Mast cell interactions with the nervous system: relationship to mechanisms of disease.
Mast cell interactions with the nervous system: relationship to mechanisms of disease.
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DOI：
10.1097/00005072-199756060-00001
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发表时间：
1997-06
影响因子：
3.2
通讯作者：
K. Dines;H. Powell
中科院分区：
文献类型：
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作者：
K. Dines;H. Powell
总之，神经系统中的肥大细胞相互作用与生理过程（即生殖）和病理状态（即炎性脱髓鞘、疼痛性疾病、毒性和代谢性疾病以及肿瘤血管生成）相关。它们的生理作用可能有助于与性别相关的炎症性疾病的脆弱性，并可能调节对疼痛的敏感性。肥大细胞普遍参与组织修复，它们释放并响应营养因子如NGF。这些细胞还产生细胞因子并与之反应，因此似乎在组织变性和修复中发挥作用。在某些神经系统疾病中，即多发性硬化症和格林-巴利综合征，肥大细胞蛋白酶降解特定髓鞘蛋白的能力表明这些细胞是脱髓鞘过程中的代理人，而不是旁观者。更有趣的是，他们最近确定的能力，有效地处理细菌抗原的活化巨噬细胞，这表明一个更关键的作用比以前怀疑可能被认为是肥大细胞在中枢神经系统和PNS脱髓鞘。在实验性代谢紊乱如半乳糖中毒和硫胺素缺乏症中，肥大细胞似乎起致病作用。因此，在半乳糖中毒时，BNB血管通透性的改变与肥大细胞增殖和脱粒有关，而在硫胺素缺乏时，大鼠丘脑中组胺水平升高（79），并与细胞死亡和增殖以及肥大细胞脱粒有关（Powell和Langlais，未发表的观察结果）。已经观察到肥大细胞和各种其他细胞之间的结构相互作用，以及肥大细胞与其中肥大细胞特别活跃的组织中的神经末梢的紧密接近。由于它们的旁分泌性质，肥大细胞可以通过爆炸性脱颗粒、零碎脱颗粒或当它们将颗粒插入相邻细胞时的“transgranulation”来调节它们微环境中的事件。最后，这些细胞在修复过程中发挥特定作用，例如血管生成，并且在肿瘤状态中具有活性，包括von Recklinghausen病（神经纤维瘤病）。迄今为止，在神经病理学研究中，由于依赖染色技术，不足以识别脱颗粒的因此活化的肥大细胞，因此可能低估了它们的参与（4）。更严格的组织化学和免疫染色程序将有助于充分认识到他们参与生理和病理过程的程度。
In summary, mast cell interactions in the nervous system are relevant to both physiological processes (i.e. reproduction) and pathologic states (i.e. inflammatory demyelination, painful disorders, toxic and metabolic disease, and tumor angiogenesis). Their physiologic roles may contribute to gender-related vulnerability to inflammatory disease and may modulate sensitivity to pain. Mast cells are universally involved in tissue repair and they release and respond to trophic factors such as NGF. These cells also produce and react to cytokines, and thus appear to play a role in tissue degeneration as well as repair. In certain neurological diseases, i.e. multiple sclerosis and Guillain-Barré syndrome, the ability of mast cell proteases to degrade specific myelin proteins suggests that these cells are agents, rather than bystanders, in the demyelinative process. Even more intriguing is their recently identified capacity to process bacterial antigen as efficiently as activated macrophages, suggesting that a more critical role than previously suspected might be considered for mast cells in CNS and PNS demyelination. In experimental metabolic disorders such as galactose intoxication and thiamine deficiency, mast cells appear to play a pathogenic role. Thus, in galactose intoxication, altered BNB vascular permeability occurs in conjunction with mast cell proliferation and degranulation, while in thiamine deficiency, increased histamine levels have been reported in the rat thalamus (79) and are associated with cell death and proliferation as well as mast cell degranulation (Powell and Langlais, unpublished observations). Structural interactions between mast cells and a variety of other cells have been observed, as well as close approximation of mast cells to nerve endings in tissues in which mast cells are especially active. Due to their paracrine nature, mast cells can modulate events in their microenvironment through explosive degranulation, piecemeal degranulation, or "transgranulation" as they insert granules into neighboring cells. Lastly, these cells play specific roles in reparative processes, e.g. angiogenesis, and are active in neoplastic states, including von Recklinghausen's disease (neurofibromatosis). Their involvement may have been underestimated in neuropathological studies, to date, by a reliance on staining techniques that are inadequate for identifying degranulated and therefore activated mast cells (4). More exacting histochemical and immunostaining procedures will help to fully realize the extent of their participation in physiological and pathological processes.