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 sepsi
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