Rozniecki J J, Hauser S L, Stein M, Lincoln R, Theoharides T C
Department of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, Boston, MA 02111.
Ann Neurol. 1995 Jan;37(1):63-6. doi: 10.1002/ana.410370112.
Multiple sclerosis (MS) lesions are associated with infiltration of T lymphocytes and macrophages that appear to mediate myelin destruction and gliosis (scarring). Mast cells are located perivascularly in the brain, are juxtaposed to neurons, and have been shown to secrete vasoactive and inflammatory mediators in response to neuropeptides and direct nerve stimulation. Mast cells have been previously identified in MS lesions, are activated by myelin basic protein, and can participate in the regulation of blood-brain barrier permeability, as well as in myelin destruction. Here, cerebrospinal fluid from MS patients and controls with other neurologic diseases was assayed for histamine, its major metabolite methylhistamine, and the specific mast cell marker tryptase. Histamine and methylhistamine were not elevated in MS. However, the mast cell specific proteolytic enzyme tryptase was significantly elevated in MS, suggesting that mast cell activation may be involved in the pathophysiology of this disease.
多发性硬化症(MS)病灶与T淋巴细胞和巨噬细胞浸润有关,这些细胞似乎介导了髓鞘破坏和胶质增生(瘢痕形成)。肥大细胞位于脑内血管周围,与神经元相邻,并且已证明其可响应神经肽和直接神经刺激而分泌血管活性和炎症介质。肥大细胞先前已在MS病灶中被鉴定出来,可被髓鞘碱性蛋白激活,并可参与血脑屏障通透性的调节以及髓鞘破坏过程。在此,对来自MS患者以及患有其他神经系统疾病的对照者的脑脊液进行了组胺、其主要代谢产物甲基组胺以及肥大细胞特异性标志物类胰蛋白酶的检测。MS患者的组胺和甲基组胺水平并未升高。然而,肥大细胞特异性蛋白水解酶类胰蛋白酶在MS患者中显著升高,这表明肥大细胞激活可能参与了该疾病的病理生理过程。