Cholinergic modulation of inflammation.

Recent studies have demonstrated that cytokine levels and inflammation can be regulated by specifically augmenting cholinergic signaling via the efferent vagus nerve and the alpha7 subunit-containing nicotinic acetylcholine receptor (alpha7nAChR). Cholinergic modalities, acting through vagus nerve- and/or alpha7nAChR-mediated mechanisms have been shown to suppress excessive inflammation in several experimental models of disease, including endotoxemic shock, sepsis, ischemia-reperfusion injury, hemorrhagic shock, colitis, postoperative ileus and pancreatitis. These studies have advanced the current understanding of the mechanisms regulating inflammation. They have also provided a rationale for exploring new possibilities to treat excessive, disease-underlying inflammation by applying selective cholinergic modalities in preclinical and clinical settings. An overview of this research is presented here.