the bone marrow of MacBlue mice, CFP+ cells displayed variable motility. On average, monocytes were slowly migratory, although cells adjacent to the vasculature moved more rapidly and in a more directed fashion, even being occasionally observed migrating on the endothelial surface of the sinusoidal vasculature (Jacquelin et al., 2013). In studies of bone marrow repopulation following chemotherapy-mediated ablation, CFP+ cells repopulated the parenchyma over 3–5 days, initially as single, blastic cells, which developed into clusters by Day 5. At this stage, highly motile monocytes were detected in the perivascular regions, and monocytes were seen to transmigrate into the sinusoidal vasculature. In a more acute model, LPS stimulation was seen to stimulate monocyte migration within 1 hour and induce egress into the sinusoidal vasculature within 2 hours (Evrard et al., 2015).
Diagnosis and management of implant debris-associated inflammation
Published in Expert Review of Medical Devices, 2020
Stuart B. Goodman, Jiri Gallo, Emmanuel Gibon, Michiaki Takagi
Yao and colleagues [137] showed that the mutant MCP-1 protein (called 7ND) was able to dramatically reduce the chemotactic effect of human MΦ when exposed to a conditioned media obtained after challenging murine MΦ with PMMA particles. 7ND acts by blocking the chemokine receptor CCR2 which is MCP-1 receptor. Keeney et al. [138] coated 7ND protein onto titanium rods. 7ND decoy was effectively released but also remained bioactive by decreasing MΦ trafficking toward MCP-1. The concept was then brought to in-vivo studies [139–141], in which biologically active rods coated with 7ND were able to mitigate UHMWPE particle-induced osteolysis and decrease systemic MΦ recruitment. Sato et al. [140] also showed that the continuous delivery of IL-4 led to increased trabecular bone volume in the presence of UHMWPE particles.