Interleukin-1.BETA. Stimulates Transendothelial Mobilization of Human Peripheral Blood Mononuclear Cells with a Potential to Differentiate into Osteoclasts in the Presence of Osteoblasts.

Abstract

Abstract.There is accumulating evidence that interleukin-1 (IL-1) levels are increased locally at the site of active bone resorption in a variety of diseases including osteoporosis, periodontal disease and rheumatoid arthritis. However, the pathogenic role of IL-1 in bone loss remains to be fully elucidated.We present here additional evidence that IL-19 enhances endothelial activation and thereby stimulates mobilization of peripheral blood mononuclear cells (PBMCs) from luminal to abluminal spaces across the endothelium. Furthermore, IL-l jl stimulates the differentiation of PBMCs into osteoclast-like cells with bone-resorbing activity in the presence of human osteoblastic SaOS-2 cells without systemic hormones.These findings provide circumstantial evidence for the hypothesis that IL-19 generated in the bone microenviroment plays a stimulatory role in PBMC mobilization from the peripheral circulation and their subsequent differentiation into osteoclast-like cells in the bone tissue. In addition, the present study supports the notion that osteoclast progenitor cells might be derived from the peripheral circulating blood mononuclear cells in human.

IL-1β Inhibits Human Osteoblast Migration

“…The most prominent function of IL-1β in bone loss is the capacity to activate osteoclastogenesis (25)(26)(27). We could show in this study that, in addition to promoting bone resorption, IL-1β also seems to influence bone formation processes as it inhibits osteoblast recruitment in the sense of a soluble repellent factor.…”

“…If IL-1β levels are increased permanently, however, severe bone loss can occur, since IL-1β has been shown to stimulate osteoclastogenesis and bone resorption by inducing RANKL secretion and suppressing OPG secretion (25)(26)(27). While activation of osteoclasts is a well-studied function of IL-1β, few studies are known concerning the inhibition of bone forming cells such as MSC and osteoblasts through IL-1β.…”

“…A different study showed that IL1 -/-hTNFtg mice were completely protected from systemic bone loss mediated through the overexpression of TNF-α (24). A possible pathogenetic role for IL-1β in bone loss is further supported by the fact that IL-1β enables peripheral blood mononuclear cells to differentiate into osteoclasts in the presence of osteoblastic SaOS-2 cells without further stimulation (25). In murine osteo blasts, IL-1β induced receptor activator of NF-κB ligand (RANKL) secretion while reducing osteoprotegerin (OPG) production and activated osteoclastogenesis (26).…”

Interaction of staphylococci with bone

“…Cell culture models support the view that IL-1 and TNFα stimulate the proliferation and differentiation of osteoclast progenitors into mature osteoclasts in the presence of osteoblasts (Mundy, 1991; Pfeilschifter et al, 1989; Tokukoda et al, 2001). TNFα and IL-1β also stimulate osteoclast-mediated bone resorption, a process which may also require the presence of osteoblasts (Azuma et al, 2000; Taubman and Kawai, 2001; Thomson et al, 1987).…”

Osteoclast differentiation by human osteoblastic cell line SaOS-2 primed with bacterial lipid A

“…SaOS‐2 cells have been shown to be able to induce the differentiation of PBMC into osteoclastic cells [41]. In the present study, we examined TRAP‐positive multinucleated cells from PBMC cocultured with SaOS‐2 cells that were primed with and without compound 506 for 24 h. In the absence of compound 506, SaOS‐2 cells induced the differentiation of PBMC into TRAP‐positive cells after a 21‐day cultivation (Fig.…”