SCOR IN ACUTE LUNG INJURY HARVESTING ALVEOLAR MACROPHAGE CELLS

该子项目是利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得主要资金， 因此可以在其他CRISP条目中表示。列出的机构是 中心，不一定是研究者的机构。 SCOR项目的总体重点是脓毒症引起的急性肺损伤。 SCOR计划并没有试图解决与脓毒症引起的急性肺损伤相关的所有基础和临床问题。 SCOR程序的具体重点和原理如下：在革兰氏败血症期间，内毒素和细菌DNA被释放并刺激巨噬细胞释放TNF。 革兰氏阳性菌的细胞壁产物模拟内毒素对巨噬细胞的作用。 TNF可触发器官和细胞功能障碍（表面活性剂产生减少）和/或损伤（通过细胞凋亡）。 项目1和2评估了人肺泡巨噬细胞（项目1）和肝脏（项目2）中细胞因子基因（包括TNF）的调节。 项目1评估MAPK的作用，项目2评估NFkB的氧化还原调节。 临床核心将为这两个项目提供人体组织和生物统计支持。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The overall focus of the SCOR program is sepsis-induced acute lung injury. The SCOR program does not try to address all of the basic and clinical issues related to sepsis-induced acute lung injury. Specific focus and rationale for the SCOR program is as follows: During gram-sepsis, endotoxin and bactrial DNA are released and stimulate macrophages to release TNF. Cell wall products of gram positive organisms mimic the effects of endotoxin on macrophages. TNF can trigger organ and cellular dysfunction (decreased surfactant production) and/or injury (by apoptosis). Projects 1 and 2 evaluate the regulation of cytokine genes (including TNF) in human alveolar macrophages (Project 1) and liver (Project 2). Project 1 evaluates the role of MAPK's and Project 2 evaluates redox regulation of NFkB. The Clinical Core will provide human tissues and biometry support for the two projects.