Saito H, Tomioka H, Watanabe T, Sato K
Infect Immun. 1986 Jan;51(1):163-7. doi: 10.1128/iai.51.1.163-167.1986.
The mechanisms by which human oligodendroglial cells, KG-1-C cells, phagocytose mycobacteria, especially Mycobacterium leprae, were studied. The ability of glial cells to phagocytose M. leprae was inhibited by azide, dinitrophenol (inhibitors of oxidative phosphorylation), and iodoacetamide but not fluoride (both are inhibitors of glycolysis). Thus, the energy metabolism dependency is somewhat different from that of peritoneal macrophages and polymorphonuclear leukocytes, the phagocytic capacities of which are mainly dependent on glycolysis. Phagocytosis of M. leprae by KG-1-C cells was markedly suppressed by a microfilament inhibitor (cytochalasin B) but not microtubule inhibitors (colchicine and vinblastine), as with macrophages. The phagocytosis of M. leprae by KG-1-C cells was dependent on the lipid and somewhat on the sugar ligands of the organism. Moreover, the phagocytosis of a given mycobacterium by KG-1-C cells correlated well with its hydrophobicity, thus revealing the importance of some lipid moieties on the surface of bacteria in the establishment of rigid binding interaction of bacteria with KG-1-C cells, before the onset of engulfment. Electric charge of a given microorganism did not correlate with its phagocytosis by KG-1-C cells.
本研究探讨了人少突胶质细胞、KG-1-C细胞吞噬分枝杆菌,尤其是麻风分枝杆菌的机制。叠氮化物、二硝基苯酚(氧化磷酸化抑制剂)和碘乙酰胺可抑制神经胶质细胞吞噬麻风分枝杆菌的能力,但氟化物(二者均为糖酵解抑制剂)则无此作用。因此,能量代谢依赖性与腹膜巨噬细胞和多形核白细胞有所不同,后二者的吞噬能力主要依赖糖酵解。与巨噬细胞一样,微丝抑制剂(细胞松弛素B)可显著抑制KG-1-C细胞对麻风分枝杆菌的吞噬作用,但微管抑制剂(秋水仙碱和长春碱)则无此作用。KG-1-C细胞对麻风分枝杆菌的吞噬作用依赖于该生物体的脂质,在一定程度上也依赖于糖类配体。此外,KG-1-C细胞对特定分枝杆菌的吞噬作用与其疏水性密切相关,这表明在吞噬开始前,细菌表面的某些脂质部分对于细菌与KG-1-C细胞建立牢固的结合相互作用至关重要。特定微生物的电荷与其被KG-1-C细胞吞噬的作用无关。