NEUTROPHILS, CYTOKINES AND CYTOKINE RECEPTORS IN SEPTIC SHOCK

严重感染导致的死亡，被称为败血症，是这个国家第13大最常见的死亡原因，造成40万到50万人死亡。来自微生物的有毒产物引发败血症，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，改进疗法的设计将需要更好地了解细胞在败血症中的作用。本研究通过研究脓毒症期间人类血细胞改变的生化和分子事件来解决这一需求。我们发现在脓毒症中促炎和抗炎基因表达失调。这种基因表达的改变与在细胞核或失调细胞的细胞质内发生的调节事件的变化有关。这些变化的结果可能对败血症患者的免疫产生不利影响。

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.