In particular, it has been shown that electric stimulation of the vagus nerve attenuates the inflammation during endotoxemia in rats [3], and that acetylcholine (ACh), the main parasympathetic neurotransmitter, effectively deactivates peripheral macrophages and inhibits the release of pro-inflammatory mediators, including the cytokine tumor necrosis factor-α (TNF-α). This evidence concerns the gene TNF and serum lipopolysaccharide activity.