Characterization of host responses during Ca/Sa polymicrobial IAI demonstrated that mortality is associated with robust inflammation, evidenced by elevated levels of hallmark sepsis-associated proinflammatory mediators (interleukin 6 [IL-6], tumor necrosis factor alpha [TNF-α], IL-1β, and prostaglandin E2 [PGE2]) both locally and systemically, which can be abrogated by treatment with nonsteroidal anti-inflammatory drugs (NSAID) or by targeting PGE2-signaling pathways (4, 5). This evidence concerns the gene IL6 and Sepsis.