NEUTROPHILS, CYTOKINES AND CYTOKINE RECEPTORS IN SEPTIC SHOCK

严重感染导致的死亡，被称为败血症，是美国第十三大常见死因，导致40万至50万人死亡。来自微生物的有毒产物引发脓毒症，但宿主对感染的反应失调是疾病发病率和死亡率的原因。人们普遍认为，设计改进的疗法将需要更好地了解细胞在脓毒症期间的作用。这项研究通过调查脓毒症期间人类血细胞中改变的生物化学和分子事件来解决这一需求。我们发现在脓毒症过程中促炎和抗炎基因的表达失调。这种基因表达的改变与调节异常细胞的细胞核或细胞质内的调节事件的变化有关。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。

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.