Weinstock J V, Elliott D
Department of Medicine, University of Iowa, Iowa City 522423, USA.
Ann N Y Acad Sci. 1998 May 1;840:532-9. doi: 10.1111/j.1749-6632.1998.tb09592.x.
Murine schistosomiasis mansoni is a parasitic disease in which flukes living in the portal vein of the host produce ova that deposit in the liver and intestines. In these organs, ova release antigens that induce chronic, focal granulomatous inflammation. IFN-gamma is an inflammatory cytokine important in macrophage activation and B-cell differentiation. A substance P (SP)/somatostatin (SOM) neurokine immunoregulatory circuit controls IFN-gamma production in schistosome granulomas. SP stimulates, while SOM inhibits IFN-gamma release, modulating IFN-gamma-dependent circuitry. SP and SOM function through interaction with authentic SP and SOM receptors located on granuloma T cells. Also, the granulomas produce authentic SP and SOM14, as evidenced by the presence of mRNA and product. The granulomas have no nerves. This, and other data suggest that the inflammatory cells make these neurokines. Granuloma macrophages produce SOM. Macrophages from various sources express SOM mRNA in response to LPS, IFN-gamma, IL-10 or several other inflammatory mediators. Thus, the inflammation of murine schistosomiasis has a complete SP/SOM immunoregulatory circuit, which in turn is subject to immunoregulation.
小鼠曼氏血吸虫病是一种寄生虫病，寄生于宿主体门静脉的吸虫产生的虫卵沉积在肝脏和肠道。在这些器官中，虫卵释放抗原，引发慢性局灶性肉芽肿炎症。干扰素-γ是一种在巨噬细胞活化和B细胞分化中起重要作用的炎性细胞因子。一种P物质（SP）/生长抑素（SOM）神经激肽免疫调节回路控制血吸虫肉芽肿中干扰素-γ的产生。SP起刺激作用，而SOM抑制干扰素-γ释放，调节依赖干扰素-γ的信号通路。SP和SOM通过与肉芽肿T细胞上的真实SP和SOM受体相互作用发挥功能。此外，肉芽肿产生真实的SP和SOM14，mRNA和产物的存在证明了这一点。肉芽肿没有神经。这一点以及其他数据表明炎性细胞产生这些神经激肽。肉芽肿巨噬细胞产生SOM。来自各种来源的巨噬细胞在接触脂多糖、干扰素-γ、白细胞介素-10或其他几种炎性介质后表达SOM mRNA。因此，小鼠血吸虫病的炎症具有完整的SP/SOM免疫调节回路，而该回路又受到免疫调节。
