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

项目B09将在分子水平上表征闭塞性细支气管炎（BOS）。在由D. Jonigk领导的DFG资助的项目中，他们发现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。分子模式描述了纤维化组织反应的效应机制。因此，该小组旨在识别早期BOS病变，以验证人肺移植物的双重打击假说。根据该模型，BO是在同种免疫环境下发生的，当继发性初始损伤如缺血或感染引起的粘膜损伤发生时。最后，该小组将使用最近建立的模拟BOS发展的大鼠肺移植模型。该模型将用于测试预防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。

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.