...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Allergy >Mast cell adhesion to bronchial smooth muscle in asthma specifically depends on CD51 and CD44 variant 6.
【24h】

Mast cell adhesion to bronchial smooth muscle in asthma specifically depends on CD51 and CD44 variant 6.

机译：哮喘中肥大细胞对支气管平滑肌的粘附具体取决于CD51和CD44变异体6。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

BACKGROUND: Mast cells infiltrate the bronchial smooth muscle (BSM) in asthmatic patients, but the mechanism of mast cell adhesion is still unknown. The adhesion molecules CD44 (i.e. hyaluronate receptor) and CD51 (i.e. vitronectin receptor) are widely expressed and bind to many extracellular matrix (ECM) proteins. The aims of the study are (i) to identify the role of ECM in mast cell adhesion to BSM and (ii) to examine the role of CD51 and CD44 in this adhesion. METHODS: Human lung mast cells, human mast cell line (HMC-1), and BSM cells from control donors or asthmatic patients were cultured in the presence/absence of various cytokines. Mast cell-BSM interaction was assessed using (3)H-thymidine-pulsed mast cells, confocal immunofluorescence, or electron microscopy. Adhesion molecules expression and collagen production on both cell types were evaluated by quantitative RT-PCR, western blot, and flow cytometry. RESULTS: Mast cell adhesion to BSM cells mostly involved type I collagen of the ECM. Such an adhesion was increased in normal BSM cells under inflammatory condition, whereas it was maximal in asthmatic BSM cells. Blockade of either CD51 or CD44 significantly decreased mast cell adhesion to BSM. At the molecular level, protein and the transcriptional expression of type I collagen, CD51 or CD44 remained unchanged in asthmatic BSM cells or in mast cells/BSM cells under inflammatory conditions, whereas that of CD44 variant isoform 6 (v6) was increased. CONCLUSIONS: Mast cell-BSM cell adhesion involved collagen, CD44, and CD51, particularly under inflammatory conditions. CD44v6 expression is increased in asthmatic BSM cells.
机译：背景：肥大细胞浸润哮喘患者的支气管平滑肌（BSM），但肥大细胞粘附的机制仍不清楚。粘附分子CD44（即透明质酸受体）和CD51（即玻连蛋白受体）广泛表达并与许多细胞外基质（ECM）蛋白结合。该研究的目的是（i）识别ECM在肥大细胞与BSM粘附中的作用，以及（ii）检查CD51和CD44在这种粘附中的作用。方法：在存在/不存在各种细胞因子的情况下，培养来自对照供体或哮喘患者的人肺肥大细胞，人肥大细胞系（HMC-1）和BSM细胞。使用（3）H-胸苷脉冲的肥大细胞，共聚焦免疫荧光或电子显微镜评估肥大细胞-BSM的相互作用。通过定量RT-PCR，蛋白质印迹和流式细胞术评估两种细胞类型上的粘附分子表达和胶原蛋白的产生。结果：肥大细胞对BSM细胞的粘附主要涉及ECM的I型胶原。在炎症条件下，正常BSM细胞中这种粘附增加，而哮喘BSM细胞中这种粘附最大。阻断CD51或CD44可以显着降低肥大细胞对BSM的粘附。在分子水平上，在炎症条件下，哮喘的BSM细胞或肥大细胞/ BSM细胞中I型胶原蛋白，CD51或CD44的蛋白质和转录表达保持不变，而CD44变异同工型6（v6）的蛋白质和转录表达却保持不变。结论：肥大细胞-BSM细胞粘附涉及胶原蛋白，CD44和CD51，特别是在炎症条件下。 CD44v6表达在哮喘BSM细胞中增加。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号