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TNF腫瘤壞死因子係免疫發炎重要的一個媒介,最近研究發現TNF產量受到迷走神經(副交感)控制. 當體內受到Endotoxemia(內毒素血整)時,藉由Cholinergic膽鹼能控制途徑會將過度發炎壓抑下來保護正常細胞
Central muscarinic cholinergic regulation of the systemic inflammatory response during endotoxemia.
Proc Natl Acad Sci U S A. 2006; 103(13):5219-23 (ISSN: 0027-8424)
Pavlov VA; Ochani M; Gallowitsch-Puerta M; Ochani K; Huston JM; Czura CJ; Al-Abed Y; Tracey KJ
Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY 11030, USA.

TNF has a critical mediator role in inflammation and is an important therapeutic target. We recently discovered that TNF production is regulated by neural signals through the vagus nerve. Activation of this "cholinergic antiinflammatory pathway" inhibits the production of TNF and other cytokines and protects animals from the inflammatory damage caused by endotoxemia and severe sepsis. Here, we describe a role for central muscarinic acetylcholine receptors in the activation of the cholinergic antiinflammatory pathway. Central muscarinic cholinergic activation by muscarine, the M1 receptor agonist McN-A-343, and the M2 receptor antagonist methoctramine inhibited serum TNF levels significantly during endotoxemia. Centrally administered methoctramine stimulated vagus-nerve activity measured by changes in instantaneous heart-rate variability. Blockade of peripheral muscarinic receptors did not abolish antiinflammatory signaling through the vagus nerve, indicating that peripheral muscarinic receptors on immune cells are not required for the cytokine-regulating activities of the cholinergic antiinflammatory pathway. The role of central muscarinic receptors in activating the cholinergic antiinflammatory pathway is of interest for the use of centrally acting muscarinic cholinergic enhancers as antiinflammatory agents.

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