Ichimiya Issei, Yoshida Kazuhide, Suzuki Masashi, Mogi Goro
Department of Immunology and Allergy (Otolaryngology), Oita Medical University, Oita, Japan.
Ann Otol Rhinol Laryngol. 2003 Aug;112(8):722-8. doi: 10.1177/000348940311200813.
Secondary cultures from murine spiral ligament (SL) fibrocytes were stimulated with proinflammatory cytokines interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), and expression of various adhesion molecules was investigated. Cultures without cytokine stimulation did not show positive immunostaining for vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), or mucosal addressin cell adhesion molecule-1 (MAdCAM-1). Although staining was also negative after stimulation with IL-1beta, VCAM-1 and ICAM-1 staining was observed after the cells were stimulated with TNF-alpha. Reverse transcription-polymerase chain reaction analysis showed messenger RNAs for both VCAM-1 and ICAM-1 expression to be present after fibrocytes were stimulated with TNF-alpha. These data suggest that activated fibrocytes may cause inflammatory cells to persist in the SL. Given that SL fibrocytes may play a role in homeostasis of cochlear fluid and ion concentrations, prolongation of the inflammatory response could lead to fibrocyte damage that might ultimately result in cochlear malfunction.
用促炎细胞因子白细胞介素 -1β(IL -1β)和肿瘤坏死因子 -α(TNF -α)刺激来自小鼠螺旋韧带(SL)纤维细胞的传代培养物,并研究各种黏附分子的表达。未用细胞因子刺激的培养物对血管细胞黏附分子 -1(VCAM -1)、细胞间黏附分子 -1(ICAM -1)或黏膜地址素细胞黏附分子 -1(MAdCAM -1)未显示阳性免疫染色。尽管用IL -1β刺激后染色也为阴性,但在用TNF -α刺激细胞后观察到VCAM -1和ICAM -1染色。逆转录 - 聚合酶链反应分析表明,在用TNF -α刺激纤维细胞后,存在VCAM -1和ICAM -1表达的信使核糖核酸。这些数据表明,活化的纤维细胞可能导致炎症细胞在螺旋韧带中持续存在。鉴于螺旋韧带纤维细胞可能在耳蜗液和离子浓度的稳态中起作用,炎症反应的延长可能导致纤维细胞损伤,最终可能导致耳蜗功能障碍。