Experimental endotoxemia as a model to study neuroimmune mechanisms in human visceral pain
Experimental endotoxemia as a model to study neuroimmune mechanisms in human visceral pain
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DOI：
10.1111/j.1749-6632.2012.06622.x
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发表时间：
2012-01-01
期刊：
影响因子：
--
通讯作者：
Elsenbruch, Sigrid
中科院分区：
文献类型：
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作者：
Benson, Sven;Engler, Harald;Elsenbruch, Sigrid
细菌内毒素（即脂多糖，LPS）的施用构成了一种完善的实验方法，用于研究急性和短暂免疫激活对动物和健康人疾病行为的生理、行为和情感方面的影响。然而，关于实验性内毒素血症对人类疼痛的可能影响知之甚少。这种知识差距在功能性内脏疼痛以及慢性炎症性胃肠道疾病的背景下尤为突出。尽管炎症过程与内脏痛的病理生理有关，但炎症介质如何与内脏痛觉过敏的自下而上（即传入输入增加）和自上而下（即中枢性疼痛加工改变）机制相互作用仍不完全清楚。考虑到近年来在人体应用LPS后出现内脏痛觉过敏的研究结果，本文提出，具有复杂外周和中枢效应的实验性内毒素血症可作为研究人类疼痛研究中神经免疫通讯的实验模型。我们总结并尝试整合内脏和躯体疼痛中神经免疫通讯的相关动物和人类研究，讨论可能的机制，并对未来的研究方向进行总结。
The administration of bacterial endotoxin (i.e., lipopolysaccharide, LPS) constitutes a well-established experimental approach to study the effects of an acute and transient immune activation on physiological, behavioral, and emotional aspects of sickness behavior in animals and healthy humans. However, little is known about possible effects of experimental endotoxemia on pain in humans. This knowledge gap is particularly striking in the context of visceral pain in functional as well as chronic-inflammatory gastrointestinal disorders. Although inflammatory processes have been implicated in the pathophysiology of visceral pain, it remains incompletely understood how inflammatory mediators interact with bottom-up (i.e., increased afferent input) and top-down (i.e., altered central pain processing) mechanisms of visceral hyperalgesia. Considering the recent findings of visceral hyperalgesia after LPS application in humans, in this review, we propose that experimental endotoxemia with its complex peripheral and central effects constitutes an experimental model to study neuroimmune communication in human pain research. We summarize and attempt to integrate relevant animal and human studies concerning neuroimmune communication in visceral and somatic pain, discuss putative mechanisms, and conclude with future research directions.