The contribution of the nervous system to inflammation and inflammatory disease.
The contribution of the nervous system to inflammation and inflammatory disease.
复制标题
神经系统对炎症和炎症性疾病的贡献。
DOI：
10.1139/y91-096
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发表时间：
1991
影响因子：
2.1
通讯作者：
Levine,JD
中科院分区：
文献类型：
--
作者：
Basbaum,AI;Levine,JD
最近的研究发现，神经系统在炎症和炎症性疾病中起着重要作用。特别是，从小直径初级传入纤维的外周终末和交感神经节后神经(SPGN)终末释放的物质与急性炎症的几个主要组成部分(例如血管扩张和血浆外渗)以及在炎症性疾病模型-实验性关节炎的组织损伤调节中有关。虽然从初级传入终末释放的多肽受到最多的关注，但我们的研究证实了肥大细胞和SPGN终末在急性炎症中的重要作用。我们描述的研究表明，激活大鼠膝关节小直径初级传入引起的血浆外渗涉及一系列事件，其中肥大细胞和交感终末依次被激活。我们的研究表明，从SPGN末端释放前列腺素，但不是去甲肾上腺素或神经肽Y，有助于增加血浆外渗。虽然通过注射缓激肽激活SPGN终末(通过肥大细胞)或更直接地激活SPGN终末，但增加血浆外渗，手术或药物交感神经切除可降低实验性关节炎的严重程度。在相关研究中，我们证明了肾上腺髓质来源的肾上腺素可以通过β受体介导的调节孤束核终末释放一种未知物质(S)来加重关节炎。我们的结果提出了重要的问题，即在疾病的背景下，急性炎症是否有助于组织修复或进一步损伤。关键词：关节炎、炎症、多肽、初级传入、交感神经系统。
Recent studies have identified a major contribution of the nervous system to inflammation and to inflammatory disease. In particular, substances released from the peripheral terminals of small diameter primary afferent fibers and from sympathetic postganglionic nerve (SPGN) terminals have been implicated in several of the major components of acute inflammation (e.g., vasodilatation and plasma extravasation) as well as in the regulation of tissue injury in an inflammatory disease model, experimental arthritis in the rat. Although the release of peptides from primary afferent terminals has received the most attention, our studies have established an important contribution of mast cells and the SPGN terminals to acute inflammation. We describe studies which indicate that plasma extravasation provoked by activation of small diameter primary afferents in the knee joint of the rat involves a cascade of events in which the mast cell and then the sympathetic terminal are sequentially activated. Our studies indicate that release of prostaglandins, but neither norepinephrine nor neuropeptide Y, from the SPGN terminal contributes to increased plasma extravasation. Although activation of the SPGN terminal (via the mast cell) or more directly, via injection of bradykinin, increased plasma extravasation, surgical or pharmacological sympathectomy decreased the severity of experimental arthritis. In related studies we demonstrated that adrenal medullary-derived epinephrine can exacerbate arthritis through a β-receptor-mediated regulation of the release of an as yet unidentified substance(s) from the SPGN terminal. Our results raise important questions as to whether acute inflammation contributes to tissue repair or to further injury in the setting of disease.Key words: arthritis, inflammation, peptides, primary afferents, sympathetic nervous system.