Lotz M, Carson D A, Vaughan J H
Science. 1987 Feb 20;235(4791):893-5. doi: 10.1126/science.2433770.
Several clinical features are consistent with nervous system involvement in the pathogenesis of rheumatoid arthritis. The neuropeptide substance P is one possible mediator of this interaction, since it can be released into joint tissues from primary sensory nerve fibers. The potential effects of the peptide on rheumatoid synoviocytes were examined. The results show that substance P stimulates prostaglandin E2 and collagenase release from synoviocytes. Furthermore, synoviocyte proliferation was increased in the presence of the neuropeptide. Similar effects were observed with a truncated form of substance P. Synoviocytes were sensitive to very small doses of the neuropeptide (10(-9) M), and its effects were inhibited by a specific antagonist. Thus, the specific stimulation of synoviocytes by the neuropeptide substance P represents a pathway by which the nervous system might be directly involved in the pathogenesis of rheumatoid arthritis.
类风湿关节炎发病机制中，有几个临床特征与神经系统受累相关。神经肽P物质是这种相互作用的一种可能介质，因为它可从初级感觉神经纤维释放至关节组织。研究了该肽对类风湿滑膜细胞的潜在影响。结果显示，P物质刺激滑膜细胞释放前列腺素E2和胶原酶。此外，在该神经肽存在的情况下，滑膜细胞增殖增加。P物质的截短形式也观察到类似效果。滑膜细胞对非常小剂量的神经肽（10(-9) M）敏感，其作用被特异性拮抗剂抑制。因此，神经肽P物质对滑膜细胞的特异性刺激代表了神经系统可能直接参与类风湿关节炎发病机制的一条途径。
