FUNCTIONAL AND METABOLIC PROPERTIES OF TOXIC NEUTROPHILS AND PATHOGENIC

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。 严重感染导致的死亡，又称败血症，是该国第十三大最常见的死亡原因，造成400,000-500,000人死亡。来自微生物的有毒产物会引发败血症，但宿主对感染的反应失调是导致疾病发病率和死亡率的原因。人们普遍认为，设计改进的治疗方法需要更好地了解细胞在脓毒症期间的作用。这项研究通过研究脓毒症期间人类血细胞中的生化和分子事件来满足这一需求。我们发现，在脓毒症期间，促炎基因和抗炎基因的表达异常。基因表达的这种变化与调控事件的变化有关，这些调控事件作用于失调细胞的细胞核或细胞质内。这些变化的结果可能会对脓毒症患者的免疫力产生不利影响。

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. Death from severe infection, referred to as sepsis, is the thirteenth most common cause of death in this country, accounting for the loss of 400,000-500,000 lives. Toxic products derived from microbes initiate sepsis, but a dysregulated host response to infection is responsible for the morbidity and mortality of disease. It is widely accepted that design of improved therapies will require a better understanding of how cells act during sepsis. This research addresses this need by investigating the biochemical and molecular events that are altered in human blood cells during sepsis. We find dysregulated expression of proinflammatory and anti-inflammatory genes during sepsis. This alteration in gene expression is associated with changes in regulatory events that act in the nucleus or within the cytoplasm of the dysregulated cells. The result of these changes can adversely affect the immunity of humans with sepsis.