Björn-Rasmussen E, Nielsen H, Hageman J, van den Dungen P
Acta Med Scand. 1986;219(3):309-13. doi: 10.1111/j.0954-6820.1986.tb03317.x.
Several observations indicate that the innate metabolic defect in hereditary hemochromatosis (HH) leads to a defective function of the monocyte-macrophage system. The present study was performed to investigate the possibility that a defect in migration of cells of the monocyte-macrophage system can explain the abnormal location of the submucosal macrophages in HH. Monocytes isolated from 14 patients with HH were investigated with regard to chemotactic responsiveness (MCR). Two different methods were used at two different laboratories. Casein and zymosan-activated serum were used as attractants. No difference in MCR was found between the control group and the group of HH patients. The conclusion can therefore be drawn that the abnormal location of the macrophages of the gut wall in HH cannot be explained by an inborn abnormality of the function of receptors responsible for the chemotactic activity of the monocyte-macrophage system. It is, however, still possible that local factors responsible for the macrophage migration (gut hormones?) may have defective activity in HH patients.
多项观察结果表明,遗传性血色素沉着症(HH)的先天性代谢缺陷会导致单核细胞 - 巨噬细胞系统功能缺陷。本研究旨在探讨单核细胞 - 巨噬细胞系统细胞迁移缺陷是否能解释HH患者黏膜下巨噬细胞的异常定位。对14例HH患者分离出的单核细胞进行趋化反应性(MCR)研究。在两个不同实验室使用了两种不同方法。酪蛋白和酵母聚糖激活血清用作趋化剂。未发现对照组与HH患者组之间的MCR有差异。因此可以得出结论,HH患者肠壁巨噬细胞的异常定位不能用负责单核细胞 - 巨噬细胞系统趋化活性的受体功能先天性异常来解释。然而,在HH患者中,负责巨噬细胞迁移的局部因素(肠道激素?)仍有可能具有缺陷活性。