Connelly M C, Kierszenbaum F
Biochem Biophys Res Commun. 1984 Jun 29;121(3):931-9. doi: 10.1016/0006-291x(84)90766-6.
The presence of phospholipase A2 (PLA2) significantly increased the association between Trypanosoma cruzi and macrophages. This effect reflected alterations to the parasite membrane since it was reproduced only when the parasite but not the macrophage was pretreated with PLA2. That PLA2 activity was responsible for the noted enhancement was indicated by the ability of the specific substrate phosphatidylcholine to block it. The presence of the PLA2 inhibitors quinacrine, 4-bromophenacyl bromide or phentermine markedly inhibited parasite-macrophage association. Quinacrine also inhibited association of the parasite with a non-phagocytic host cell. These results suggested a role for endogenous PLA2 in the initial stages of cell infection by T. cruzi.
磷脂酶A2（PLA2）的存在显著增强了克氏锥虫与巨噬细胞之间的结合。这种效应反映了寄生虫膜的改变，因为只有当寄生虫而非巨噬细胞用PLA2预处理时才会重现这种效应。特定底物磷脂酰胆碱能够阻断这种效应，这表明PLA2活性是导致上述增强作用的原因。PLA2抑制剂奎纳克林、4-溴苯甲酰溴或芬特明的存在显著抑制了寄生虫与巨噬细胞的结合。奎纳克林还抑制了寄生虫与非吞噬性宿主细胞的结合。这些结果表明内源性PLA2在克氏锥虫细胞感染的初始阶段发挥作用。
