Flescher E, Keisari Y, Lengy J, Gold D
Department of Medicine, University of Texas Health Science Center, San Antonio 78284.
Parasitology. 1991 Aug;103 Pt 1:61-4. doi: 10.1017/s0031182000059291.
Lysozyme secretion from macrophages of Schistosoma mansoni-infected mice was time dependent, rising significantly from the 8th week post-infection, the macrophages thereafter exhibiting very high levels (greater than 90%) of schistosomulicidal activity. Despite the ability of lysozyme to kill schistosomula in vitro, the concentrations required for such killing were several hundred-fold to several thousand-fold higher than those detected in the supernatants from infected-mice macrophages cultured with or without schistosomula. An in vitro lysozyme inhibitor, N,N,N-triacetyl chitobiose, did not abrogate the cytotoxic ability of macrophages from schistosome-infected mice, but an inhibitor of arginine-dependent cytotoxicity, NG-monomethyl arginine, markedly inhibited schistosomulicidal activity. Evidently, concentrations of ambient lysozyme from macrophage cultures are too low to affect schistosomula in culture, while the main schistosomulicidal pathway in vitro seems to be arginine dependent.
曼氏血吸虫感染小鼠巨噬细胞的溶菌酶分泌具有时间依赖性，感染后第8周显著升高，此后巨噬细胞表现出非常高的（大于90%）杀血吸虫活性。尽管溶菌酶在体外具有杀死血吸虫幼虫的能力，但这种杀伤所需的浓度比在有或没有血吸虫幼虫培养的感染小鼠巨噬细胞上清液中检测到的浓度高出数百倍至数千倍。一种体外溶菌酶抑制剂N，N，N-三乙酰壳二糖并未消除血吸虫感染小鼠巨噬细胞的细胞毒性能力，但精氨酸依赖性细胞毒性抑制剂NG-单甲基精氨酸显著抑制了杀血吸虫活性。显然，巨噬细胞培养物中环境溶菌酶的浓度过低，无法影响培养中的血吸虫幼虫，而体外主要的杀血吸虫途径似乎是精氨酸依赖性的。
