SCOR IN ACUTE LUNG INJURY HARVESTING ALVEOLAR MACROPHAGE CELLS

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 SCOR计划的总体重点是脓毒症所致的急性肺损伤。SCOR计划并不试图解决与脓毒症引起的急性肺损伤相关的所有基本和临床问题。SCOR计划的具体重点和基本原理如下：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肿瘤坏死因子。革兰氏阳性菌的细胞壁产物模拟内毒素对巨噬细胞的影响。肿瘤坏死因子可引发器官和细胞功能障碍(表面活性物质产生减少)和/或损伤(通过细胞凋亡)。项目1和2评估人肺泡巨噬细胞(项目1)和肝脏(项目2)中细胞因子基因(包括肿瘤坏死因子)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测量支持。

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.