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Interleukin-10 이 $interleukin-1{\beta}$로 유도되는 골흡수에 미치는 효과
유윤정,강윤선,이승일,Yu, Yun-Jung,Kang, Yun-Sun,Lee, Syng-Ill 대한치주과학회 1994 Journal of Periodontal & Implant Science Vol.24 No.2
The cytokines released by osteoblasts induce bone resorption via the differentiation of osteoclast precursors. In this process, $interleukin-1{\beta}$($IL-1{\beta}$)-induced bone resorption is mediated by granulocyte macrophage-colony stimulation factor(GM-CSF), interleukin-6 (IL-6), and tumor necrosis factor ${\alpha}$($TNF-{\alpha}$) released from osteoblasts. Since these cytokines (GM-CSF, IL-6, $TNF-{\alpha}$) are produced by not only osteoblasts but also monocytes, and interleukin-10(I1-10) inhibits the secretion of these cytokines from monocytes, it may be speculated that IL 10 could modulate the production of GM-CSF, IL-6, and $TNF-{\alpha}$ by osteoblasts, then control $IL-1{\beta}-induced$ bone resorption. Therefore, the aims of the present study were to examine the effects of IL-10 on bone resorption. The sixten or seventeen-day pregnant ICR mice were injected with $^{45}Ca$ and sacrificed one day after injection. Then fetal mouse calvaria prelabeled with $^{45}Ca$ were dissected out. In order to confirm the degree of bone resorption, mouse calvaria were treated with Lipopolysaccharide(LPS), $TNF-{\alpha}$, $IL-1{\alpha}$, IL-8, $IL-1{\beta}$, and $IL-1{\alpha}$, Then, IL-10 and $interferon-{\gamma}$ ($IFN-{\gamma}$) were added to calvarial medium, in an attempt to evaluate the effect of $IL-1{\beta}-induced$ bone resorption. In addition, osteoclasts formation in bone marrow cell cultures, and the concentration of IL-6, $TNF-{\alpha}$, and GM-CSF produced from mouse calvarial cells were investigated in response to $IL-1{\beta}$ alone and simultaneously adding f $IL-1{\beta}$ and IL-10. The degree of bone resorption was expressed as the ratio of $^{45}Ca$ release(the treated/the control). The osteoclasts in bone marrow cultures were indentified by tartrate resistant acid phosphatase(TRAP) stain and the concentration of the cytokines was quantified using enzyme linked immunosorbent method. As results of these studies, bone resorption was induced by LPS(1 ng/ml ; the ratio of $^{45}Ca$ release, $1.14{\pm}0.07$). Also $IL-1{\beta}$(1 ng/ml), $IL-1{\alpha}$(1 ng/ml), and $TNF-{\alpha}$(1 ng/ml) resulted in bone resorption(the rations of $^{45}Ca$ release, $1.61{\pm}0.26$, $1.77{\pm}0.03$, $1.20{\pm}0.15$ respectively), but IL-8 did not(the ratio of $^{45}Ca$ release, $0.93{\pm}0.21$). The ratios of $^{45}Ca$ release in response to IL-10(400 ng/ml) and $IFN-{\gamma}$(100 ng/ml) were $1.24{\pm}0.12$ and $1.08{\pm}0.04$ respectively, hence these cytokines inhibited $IL-1{\beta}$(1 ng/ml)-induced bone resorption(the ratio of $^{45}Ca$ release $1.65{\pm}0.24$). While $IL-1{\beta}$(1 ng/ml) increased the number of TRAP positive multinulcleated cells in bone marrow cultures($20{\pm}11$), simultaneously adding $IL-1{\beta}$(1 ng/ml) and IL-10(400 ng/ml) decreased the number of these cells($2{\pm}2$). Nevertheless, IL-10(400 ng/ml) did not affect the IL-6, GM-CSF, and $TNF-{\alpha}$ secretion from $IL-1{\beta}$(1 ng/ml)-activated mouse calvarial cells. From the above results, it may be suggested that IL-10 inhibites $IL-1{\beta}-induced$ osteoclast differntiation and bone resorption. However, the inhibitory effect of IL-10 on the osteoclast formation seems to be mediated not by the reduction of IL-6, GM-CSF, and $TNF-{\alpha}$ production, but by other mechanisms.
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Interleukin-1β에 의하여 치주인대세포에서 유리된 cytokine이 파골세포형성에 미치는 영향
이종갑,곽월아,유윤정,이승일,김태선 大韓小兒齒科學會 1996 大韓小兒齒科學會誌 Vol.23 No.1
Tooth movement is induced by bone remodeling during orthodontic treatment. Bone remodeling is regulated by various cytokines. Especially interleukin-1 (IL-1β), a cytokine present in periodontal ligaments of experimentally moved teeth, elicits bone resorption. In these processes, IL-1-induced bone resorption is mediated by interleukin-6 (IL-6) and granulocyte macrophage-colony stimulating fector (GM-CSF) secreted from osteoblasts. Periodontal ligament cells, which function as an anchorage for tooth, lie between alveolar bone and cementum. Therefore cytokines produced in the periodontal ligament (PDL) cells may also directly affect alveolar bone resorption in orthodontic tooth movement. Here I have examined whether PDL cells express IL-1β,interleukin-6 (IL-6) and granulocyte macrophage-colony stimulating factor (GM-CSF) mRNA and secrete those cytokines in response to IL-1β. Finally I have investigated whether IL-6 produced from PDL cells induces osteoclast formation in mouse bone marrow cell cultures. The expression of mRNA was estimated by polymerase chain reaction (PCR). The concentration of cytokines was quantified using enzyme linked immunosorbent method and the osteoclasts in bone marrow cultures were identified by tartrate resistant acid phosphatase (TRAP) stain. As results of these studies, IL-1βstimulated the expression of IL-1β, IL-6 and GM-CSF mRNA in PDL cells. 0.05 ng/ml IL-1βalso induced maximum production of Il-6 and GM-CSF in these cells. After an addition of IL-1β(0.05 ng/ml), IL-6 production increased from 2 hours to 8 hours and GM-CSF production also increased from 4 hours to 8 hours. IL-6 (100 ng/ml) increased the number of TRAP positive multinucleated cells in the presence of soluble interleukin-6 receptor (sIL-6R, 100 ng/ml). These results suggest that IL-1βmay stimulate alveolar bone resorption by inducing IL-6 and GM-CSF production in PDL cells which enhance osteoclast differentiation and IL-6 enhances osteoclast formation in the presence of sIL-6R. And this process by IL-1βmay be closely associated with alveolar bone resorption induced by orthodontic force.
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