Role of prostaglandins in interleukin‐1‐induced bone resorption in mice in vitro
Role of prostaglandins in interleukin‐1‐induced bone resorption in mice in vitro
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DOI：
10.1002/jbmr.5650060212
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发表时间：
1991-02
影响因子：
6.2
通讯作者：
T. Akatsu;N. Takahashi;N. Udagawa;Kazunobu Imamura;A. Yamaguchi;Kanji Sato;N. Nagata;T. Suda
中科院分区：
文献类型：
--
作者：
T. Akatsu;N. Takahashi;N. Udagawa;Kazunobu Imamura;A. Yamaguchi;Kanji Sato;N. Nagata;T. Suda
使用三种不同的体外试验系统在小鼠中检查了白细胞介素1（IL-1）诱导的骨吸收机制：胎儿长骨器官培养系统、骨髓培养系统以及原代成骨细胞群和脾细胞的共培养系统。在器官培养系统中，重组人IL-1α（rhIL-1α）增加骨吸收和破骨细胞数量。在消炎痛的存在下，两者都被部分抑制。在骨髓培养中，rhIL-1α和rhIL-1β均刺激破骨细胞样细胞的形成，同时加入吲哚美辛可完全抑制破骨细胞样细胞的形成。此外，破骨细胞样细胞形成的数量和释放到培养基中的前列腺素E2（PGE 2）的量之间有很好的相关性。这表明PGE 2参与了IL-1介导的破骨细胞样细胞形成的机制。在原代成骨细胞群和脾细胞的共培养中，rhIL-1再次刺激破骨细胞样细胞的形成，这被加入吲哚美辛抑制。在成骨细胞和脾细胞之间的直接相互作用被抑制的共培养物中，PGE 2的合成同样增加，但没有破骨细胞样细胞形成。这些结果表明，IL-1通过涉及PG（最有可能是PGE 2）的机制诱导破骨细胞形成。此外，破骨细胞祖细胞和成骨细胞之间的直接相互作用是由IL-1诱导的破骨细胞募集所必需的。
The mechanism of bone resorption induced by interleukin 1 (IL‐1) was examined in mice using three different in vitro assay systems: a fetal long bone organ culture system, a bone marrow culture system, and a co‐culture system of primary osteoblastic cell populations and spleen cells. In the organ culture system, recombinant human IL‐1α (rhIL‐1α) increased both bone resorption and osteoclast number. Both were partially suppressed in the presence of indomethacin. In the marrow culture, both rhIL‐1α and rhIL‐1β stimulated osteoclastlike cell formation, which was completely inhibited by adding indomethacin concurrently. Furthermore, there was a good correlation between the number of osteoclastlike cells formed and the amount of prostaglandin E2 (PGE2) released into the culture media. This indicates that PGE2 is involved in the mechanism of IL‐1‐mediated osteoclastlike cell formation. In the coculture of primary osteoblastic cell populations and spleen cells, rhIL‐1 again stimulated osteoclastlike cell formation, which was inhibited by adding indomethacin. In the cocultures in which direct interaction between osteoblastic cells and spleen cells was inhibited, PGE2 synthesis was similarly increased but no osteoclastlike cells were formed. These results indicate that IL‐1 induces osteoclast formation by a mechanism involving PG (most likely PGE2). Furthermore, direct interaction between osteoclast progenitors and osteoblastic cells is required in the osteoclast recruitment induced by IL‐1.