Bacterial LPS elicits the overproduction of inflammatory mediators, such as interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), nitric oxide, and prostaglandin E2 and the large number of inflammatory mediators produced in the body are thought to contribute to the LPS-induced symptoms of sepsis [14,15]. This evidence concerns the gene IL6 and Sepsis.