Vital fluorescence microscopy of lysosomes in cultured mouse peritoneal macrophages during their interactions with microorganisms and active substances. III. Interactions of macrophages with endozoits of Toxoplasma gondii RH strain and their soluble substance.

T N Khavkin, I S Freidlin, A K Shustrov
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Abstract

Macrophages with lysosomes pinpointed by quinacrine-induced fluorescence were infected with the endozoits of Toxoplasma gondii RH strain (peritoneal exudate of infected mouse), or treated with liquid (acellular) fraction of the same exudate. Dead toxoplasmas ingested by macrophages come into contact with the stained lysosomes of the cell and acquire a diffuse fluorescence. Viable toxoplasmas do not give fluorescence, which means that they do not come into contact with lysosomes, either primary or secondary. This supports the hypothesis that toxoplasmas can prevent lysosomes from fusing with the phagosomes of the host cell. Moderate doses of soluble products of toxoplasmas contained in peritoneal exudate cause an excessive output of macrophage lysosomes which points to the activation of macrophages; high doses of challenge inhibit the phagocytosis of toxoplasmas and damage macrophages. The pathogenicity of toxoplasmas due to their ability to inhibit the fusion of lysosomes and phagosomes and the cellular action of their soluble products is discussed.

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培养的小鼠腹膜巨噬细胞与微生物和活性物质相互作用时溶酶体的荧光显微镜。3刚地弓形虫RH株巨噬细胞与内殖体及其可溶性物质的相互作用。
用刚地弓形虫RH株(感染小鼠的腹膜渗出液)内殖体感染带有溶酶体的巨噬细胞,或用同一渗出液的液体(无细胞)部分处理。被巨噬细胞吞噬的死亡弓形虫与细胞的染色溶酶体接触并获得弥漫荧光。活的弓形虫不发出荧光,这意味着它们不与溶酶体接触,无论是原发性的还是继发性的。这支持了弓形虫可以阻止溶酶体与宿主细胞吞噬体融合的假设。腹膜渗出液中含有适量的可溶性弓形虫产物,可引起巨噬细胞溶酶体的过量输出,这表明巨噬细胞被激活;高剂量的攻毒抑制弓形虫的吞噬作用并损伤巨噬细胞。讨论了弓形虫的致病性,因为它们能够抑制溶酶体和吞噬体的融合,以及它们的可溶性产物的细胞作用。
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