Huston JM, Tracey KJ (Department of Surgery, Division of General Surgery, Trauma, Surgical Critical Care, and Burns, Stony Brook University Medical Center, Health Sciences Center, Stony Brook; and Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, Manhasset; NY, USA). The pulse of inflammation: heart rate variability, the cholinergic anti-inflammatory pathway, and implications for therapy (Key Symposium). J Intern Med 2011; 269: 45–53.
Biological therapeutics targeting TNF, IL-1 and IL-6 arewidelyused for treatment of rheumatoidarthritis, inflammatory bowel disease and a growing list of other syndromes, often with remarkable success. Nowadvances inneurosciencehave collidedwiththis therapeutic approach, perhaps rendering possible the development of nerve stimulators to inhibit cytokines. Action potentials transmitted in the vagus nerve culminate in the release of acetylcholine that blocks cytokine production by cells expressing acetylcholine receptors. The molecular mechanism of this cholinergic anti-inflammatory pathway is attributable to signal transduction by the nicotinic alpha 7
acetylcholine receptor subunit, a regulator of the intracellular signals that control cytokine transcription and translation. Favourable preclinical data support the possibility that nerve stimulatorsmay be added to the future therapeutic armamentarium, possibly replacing somedrugs to inhibit cytokines.
Keywords: heart rate variability, inflammation, neuroimmunology, therapeutics, vagus nerve stimulation.
瞄準TNF，IL-1，IL-6之生物治療法對類風濕性發炎，發炎性腸胃炎及其他炎症都有意想不到的效果。神經科學之最新進展更推高其可能性，使到用神經刺激方法來抑制細胞激素之產生是一種可行之治療方法。在迷走神經所發之位能會使其釋出乙醯膽鹼，細胞中之乙醯膽鹼接受器會在接受乙醯膽鹼後便會阻斷細胞激素之產生。這些接受器就是叫做尼古丁α-7分子 --- 一個調整細胞激素之分子。正面的臨床前的數據支持下面所說的一個可能性；即神經刺激可代替藥物來抑制細胞激素的產生。