Following the infection, endotoxemia or endotoxic shock is induced, which are characterized by a cascade of cytokines that are expressed and released, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6, followed by an anti-inflammatory response with the production of anti-inflammatory cytokines, such as IL-10 [2, 3]. This evidence concerns the gene IL1B and serum lipopolysaccharide activity.