Pompeu M L, Freitas L A, Santos M L, Barral A, Barral-Netto M
Faculdade de Medicina, Universidade Federal da Bahia R. Joao das Botas, Salvador-Bahia, Brazil.
Exp Parasitol. 1992 Mar;74(2):169-76. doi: 10.1016/0014-4894(92)90044-b.
In vitro studies have shown that both macrophage activation and destruction of parasitized macrophages lead to leishmania destruction. The relative role played by such mechanisms in vivo have not been properly evaluated. We took advantage of the model of intravenous immunization with solubilized leishmanial antigen which renders partially resistant the otherwise highly susceptible BALB/c mice to address this issue avoiding the interference of different genetic backgrounds. Leishmania destruction occurred in three situations: destruction of the parasitized macrophage, which were in close contact with lymphocytes or eosinophils; extracellular damage, always surrounded by small foci of granulocytes; and parasite damage inside activated macrophages. Destruction of the parasitized macrophages was frequently seen in immunized and protected animals. Our observations suggest that destruction of parasite-loaded macrophages is an important mechanism of host protection in experimental cutaneous leishmaniasis.
体外研究表明，巨噬细胞的激活以及被寄生巨噬细胞的破坏都会导致利什曼原虫的破坏。这些机制在体内所起的相对作用尚未得到恰当评估。我们利用了用可溶性利什曼原虫抗原进行静脉免疫的模型，该模型使原本高度易感的BALB/c小鼠产生部分抗性，以解决这一问题，避免不同遗传背景的干扰。利什曼原虫的破坏发生在三种情况下：与淋巴细胞或嗜酸性粒细胞紧密接触的被寄生巨噬细胞的破坏；总是被粒细胞小病灶包围的细胞外损伤；以及活化巨噬细胞内的寄生虫损伤。在免疫和受保护的动物中经常可以看到被寄生巨噬细胞的破坏。我们的观察结果表明，在实验性皮肤利什曼病中，负载寄生虫的巨噬细胞的破坏是宿主保护的重要机制。
