Inflammation and fibrogenesis in early lesions of chronic lung allograft dysfunction (B09*)

慢性肺同种异体移植功能障碍早期病变中的炎症和纤维发生（B09*）

• 批准号: 278147159
• 金额: --
• 依托单位: Institut für Pathologie
• 依托单位国家: 德国
• 项目类别: Collaborative Research Centres
• 财政年份: 2015
• 资助国家: 德国
• 起止时间: 2014-12-31 至 2018-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/278147159?language=en
• 关键词: Inflammation; fibrogenesis; early; lesions; chronic

Project B09 will characterize bronchiolitis obliterans (BOS) on the molecular level. During a DFG funded project headed by D. Jonigk, they identified a specific expression pattern helpful in diagnosing and even predicting the subsequent development of BOS. The molecular pattern rather described effector mechanisms of a fibrogenic tissue response. Therefore, the group aims to identify the early BOS lesions to test the double-hit hypothesis in human lung grafts. According to this model, BO develops in an alloimmune setting when a secondary initiating damage like mucosal damage by ischemia or infection occurs. Finally, the group will use a recently established rat lung transplant model mimicking the development of BOS. The model will be used to test various therapeutic interventions preventing (antibiotics, immunosuppression) the development of BOS, which could pave the way for future clinical trials.

B09项目将在分子水平上描述闭塞性细支气管炎(BOS)的特征。在由D.Jonigk领导的DFG资助的一个项目中，他们确定了一种特定的表达模式，有助于诊断甚至预测BOS的后续发展。分子模式更好地描述了纤维化组织反应的效应机制。因此，该小组的目标是识别早期的BOS损害，以检验人类肺移植中的双重打击假说。根据这一模型，当发生二次起始损伤，如缺血或感染造成的粘膜损伤时，BO在同种免疫环境中发展。最后，该小组将使用最近建立的大鼠肺移植模型来模拟BOS的发展。该模型将用于测试防止BOS发展的各种治疗干预措施(抗生素、免疫抑制)，这可能为未来的临床试验铺平道路。