In eukaryotic systems, inflammation and activation of innate immunity are fundamental host responses to microbial invasion and endogenous danger signals. Blood leukocytes contribute to this inflammatory response, and exposure to a prototypical stimulus such as LPS leads first to changes in gene expression, then production of cytokines which are secreted and cause secondary transcriptional and other responses [15]. In previous work, we and others generated a set of gene expression profiles from human subjects over 24 hours following the intravenous administration of bacterial endotoxin LPS [16]. Experimental endotoxicosis produces in the previously healthy individual a transient but significant systemic inflammatory response, characterized by fever, tachycardia, malaise, and a hepatic acute phase response. Administration of endotoxin is presumed to model the early inflammatory changes associated with a microbial invasion, sepsis and the systemic inflammatory response syndrome [17]. We used this **data** to determine important clusters of genes involved in the early inflammatory response, as well as to depict the temporal changes in gene expression as inflammation resolved over the first twenty-four hours. In this study, we calculated transcription factor activities and regulatory influences in the above **dataset** using NCA, and interpreted the results to develop a dynamic network of transcription events following experimental endotoxicosis in humans.