The calcium-binding protein S100A12 induces neutrophil adhesion, migration, and release from bone marrow in mouse at concentrations similar to those found in human inflammatory arthritis

The calcium-binding protein S100A12 induces neutrophil adhesion, migration, and release from bone marrow in mouse at concentrations similar to those found in human inflammatory arthritis
复制标题

DOI:
10.1016/s1521-6616(02)00043-8
复制
发表时间:
2003-04-01
影响因子:
8.6
通讯作者:
Tessier, PA
Tessier, PA
中科院分区:
医学3区
文献类型:
--
作者:
Rouleau, P;Vandal, K;Tessier, PA

文献摘要

被引文献

相似文献

我们研究了 S100A12 在滑膜炎症中的促炎活性。痛风、类风湿性关节炎、银屑病关节炎患者的滑液和血浆中 S100A12 水平升高,而骨关节炎(一种非炎症性疾病)患者的 S100A12 水平检测不到。事实证明,S100A12 可以通过 Mac-1 诱导中性粒细胞粘附到纤维蛋白原上,其浓度与滑液中的浓度相似。相似的浓度诱导小鼠气囊模型中大量中性粒细胞和单核细胞的募集。为了表征 S100A12 血浆水平增加的影响,对小鼠静脉注射 S100A12。这导致中性粒细胞从骨髓动员到外周血。这些结果表明,S100A12 通过诱导中性粒细胞从骨髓中释放以及激活中性粒细胞向炎症部位的粘附和迁移来刺激中性粒细胞的积累。 (C) 2003 年爱思唯尔科学(美国)。版权所有。
We investigated the proinflammatory activities of S100A12 in the context of synovial inflammation. S100A12 levels were increased in the synovial fluids and plasma of patients with gout, rheumatoid arthritis, psoriatic arthritis, and undetectable in osteoarthritis, a noninflammatory disorder. S100A12 proved to induce neutrophil adhesion to fibrinogen via Mac-1 at concentrations similar to those found in the synovial fluids. Similar concentrations induced the recruitment of large numbers of neutrophils and monocytes in the murine air pouch model. To characterize the effect of increased S100A12 plasma levels, mice were injected intravenously with S100A12. This led to the mobilization of neutrophils from the bone marrow to the peripheral blood. These results suggest that S100A12 stimulates the accumulation of neutrophil by inducing their release from the bone marrow, as well as by activating their adhesion and migration toward inflammatory sites. (C) 2003 Elsevier Science (USA). All rights reserved.