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促炎细胞因子刺激培养的螺旋韧带成纤维细胞后粘附分子的表达

Expression of adhesion molecules by cultured spiral ligament fibrocytes stimulated with proinflammatory cytokines.

作者信息

Ichimiya Issei, Yoshida Kazuhide, Suzuki Masashi, Mogi Goro

机构信息

Department of Immunology and Allergy (Otolaryngology), Oita Medical University, Oita, Japan.

出版信息

Ann Otol Rhinol Laryngol. 2003 Aug;112(8):722-8. doi: 10.1177/000348940311200813.

Abstract

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.

摘要

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。

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