首页> 美国卫生研究院文献>Journal of the Canadian Association of Gastroenterology >A12 INTESINAL TREFOIL FACTOR (ITF) PLAYS CRITICAL ROLES IN INNATE PROTECTION AGAINST AND RECOVERY FROM CLOSTRIDIUM DIFFICILE COLITIS
【2h】

A12 INTESINAL TREFOIL FACTOR (ITF) PLAYS CRITICAL ROLES IN INNATE PROTECTION AGAINST AND RECOVERY FROM CLOSTRIDIUM DIFFICILE COLITIS

机译:A12肠三叶因子(ITF)在预防和预防艰难梭菌结肠炎中发挥重要作用

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

BackgroundClostridium Difficile (Cdif) colitis is a leading cause of morbidity & mortality in many patients including: hospitalized elderly, those with IBD, and immunocompromised. Little is known of the mechanisms involved in protection against, and recovery from, Cdif toxin-induced injury. Histological findings of Cdif colitis include; epithelial disruption, inflammatory cell infiltration, goblet cell depletion & when severe, pseudomembranous colitis (PMC). We previously showed Keratinocyte Growth Factor (KGF) plays protective roles on Cdif exposure. KGF-/- mice had more severe Cdif toxin-induced injury & greater depletion of goblet cells and the goblet cell derived growth factor ITF. Since KGF directly binds the ITF promoter (increasing ITF) and Cdif colitis is associated with goblet cell depletion & loss of ITF we developed the following aim.
机译:背景艰难梭菌(Cdif)结肠炎是许多患者发病和死亡的主要原因,这些患者包括:住院的老年人,IBD患者和免疫功能低下的患者。关于防止Cdif毒素引起的损伤并从中恢复的机制知之甚少。 Cdif结肠炎的组织学发现包括:上皮破坏,炎性细胞浸润,杯状细胞耗竭以及严重的伪膜性结肠炎(PMC)。我们先前显示,角质形成细胞生长因子(KGF)在Cdif暴露中起保护作用。 KGF-/-小鼠具有更严重的Cdif毒素诱导的损伤以及杯状细胞和杯状细胞衍生的生长因子ITF的更大耗竭。由于KGF直接结合ITF启动子(增加ITF),而Cdif结肠炎与杯状细胞消耗和ITF丧失有关,因此我们制定了以下目标。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

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