Moriguchi S, Kishino Y
J Nutr. 1984 May;114(5):888-93. doi: 10.1093/jn/114.5.888.
We measured phagocytosis of opsonized sheep red blood cells by alveolar macrophages (AM) of rats fed a diet with or without pyridoxine for 4 weeks. In pyridoxine-deficient (DEF) and pair-fed control (PF) groups AM showed a higher degree of phagocytosis than those of rats in the ad libitum-fed control (AL) group. After in vitro treatment with a macrophage-activating factor (MAF), such as lymphokines, for 4 hours at 37 degrees C, AM from the PF and AL groups showed a greater enhancement of phagocytic activity than AM from the DEF group, which was slightly enhanced. When the effect of MAF prepared from splenic cells of rats of the PF or DEF groups on the phagocytosis of AM was observed, MAF from the PF group showed an approximate 35% increase of phagocytic ability compared to the supernatant of splenic cells cultured with medium only. However, MAF from the DEF group had no effect on phagocytosis. These results suggest that pyridoxine deficiency affects not only phagocytic function of AM responsible for host defense in the lung but also MAF production by splenic cells.
我们测定了喂食含或不含吡哆醇饮食4周的大鼠肺泡巨噬细胞（AM）对调理素化绵羊红细胞的吞噬作用。在吡哆醇缺乏（DEF）组和配对喂养对照（PF）组中，AM的吞噬程度高于随意进食对照（AL）组的大鼠。在37℃下用巨噬细胞激活因子（MAF）如淋巴因子进行体外处理4小时后，PF组和AL组的AM吞噬活性增强程度大于DEF组，DEF组仅略有增强。当观察PF组或DEF组大鼠脾细胞制备的MAF对AM吞噬作用的影响时，与仅用培养基培养的脾细胞上清液相比，PF组的MAF吞噬能力提高了约35%。然而，DEF组的MAF对吞噬作用没有影响。这些结果表明，吡哆醇缺乏不仅影响肺部负责宿主防御的AM的吞噬功能，还影响脾细胞产生MAF。
