• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Neutrophil elastase induces mucus cell metaplasia in mouse lung.
【24h】

Neutrophil elastase induces mucus cell metaplasia in mouse lung.

机译：中性粒细胞弹性蛋白酶诱导小鼠肺中的粘液细胞化生。

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

Goblet cell hyperplasia in the superficial airway epithelia is a signature pathological feature of chronic bronchitis and cystic fibrosis. In these chronic inflammatory airway diseases, neutrophil elastase (NE) is found in high concentrations in the epithelial lining fluid. NE has been reported to trigger mucin secretion and increase mucin gene expression in vitro. We hypothesized that chronic NE exposure to murine airways in vivo would induce goblet cell metaplasia. Human NE (50 microg) or PBS saline was aspirated intratracheally by male Balb/c (6 wk of age) mice on days 1, 4, and 7. On days 8, 11, and 14, lung tissues for histology and bronchoalveolar lavage (BAL) samples for cell counts and cytokine levels were obtained. NE induced Muc5ac mRNA and protein expression and goblet cell metaplasia on days 8, 11, and 14. These cellular changes were the result of proteolytic activity, since the addition of an elastase inhibitor, methoxysuccinyl Ala-Ala-Pro-Val chloromethylketone (AAPV-CMK), blocked NE-induced Muc5ac expression and goblet cell metaplasia. NE significantly increased keratinocyte-derived chemokine and IL-5 in BAL and increased lung tissue inflammation and BAL leukocyte counts. The addition of AAPV-CMK reduced these measures of inflammation to control levels. These experiments suggest that NE proteolytic activity initiates an inflammatory process leading to goblet cell metaplasia.
机译：浅表气道上皮中的杯状细胞增生是慢性支气管炎和囊性纤维化的标志性病理特征。在这些慢性炎症性气道疾病中，中性粒细胞弹性蛋白酶（NE）在上皮内衬液中浓度很高。据报道，NE在体外触发粘蛋白分泌并增加粘蛋白基因表达。我们假设慢性NE体内暴露于鼠气道会诱导杯状细胞化生。在第1、4和7天，由雄性Balb / c（6周龄）小鼠气管内抽吸人NE（50微克）或PBS盐水。在第8、11和14天，用肺组织进行组织学检查和支气管肺泡灌洗（获得BAL）样品的细胞计数和细胞因子水平。 NE在第8、11和14天诱导Muc5ac mRNA和蛋白表达以及杯状细胞化生。这些细胞变化是蛋白水解活性的结果，因为添加了弹性蛋白酶抑制剂甲氧基琥珀酰Ala-Ala-Pro-Val氯甲基酮（AAPV- CMK），阻止NE诱导的Muc5ac表达和杯状细胞化生。 NE显着增加了BAL中角化细胞衍生的趋化因子和IL-5，并增加了肺组织炎症和BAL白细胞计数。添加AAPV-CMK可将这些炎症措施降至控制水平。这些实验表明，NE蛋白水解活性引发了导致杯状细胞化生的炎症过程。

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