Gene expression data from compstatin treated E.coli-Induced primate sepsis model

Severe sepsis leads to massive activation of coagulation and complement cascades that could contribute to multiple organ failure (MOF) and death. To investigate the role of the complement and its crosstalk with the hemostatic system in the pathophysiology and therapeutics of sepsis, we have used a potent inhibitor (compstatin) administered early or late post E. coli challenge in a baboon model of sepsis-induced MOF. Microarray was used to study the affect of complement pathway on global gene expression pattern in sepsis, aims on exploring and discovering the new target genes as potential drugs for the early treatment and prevention of sepsis. Lung and liver tissues were obtained from three normal healthy animals (as Ctl), three animals challenged with sublethal dose of E. coli as SLEC, three animals treated with Compstatin at different sepsis stages after E.coli challenge as SLEC-CST0 and SLEC-CST5. All the animals challenged with E. coli were sacrified at 24 hours post challenge. Total RNAs were isolated from these tissues, hybridized with Affymetrix Human Genome GeneChip U133A 2.0.